NCI Drug Dictionary

807 results found for: P

p-cadherin antagonist PF-03732010: An agent that inhibits p-cadherin (cdh3), with potential antineoplastic activity. PF-03732010 binds to and inhibits the activity of p-cadherin. Inhibition of the activity of p-cadherin may inhibit tumor cell invasion and proliferation in p-cadherin expressing tumor cells. P-cadherin, a cell-surface protein and member of the cadherin family, is overexpressed in a variety of solid tumors, and plays a role in cell adhesion, motility, invasion and proliferation.
P-cadherin inhibitor PCA062: An agent that inhibits p-cadherin, with potential antineoplastic activity. Upon intravenous infusion, PCA062 binds to and inhibits the activity of p-cadherin. Inhibition of the activity of p-cadherin may inhibit both invasion and proliferation of p-cadherin expressing tumor cells. P-cadherin, a cell-surface protein and member of the cadherin family, is overexpressed in a variety of tumors and plays a role in cell adhesion, motility, invasion, and proliferation.
P-cadherin-targeting agent PF-06671008: An agent that targets p-cadherin (CDH3), with potential antineoplastic activity. Upon administration, PF-06671008 binds to and inhibits the activity of p-cadherin; this may inhibit both invasion and proliferation of p-cadherin-expressing tumor cells. P-cadherin, a cell-surface protein and member of the cadherin family, is overexpressed in a variety of tumors and plays a role in cell adhesion, motility, invasion, and proliferation.
P-glycoprotein inhibitor HM30181AK: An inhibitor of the adenosine triphosphate (ATP)-binding cassette (ABC) transporter P-glycoprotein (P-gp), with adjuvant activity. Upon oral administration, P-gp inhibitor HM30181AK selectively binds to and inhibits the multidrug resistance (MDR) efflux pump P-gp, which prevents the efflux of various chemotherapeutic agents from intestinal epithelial cells to the gastrointestinal tract. This leads to an increase in both oral bioavailability and therapeutic efficacy. P-gp prevents the intestinal uptake and intracellular accumulation of various cytotoxic agents. HM30181AK is not systemically absorbed.
P-p68 inhibitor RX-5902: An orally bioavailable small molecule inhibitor of phosphorylated-p68 RNA helicase (P-p68), with potential anti-proliferative and antineoplastic activity. Upon oral administration, P-p68 inhibitor RX-5902 may both inhibit the activity of the anti-apoptotic B-cell lymphoma 2 (Bcl-2) protein and facilitate the induction of cyclin-dependent kinase inhibitor 1 (p21). This may prevent G2/M cell cycle progression and lead to growth inhibition in tumor cells. P-p68 is overexpressed in various types of solid tumors but absent in normal tissues, and plays a role in tumor progression and metastasis. p21 is a potent cyclin-dependent kinase inhibitor which regulates cell cycle progression and mediates both growth arrest and cellular senescence.
p.DOM-WT1-126 DNA vaccine: A fusion DNA vaccine containing the first domain of fragment C (FrC) of tetanus toxin (TT865-1120) (p.DOM) fused to the human Wilms' Tumor gene-1 (WT1)-derived MHC class I-binding epitope WT1.126, with potential antitumor activity. Upon vaccination with p.DOM-WT1-126 DNA and subsequent electroporation, this vaccine may induce a WT1 epitope-specific cytotoxic T-lymphocyte (CTL) response against WT1 expressing cells, resulting in cell lysis and inhibition of cancer cell proliferation in WT1-overexpressing cancer cells. WT1, a tumor associated antigen, is overexpressed in most types of leukemia and in a variety of solid cancers. The FrC of tetanus toxin contains the MHC II-binding sequence, p30, which induces T-helper cell activation for long-lasting immunity.
p.DOM-WT1-37 DNA vaccine: A fusion DNA vaccine containing the first domain of fragment C (FrC) of tetanus toxin (TT865-1120) (p.DOM) fused to the human Wilms' Tumor gene-1 (WT1)-derived MHC class I-binding epitope WT1.37, with potential antitumor activity. Upon vaccination with p.DOM-WT1-37 DNA and subsequent electroporation, this vaccine may induce a WT1 epitope-specific cytotoxic T-lymphocyte (CTL) response against WT1 expressing cells, resulting in cell lysis and inhibition of cancer cell proliferation in WT1-overexpressing cancer cells. WT1, a tumor associated antigen, is overexpressed in most types of leukemia and in a variety of solid cancers. The FrC of tetanus toxin contains the MHC II-binding sequence, p30, which induces T-helper cell activation for long-lasting immunity.
p21 gene activator saRNA RAG-01: A small activating RNA (saRNA) targeting the tumor suppressor gene p21, with potential antineoplastic activity. Upon intravesical instillation of p21 gene activator saRNA RAG-01, the saRNA targets and activates the expression of the p21 gene and restores p21 therapeutic protein levels. This may decrease bladder tumor cell growth. Downregulation of p21 plays a key role in tumorigenesis. p21 is crucial for regulating the progression of the cell cycle and plays an essential role in halting the proliferation of cancer cells.
P2RX3 antagonist BAY 1817080: An orally bioavailable antagonist of the purinergic receptor P2X ligand-gated ion channel 3 (P2RX3), which may potentially be used to suppress pain and chronic cough. Upon oral administration, P2RX3 antagonist BAY1817080 selectively binds to and inhibits P2RX3 expressed on sensory nerve fibers. This may inhibit P2RX3-mediated afferent nerve fiber signaling including respiratory tract afferent nerve fiber signaling, and result in the suppression of pain and chronic cough. P2RX3 plays an important role in the cough reflex. It is also a natural mediator of pain and neurogenic inflammation.
P30-linked EphA2/CMV pp65/survivin peptide vaccine P30-EPS: A peptide vaccine comprised of three immunogenic tetanus toxoid epitope P30-linked tumor-associated antigen (TAA) peptides, P30-linked Ephrin receptor A2 (EphA2), P30-linked cytomegalovirus (CMV) matrix protein pp65 (65 kDa lower matrix phosphoprotein; UL83) and P30-linked survivin, with potential immunostimulating and antineoplastic activities. Upon administration, P30-linked EphA2/CMV pp65/survivin peptide vaccine P30-EPS may elicit a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing EphA2, CMV pp65 and survivin. The tyrosine kinase receptor EphA2 and the inhibitor of apoptosis (IAP) family member survivin, overexpressed in certain tumor types, play key roles in tumor cell proliferation. The CMV pp65 protein is expressed in certain tumor types. The covalent linkage of P30 to the TAA peptides enhances TAA-specific anti-tumor immune responses, compared with the administration of the TAA peptides alone.
p300/CBP bromodomain inhibitor CCS1477: An orally bioavailable, small molecule inhibitor of the highly conserved bromodomains of the histone acetyltransferase (HAT) paralogs, p300 (E1A-associated protein p300; p300 HAT) and CREB binding protein (CBP), with potential antineoplastic activity. Upon oral administration, p300/CBP bromodomain inhibitor CCS1477 selectively and reversibly binds to the bromodomains of p300 and CBP. This disrupts the acetylation of histones and other proteins and prevents the co-activation of key transcription factors that contribute to tumor progression including the androgen receptor (AR), androgen receptor splice variants (AR-SV), hypoxia-inducible factor 1-alpha (HIF-1-alpha) and Myc proto-oncogene protein (c-Myc). The HAT paralogs p300 and CBP are key transcriptional co-activators that are essential for a multitude of cellular processes and are implicated in the progression and therapeutic resistance of certain cancers.
p38 MAPK inhibitor LY2228820 dimesylate: The dimesylate salt form of LY2228820, a tri-substituted imidazole derivative and orally available, p38 mitogen-activated protein kinase (MAPK) inhibitor with potential anti-inflammatory and antineoplastic activities. Upon administration, LY2228820 inhibits the activity of p38, particularly the alpha and beta isoforms, thereby inhibiting MAPKAPK2 phosphorylation and preventing p38 MAPK-mediated signaling. This may inhibit the production of a variety of cytokines involved in inflammation, cellular proliferation and angiogenesis such as tumor necrosis factor alpha (TNFa), interleukin (IL)-1, -6 and -8, vascular endothelial growth factor, and macrophage inflammatory protein-1 alpha. Ultimately this induces apoptosis and reduces tumor cell proliferation. In addition, inhibition of the p38 MAPK pathway by LY2228820 increases the antineoplastic activity of certain chemotherapeutic agents. p38 MAPK, a serine/threonine protein kinase that is often upregulated in cancer cells, plays a crucial role in tumor cell proliferation, angiogenesis and metastasis.
p38 MAPK inhibitor LY3007113: An orally active p38 mitogen-activated protein kinase (MAPK) inhibitor with potential immunomodulating, anti-inflammatory, and antineoplastic activity. Upon administration, LY3007113 inhibits the activity of p38, thereby preventing p38 MAPK-mediated signaling. This may result in the inhibition of the production of proinflammatory cytokines and the induction of tumor cell apoptosis. p38 MAPK, a serine/threonine protein kinase often upregulated in cancer cells, plays a crucial part in the production of a variety of cytokines involved in inflammation and cellular proliferation such as tumor necrosis factor (TNF) and interleukin (IL)-1 and -6.
p53 mutant reactivator APR-548: An analog of eprenetapopt and an orally bioavailable, small molecule prodrug and reactivator of p53 mutants, with potential antineoplastic activity. Upon oral administration of p53 mutant reactivator APR-548, as a prodrug APR-548 is converted to its active form, 2-methylene-quinuclidin-3-one (MQ), which binds to mutant p53 proteins at their DNA-binding domain and restores wild-type p53 protein structure and activity. This reconstitutes endogenous p53 activity, blocks tumor cell cycle progression and induces apoptosis in tumor cells expressing the TP53 mutations. p53, a tumor suppressor and transcription factor normally activated upon DNA damage, is frequently mutated and overexpressed in cancer cells; it plays a key role in both DNA repair and the induction of apoptosis.
p53 peptide vaccine: A peptide-based cancer vaccine composed of amino acids 264 to 272 of the wild-type protein encoded by the P53 gene. p53 peptide vaccine may elicit an HLA-A2.1-restricted cytotoxic T lymphocyte immune response against tumor cells that overexpress p53 protein.
p53 synthetic long peptide (70-251) vaccine: A peptide vaccine consisting of 10 synthetic long peptides (SLPs), 25-30 amino acids in size and derived from the middle portion of p53 (amino acids 70-251), mixed with the adjuvant Montanide ISA-51 with potential immunostimulatory and antitumor activities. Upon administration, p53 synthetic long peptide (70-251) vaccine may stimulate the host immune system to mount a cytotoxic T-cell lymphocyte (CTL) response against p53-expressing tumor cells. p53, a tumor associated antigen (TAA), may be overexpressed in variety of cancer cell types.
p53 Y220C mutant reactivator PC14586: An orally bioavailable, small molecule reactivator of the p53 Y220C mutant, with potential antineoplastic activity. Upon oral administration, p53 Y220C mutant reactivator PC14586 selectively targets and binds to the crevice created by the p53 Y220C mutation, which normalizes and restores wild-type p53 protein structure and activity. This blocks tumor cell cycle progression and induces apoptosis in tumor cells expressing the p53 Y220C mutant. The p53 gene, a tumor suppressor gene, is mutated in many tumor types. The p53 protein plays a key role in the regulation of apoptosis and cellular proliferation.
p53 Y220C reactivator JAB-30355: An orally bioavailable reactivator of the tumor suppressor protein p53 mutation TP53 Y220C, with potential antineoplastic activity. Upon oral administration, p53 Y220C reactivator JAB-30355 selectively targets, binds to and restores the conformation of TP53 Y220C. This restores the transcriptional activity of TP53 Y220C, reactivates p53-mediated signaling and restores p53 function. This induces cell cycle arrest and apoptosis in tumor cells expressing the TP53 Y220C mutation and inhibits proliferation of tumor cells expressing the TP53 Y220C mutant. p53, a tumor suppressor gene, plays a key role in the regulation of cell cycle arrest, apoptosis, senescence and DNA repair. P53 is often mutated in many tumor cells, resulting in the loss of apoptosis regulation and abnormal cell proliferation. TP53 Y220C is a hotspot loss-of-function mutation.
p53-HDM2 protein-protein interaction inhibitor MI-773: An orally available spiro-oxindole HDM2 (human double minute 2) antagonist with potential antineoplastic activity. Upon oral administration, the p53-HDM2 protein-protein interaction inhibitor MI-773 binds to HDM2, preventing the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the proteosome-mediated enzymatic degradation of p53 is inhibited and the transcriptional activity of p53 is restored, which may result in the restoration of p53 signaling and lead to the p53-mediated induction of tumor cell apoptosis. HDM2, a zinc finger protein and a negative regulator of the p53 pathway, is often overexpressed in cancer cells. It has been implicated in cancer cell proliferation and survival.
p53/HDM2 interaction inhibitor CGM097: An orally bioavailable HDM2 (human homolog of double minute 2) antagonist with potential antineoplastic activity. Upon oral administration, p53/HDM2 interaction inhibitor CGM097 inhibits the binding of the HDM2 protein to the transcriptional activation domain of the tumor suppressor protein p53. By preventing this HDM2-p53 interaction, the proteosome-mediated enzymatic degradation of p53 is inhibited, which may result in the restoration of p53 signaling and, thus, the p53-mediated induction of tumor cell apoptosis. HDM2, a zinc finger nuclear phosphoprotein, is a negative regulator of the p53 pathway, often overexpressed in cancer cells and has been implicated in cancer cell proliferation and survival.
p70S6K inhibitor LY2584702: An orally available inhibitor of p70S6K signaling, with potential antineoplastic activity. p70S6K inhibitor LY2584702 inhibits ribosomal protein S6 Kinase (p70S6K), and prevents phosphorylation of the S6 subunit of ribosomes, thereby inhibiting normal ribosomal function within tumor cells leading to a decrease in protein synthesis and in cellular proliferation. P70S6K, a serine/threonine kinase, acts downstream of PIP3 and phosphoinositide-dependent kinase-1 in the PI3 kinase pathway, is often upregulated in a variety of cancer cells, and is involved in the regulation of cell growth, proliferation, motility, and survival.
p70S6K/Akt inhibitor M-2698: An orally available inhibitor of the serine/threonine protein kinases ribosomal protein S6 Kinase (p70S6K) and Akt (protein kinase B), with potential antineoplastic activity. Upon administration, p70S6K/Akt inhibitor M-2698 binds to and inhibits the activity of p70S6K and Akt. This prevents the activation of the PI3K/Akt/p70S6K signaling pathway and inhibits tumor cell proliferation in cancer cells that have an overactivated PI3K/Akt/p70S6K signaling pathway. Constitutive activation and dysregulated signaling of the PI3K/Akt/p70S6K pathway are frequently associated with tumorigenesis of many tumor types; targeting multiple kinases in this pathway is more efficacious than targeting a single kinase.
p97 inhibitor CB-5083: An orally bioavailable inhibitor of valosin-containing protein (VCP) p97, with potential antineoplastic activity. Upon oral administration, CB-5083 specifically binds to and inhibits the activity of p97. This prevents ubiquitin-dependent protein degradation and causes cellular accumulation of poly-ubiquitinated proteins. The inhibition of endoplasmic reticulum (ER)-associated protein degradation activates the ER-dependent stress response pathway, and leads to both an induction of apoptosis and inhibition of cell proliferation in susceptible tumor cells. p97, a type II AAA ATPase, plays a key role in cellular protein homeostasis. Its overexpression in many tumor cell types is associated with increased tumor cell proliferation and survival.
p97 Inhibitor CB-5339: An orally bioavailable, selective, second-generation inhibitor of valosin-containing protein (VCP)/p97, with potential antineoplastic activity. Upon oral administration, p97 inhibitor CB-5339 binds to and inhibits the activity of p97. This prevents ubiquitin-dependent protein degradation and causes cellular accumulation of poly-ubiquitinated proteins. The inhibition of endoplasmic reticulum (ER)-associated protein degradation activates the ER-dependent stress response pathway, and leads to both an induction of apoptosis and the inhibition of cell proliferation in susceptible tumor cells. VCP/p97, a type II AAA+ ATPase, plays a key role in cellular protein homeostasis processes including ER-associated degradation (ERAD), chromatin associated degradation (CAD) and the DNA damage response (DDR). Its overexpression in many tumor cell types is associated with increased tumor cell proliferation and survival.
p97 inhibitor CB-5339 tosylate: The tosylate salt of CB-5339, an orally bioavailable, selective, second-generation inhibitor of valosin-containing protein (VCP)/p97, with potential antineoplastic activity. Upon oral administration, p97 inhibitor CB-5339 binds to and inhibits the activity of p97. This prevents ubiquitin-dependent protein degradation and causes cellular accumulation of poly-ubiquitinated proteins. The inhibition of endoplasmic reticulum (ER)-associated protein degradation activates the ER-dependent stress response pathway, and leads to both an induction of apoptosis and the inhibition of cell proliferation in susceptible tumor cells. VCP/p97, a type II AAA+ ATPase, plays a key role in cellular protein homeostasis processes including endoplasmic reticulum associated degradation (ERAD), chromatin associated degradation (CAD) and the DNA damage response (DDR). Its overexpression in many tumor cell types is associated with increased tumor cell proliferation and survival.
PA-1-STK ovarian carcinoma vaccine: A cell-based cancer vaccine with potential antineoplastic activity. PA-1-STK ovarian carcinoma vaccine is produced by transducing the ovarian cancer cell line, PA-1, with the herpes simplex thymidine kinase (HSV-tk) gene, resulting in a cell line, PA-1-STK, that permanently expresses the HSV tk gene. Upon transfection into malignant cells, this vaccine is capable of sensitizing tumor cells in response to an antiviral drug such as ganciclovir, which is readily phosphorylated by the TK enzyme to its active form. Administration of ganciclovir following PA-1 STK transfection results in enhanced cytotoxicity of the transfected tumor cells. Additionally, adjacent non-transfected cells are also killed by the activated antiviral drug, a phenomenon referred to as the bystander effect that occurs with this type of suicide-gene transfer technique.
Pabal: (Other name for: carbetocin)
pacanalotamab: A short half-life bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; TNFRSF17), fused to one that is directed against the CD3 antigen found on T lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration of pacanalotamab, this bispecific antibody binds to both CD3 on cytotoxic T lymphocytes (CTLs) and BCMA found on BCMA-expressing tumor cells. This activates and redirects CTLs to BCMA-expressing tumor cells, which results in the CTL-mediated cell death of BCMA-expressing tumor cells. BCMA, a member of the tumor necrosis factor receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival.
paclitaxel: A compound extracted from the Pacific yew tree Taxus brevifolia with antineoplastic activity. Paclitaxel binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell Leukemia 2).
paclitaxel and hyaluronic acid: A water soluble, muco-adhesive co-formulation composed of the natural taxane paclitaxel conjugated to the naturally occurring proteoglycan hyaluronic acid, with potential antineoplastic activity. Upon intravesical administration of paclitaxel and hyaluronic acid, HA targets and binds to CD44 expressed on cancer cells. In turn, paclitaxel binds to and stabilizes microtubules, preventing their depolymerization and inhibiting cellular motility, mitosis, and replication in CD44-expressing tumor cells. CD44, a transmembrane glycoprotein and HA receptor expressed in healthy tissue, is overexpressed in a variety of cancer cell types and plays a key role in tumor cell proliferation, migration and survival.
paclitaxel injection concentrate for nanodispersion: A nanoparticle-based injectable concentrate containing the water-insoluble taxane paclitaxel, with potential antineoplastic activity. Upon reconstitution and administration, paclitaxel binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. Compared to paclitaxel alone, the nanodispersion-based formulation uses less toxic solvents and allows for administration of higher doses resulting in higher concentrations of paclitaxel at the tumor site, and an increased safety profile.
paclitaxel liposome: A liposome-encapsulated formulation of paclitaxel, a taxoid compound extracted from the Pacific yew tree Taxus brevifolia, with antineoplastic property. Paclitaxel binds to tubulin and interferes with the assembly/disassembly dynamics of microtubules, thereby resulting in the inhibition of cell division. This agent also induces apoptosis via inactivation of the apoptosis inhibitor, B-cell Leukemia 2 (Bcl-2) protein. Paclitaxel liposome formulation potentially enhances delivery of higher doses of paclitaxel to the target tissues and exhibits lower systemic toxicity.
paclitaxel poliglumex: The agent paclitaxel linked to a biodegradable, water-soluble polyglutamate polymer with antineoplastic properties. The polyglutamate residue increases the water solubility of paclitaxel and allows delivery of higher doses than those achievable with paclitaxel alone. Paclitaxel promotes microtubule assembly and prevents microtubule depolymerization, thus interfering with normal mitosis.
paclitaxel polymeric micelle formulation NANT-008: A nanoparticle-based formulation consisting of polymeric micelles encapsulating the taxane paclitaxel, with potential antineoplastic activity. Paclitaxel is covalently bound to polyethylene glycol (PEG)-based block copolymers which forms a micellar structure with an outer hydrophilic PEG shell surrounding the hydrophobic paclitaxel. Upon administration of the paclitaxel polymeric micelle formulation NANT-008, the nanoparticles are stable in the bloodstream and specifically accumulate in the tumor tissue. Due to the acidic conditions in the tumor and the pH-responsive nature of the micelles, paclitaxel is released in the tumor environment. Paclitaxel binds to microtubules, promotes microtubule assembly, and prevents depolymerization, thus interfering with normal mitosis. Compared to the administration of paclitaxel alone, this formulation increases the solubility of paclitaxel, enhances its specific retention in cancer tissue, and increases its therapeutic effect, while decreasing its toxicity. In addition, the micellar formulation allows the delivery of higher doses of paclitaxel to target tissues while minimizing systemic toxicity.
paclitaxel vitamin E-based emulsion formulation: A cremophor-free, P-glycoprotein-inhibiting, vitamin E-based emulsion particle formulation of paclitaxel with antineoplastic activity. Paclitaxel binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. This agent also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell Leukemia 2). The vitamin-E based emulsion allows bolus infusion without steroid premedication and may diminish hypersensitivity reactions; tumor tissue may be passively targeted due to preferential deposition of emulsion particles while an emulsion formulation component inhibits the P-glycoprotein drug efflux pump.
paclitaxel-conjugated CXCR4 peptide antagonist MB1707: A peptide-drug conjugate (PDC) of paclitaxel with an inhibitor of CXC chemokine receptor 4 (CXCR4), with potential antineoplastic activity. Upon administration of paclitaxel-conjugated CXCR4 peptide antagonist MB1707, the CXCR4 inhibitor moiety binds to the chemokine receptor CXCR4 expressed on tumor cells, thereby preventing CXCR4 binding to its ligand, stromal derived factor-1 (SDF-1), and subsequent receptor activation. This may result in decreased tumor cell proliferation and migration. In addition, paclitaxel binds to tubulin inside CXCR4-expressing tumor cells and inhibits the disassembly-assembly dynamics of microtubules, resulting in cell cycle arrest and cell death. CXCR4, a chemokine receptor belonging to the G protein-coupled receptor (GPCR) gene family, plays an important role in chemotaxis and angiogenesis and is upregulated in several tumor cell types. By targeting CXCR4-expressing tumor cells specifically, paclitaxel's efficacy is increased while minimizing systemic toxiciy.
pacritinib citrate: The citrate salt form of pacritinib, an orally bioavailable inhibitor of Janus kinase 2 (JAK2), the JAK2 mutant JAK2V617F and FMS-like tyrosine kinase 3 (FLT3; CD135; STK1; FLK2), with potential antineoplastic activity. Upon oral administration of pacritinib citrate, pacritinib competes with JAK2 and the JAK2 mutant JAK2V617F for ATP binding, which may result in inhibition of JAK2 activation, inhibition of the JAK-signal transducer and activator of transcription (STAT) signaling pathway, and the induction of apoptosis. In addition, pacritinib targets, binds to and inhibits the activity of FLT3. This inhibits FLT3-mediated signaling and the proliferation of FLT3-expressing cancer cells. JAK2, often upregulated or mutated in a variety of cancer cells, plays a key role in tumor cell proliferation and survival. The JAK2V617F gain-of-function mutation involves a valine-to-phenylalanine modification at position 617. The JAK-STAT signaling pathway is a major mediator of cytokine activity. FLT3, a class III receptor tyrosine kinase (RTK), is overexpressed or mutated in most B-lineage neoplasms and in acute myeloid leukemias. In addition, JAK2 and FLT3 play a key role in the regulation of the inflammatory response and dendritic cell (DC) proliferation, differentiation and function. Inhibition of JAK2- and FLT3-mediated signaling may suppress the generation and differentiation of DCs, and may regulate inflammatory and immune responses.
PAD regimen: A chemotherapy regimen containing bortezomib, doxorubicin and dexamethasone regimen used in the treatment of plasma cell myeloma.
Padcev: (Other name for: enfortumab vedotin-ejfv)
padeliporfin: A vascular-acting photosensitizer consisting of a water-soluble, palladium-substituted bacteriochlorophyll derivative with potential antineoplastic activity. Upon administration, paldeliporfin is activated locally when the tumor bed is exposed to low-power laser light; reactive oxygen species (ROS) are formed upon activation and ROS-mediated necrosis may occur at the site of interaction between the photosensitizer, light and oxygen. Vascular-targeted photodynamic therapy (VTP) with padeliporfin may allow tumor-site specific cytotoxicity while sparing adjacent normal tissues.
PADRE 965.10: Pan-DR epitope (PADRE) 965.10 is a helper peptide. PADRE peptides have been shown the capacity to deliver help for antibody responses in vivo. They were also found to be able to provide significant helper T-cell activity in vivo. Acts as an adjuvant.
PADRE-CMV fusion peptide vaccine: A peptide-based vaccine containing a pan HLA DR-binding epitope (PADRE) fused to a cytomegalovirus (CMV) peptide epitope, with potential anti-viral and immunomodulating activities. Upon administration, PADRE-CMV fusion peptide may stimulate a cytotoxic T-lymphocyte (CTL) response against CMV in the CMV-infected host. The synthetic peptide PADRE is a universal helper T cell epitope.
pafolacianine sodium: The sodium salt form of pafolacianine, a fluorescent imaging agent composed of a folate receptor-alpha (FRa)-targeting ligand conjugated to a fluorescent near infrared (NIR) dye, that can be used for imaging of FRa-expressing tumor cells. Upon administration, the FRa-targeting moiety of pafolacianine specifically binds to FRa expressed on tumor cells thus selectively delivering the fluorescent dye to FRa-expressing tumor cells. Upon NIR imaging, tumor cells fluoresce, which allows for the visualization and identification of FRa-overexpressing tumor cells. FRa, a high-affinity folate-binding protein and a member of the folate receptor family, is overexpressed in various cancer cell types.
PAI-1 inhibitor ACT001: The fumarate salt form of the parthenolide derivative micheliolide (MCL), and an orally bioavailable guaianolide sesquiterpene lactone and inhibitor of the protease plasminogen activator inhibitor-1 (PAI-1), with potential immunomodulating and antineoplastic activities. Upon oral administration, PAI-1 inhibitor ACT001 targets and binds to PAI-1, thereby inhibiting the PAI-1/phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway. This induces apoptosis in and inhibits the proliferation, migration and invasion of tumor cells in which the PI3K/AKT pathway is overexpressed. In addition, ACT001 binds to and inhibits the activity of inhibitor of nuclear factor kappa-B kinase subunit beta (IKK-beta), thereby inhibiting nuclear factor kappa B (NF-kB) signaling. This leads to the downregulation of manganese superoxide dismutase (MnSOD) and induces the generation of reactive oxygen species (ROS). This induces G2/M phase arrest and tumor cell apoptosis. Also, ACT001 binds to and inhibits the phosphorylation of signal transducer and activator of transcription 3 (STAT3), and reduces the expression of programmed death-ligand 1 (PD-L1). This may modulate the anti-tumor immune response. ACT001 may also affect tissue remodeling and cancer metabolism. PAI-1 plays a key role in the proliferation, migration, invasion and adhesion of cancer cells as well as multidrug resistance. It is highly expressed in certain tumors, such as gliomas. ACT001 is able to cross the blood-brain barrier (BBB).
PAK4 inhibitor PF-03758309: An orally bioavailable small-molecule inhibitor of p21-activated kinase 4 (PAK4) with potential antineoplastic activity. PAK4 inhibitor PF-03758309 binds to PAK4, inhibiting PAK4 activity and cancer cell growth. PAK4, a serine/threonine kinase belonging to the p21-activated kinase (PAK) family, is often upregulated in a variety of cancer cell types and plays an important role in cancer cell motility, proliferation, and survival.
PAK4/NAMPT inhibitor ATG-019: An orally bioavailable inhibitor of both the serine/threonine kinase P21-activated kinase 4 (PAK4) and the nicotinamide adenine dinucleotide (NAD)-synthesizing enzyme nicotinamide phosphoribosyltransferase (NAMPT; NAMPRTase), with potential antineoplastic activity. Upon administration, ATG-019 allosterically binds to, destabilizes and causes degradation of PAK4. This inhibits PAK4-mediated signaling, induces cell death in, and inhibits the proliferation of PAK4-overexpressing tumor cells. In addition, ATG-019 binds to and inhibits the activity of NAMPT. This depletes cellular NAD and inhibits NAD-dependent enzymes, both of which are needed for rapid cell proliferation; this results in tumor cell death in NAMPT-overexpressing cancer cells. PAK4, a serine/threonine kinase and member of the PAK family of proteins upregulated in various cancer cell types, regulates cell motility, proliferation and survival. NAMPT, an enzyme that is responsible for maintaining the intracellular NAD pool, plays a key role in the regulation of cellular metabolism and has cytokine-like activities. NAMPT is often overexpressed in a variety of cancers and metabolic disorders and tumor cells rely on NAMPT activity for their NAD supply.
palacaparib: An orally bioavailable central nervous system (CNS) penetrant and inhibitor of nuclear enzyme poly(ADP-ribose) polymerase (PARP) 1, with potential antineoplastic activity. Upon oral administration, palacaparib selectively binds to PARP1, thereby preventing repair of damaged DNA via the base excision repair (BER) pathway. This agent enhances the accumulation of DNA strand breaks and promotes genomic instability eventually leading to apoptosis. Palacaparib may enhance the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance. PARP1 catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and plays a key role in the repair of single strand DNA (ssDNA) breaks and double-strand break (DSBs). Palacaparib is able to penetrate the blood-brain barrier (BBB).
palazestrant: An orally available, small molecule antagonist of estrogen receptor alpha (ERalpha; ERa; ESR1; nuclear receptor subfamily 3, group A, member 1; NR3A1) and a selective ER degrader (SERD), with potential antineoplastic activity. Upon oral administration, palazestrant competes with the endogenous activating estrogenic ligand 17-beta estradiol for binding in the ligand binding pocket of ERalpha, thereby inhibiting the activity of ERalpha. Palazestrant blocks estrogen-driven transcriptional activity and induces degradation of ERalpha. This inhibits the growth and survival of ERalpha-expressing cancer cells. ERalpha, a nuclear hormone receptor, is often overexpressed and/or mutated in a variety of cancer cell types. It plays a key role in tumor cell proliferation and survival.
Palbociclib: An orally available cyclin-dependent kinase (CDK) inhibitor with potential antineoplastic activity. Palbociclib selectively inhibits cyclin-dependent kinase 4 (CDK4) and 6 (CDK6), thereby inhibiting retinoblastoma (Rb) protein phosphorylation early in the G1 phase leading to cell cycle arrest. This suppresses DNA replication and decreases tumor cell proliferation. CDK4 and 6 are serine/threonine kinases that are upregulated in many tumor cell types and play a key role in the regulation of cell cycle progression.
Palestrol: (Other name for: diethylstilbestrol)
palifermin: A recombinant form of the endogenous human keratinocyte growth factor. Palifermin binds to epithelial cell surface receptors in the lining of the mouth and gastrointestinal tract, resulting in stimulation of epithelial cell proliferation, differentiation and upregulation of cytoprotective mechanisms.
palifosfamide: A synthetic mustard compound with potential antineoplastic activity. An active metabolite of ifosfamide covalently linked to the amino acid lysine for stability, palifosfamide irreversibly alkylates and cross-links DNA through GC base pairs, resulting in irreparable 7-atom inter-strand cross-links; inhibition of DNA replication and cell death follow. Unlike ifosfamide, this agent is not metabolized to acrolein or chloroacetaldehyde, metabolites associated with bladder and CNS toxicities. In addition, because palifosfamide does not require activation by aldehyde dehydrogenase, it may overcome the tumor resistance seen with ifosfamide.
palifosfamide tromethamine: A synthetic mustard compound of the tromethamine (tris) salt of palifosfamide (Isophosphamide mustard), with potential antineoplastic activity. As the stabilized active metabolite of ifosfamide, palifosfamide irreversibly alkylates and crosslinks DNA through GC base pairs, resulting in irreparable 7-atom interstrand crosslinks. This leads to an inhibition of DNA replication and ultimately cell death. Unlike ifosfamide, this agent is not metabolized to acrolein or chloroacetaldehyde, metabolites associated with bladder and CNS toxicities. In addition, because palifosfamide does not require activation by aldehyde dehydrogenase, it may overcome the tumor resistance seen with ifosfamide. Stabilization with tris instead of lysine further increases stability and may further decrease nephrotoxicity.
palivizumab: A humanized monoclonal antibody against the fusion protein (F protein) of human respiratory syncytial virus (RSV), with prophylactic application in respiratory syncytial virus infections. RSV F protein, a small envelop glycoprotein, is not only required for cytopathic syncytia resulting from cell-to-cell fusion, but is also necessary for viral spreading and evading neutralizing antibody. Palivizumab neutralizes and inhibits fusion activity of RSV, thereby preventing syncytia formation. Administration of this antibody does not interfere with other immunizations.
palladium Pd-103: A radioisotope of the metal palladium used in brachytherapy implants or 'seed'. With a half-life of 17 days, palladium 103 administered with brachytherapy allows continuous, tumor-site specific low-energy irradiation to the tumor cell population while sparing normal adjacent tissues from radiotoxicity.
palladium-bacteriopheophorbide: A novel palladium-substituted bacteriochlorophyll derivative and photosensitizer with potential antitumor activity. Upon administration, inactive palladium-bacteriophephorbide is activated locally when the tumor bed is exposed to photoirradiation; the activated form induces local cytotoxic processes, resulting in local tissue damage, disruption of tumor vasculature, and tumor hypoxia and necrosis.
palmidrol: A natural fatty acid amide that is both a food component and an endogenously synthesized compound, with potential analgesic and anti-inflammatory activities. Upon administration, palmidrol may inhibit the release of pro-inflammatory mediators from activated mast cells. This may reduce inflammation and pain.
palonosetron hydrochloride: The hydrochloride salt of palonosetron, a carbazole derivative and a selective serotonin receptor antagonist with antiemetic activity. Palonosetron competitively blocks the action of serotonin at 5-hydroxytryptamine type 3 (5-HT3) receptors located on vagal afferents in the chemoreceptor trigger zone (CTZ), resulting in suppression of chemotherapy-induced nausea and vomiting. The CTZ is located in the area postrema on the dorsal surface of the medulla oblongata at the caudal end of the fourth ventricle and outside the blood-brain barrier (BBB).
pamidronate disodium: The disodium salt of the synthetic bisphosphonate pamidronate. Although its mechanism of action is not completely understood, pamidronate appears to adsorb to calcium phosphate crystals in bone, blocking their dissolution by inhibiting osteoclast-mediated bone resorption. This agent does not inhibit bone mineralization and formation.
pamiparib: An orally bioavailable inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP), with potential antineoplastic activity. Upon administration, pamiparib selectively binds to PARP and prevents PARP-mediated repair of single-strand DNA breaks via the base-excision repair (BER) pathway. This enhances the accumulation of DNA strand breaks, promotes genomic instability, and eventually leads to apoptosis. PARP is activated by single-strand DNA breaks and, subsequently, catalyzes post-translational ADP-ribosylation of nuclear proteins which then transduce signals to recruit other proteins to repair damaged DNA. Pamiparib may both potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance.
Pamolyn 300: (Other name for: conjugated linoleic acid)
pamrevlumab: A human monoclonal antibody targeting connective tissue growth factor (CTGF) with potential anti-fibrotic and antineoplastic activities. Pamrevlumab binds to CTGF thereby preventing the binding of the ligand to the receptor and subsequent receptor activation. As CTGF enhances the production of collagen and fibronectin, FG-319 may prevent and reverse fibrosis. In addition, FG-3019 may prevent tumor cell proliferation in CTGF-expressing tumor cells. CTGF, a member of the CCN family (CTGF, CYR61/CEF and NOV), is expressed in a variety of tumor cell types and is involved in processes such as cell proliferation, cell migration, cell adhesion, differentiation and angiogenesis.
pan FGFR inhibitor PRN1371: A highly specific covalent inhibitor of human fibroblast growth factor receptor types 1, 2, 3 and 4 (FGFR1-4) with potential antiangiogenic and antineoplastic activities. FGFR1-4 tyrosine kinase inhibitor PRN1371 specifically binds to a conserved cysteine residue in the glycine-rich loop in FGFRs and inhibits their tyrosine kinase activity, which may result in the inhibition of both tumor angiogenesis and tumor cell proliferation, and the induction of tumor cell death. FGFRs are a family of receptor tyrosine kinases, which may be upregulated in various tumor cell types and may be involved in tumor cell differentiation, proliferation and survival, and in tumor angiogenesis. This agent potently inhibits FGFR1-4 but does not inhibit other tyrosine kinases, even those that share the conserved cysteine, which may improve therapeutic responses and decrease toxicity when compared with less selective inhibitors.
pan-AKT inhibitor ARQ 751: An orally bioavailable pan inhibitor of the serine/threonine protein kinase AKT (protein kinase B) enzyme family with potential antineoplastic activity. Upon oral administration, AKT inhibitor ARQ 751 selectively binds to and inhibits the activity of the AKT isoforms 1, 2 and 3, which may result in the inhibition of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway. This may lead to a reduction in tumor cell proliferation and the induction of tumor cell apoptosis. The AKT signaling pathway is often deregulated in cancer and is associated with tumor cell proliferation, survival and migration.
pan-AKT kinase inhibitor GSK690693: An aminofurazan-derived inhibitor of Akt kinases with potential antineoplastic activity. Pan-AKT kinase inhibitor GSK-690693 binds to and inhibits Akt kinases 1, 2, and 3, which may result in the inhibition of protein phosphorylation events downstream from Akt kinases in the PI3K/Akt signaling pathway, and, subsequently, the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. In addition, this agent may inhibit other protein kinases including protein kinase C (PKC) and protein kinase A (PKA). As serine/threonine protein kinases which are involved in a number of biological processes, AKT kinases promote cell survival by inhibiting apoptosis and are required for glucose transport.
pan-DDR DNA decoy-cholesterol conjugate VIO-01: A pan-DNA damage response (DDR) DNA decoy linked to a cholesterol molecule, with potential immunomodulatory and antineoplastic activities. Upon administration of pan-DDR DNA decoy-cholesterol conjugate VIO-01, the cholesterol moiety enables tumoral and nuclear uptake of the DNA, and mimics DNA double-strand breaks (DSBs) inside the tumor cells. This triggers false DNA break signals, binding to and activating DNA repair proteins including poly(ADP-ribose) polymerase (PARP) 1, KU70/80, MRN complex and MSH2/MSH3. This prevents the recruitment of these repair proteins at the actual damage site and inhibits various DNA DSB repair pathways. This promotes genetic instability and enhances the accumulation of single and double strand DNA breaks, ultimately leading to apoptosis of tumor cells. VIO-01 also triggers the activation of the stimulator of interferon genes protein (STING; transmembrane protein 173; TMEM173) pathway in immune cells in the tumor microenvironment (TME). This leads to the production of pro-inflammatory cytokines, including interferons (IFNs), enhances the cross-presentation of tumor-associated antigens (TAAs) by dendritic cells (DCs), and induces a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. PARP1 catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and plays a key role in the repair of single strand DNA (ssDNA) breaks and DSBs. STING, a transmembrane protein that activates immune cells in the TME, plays a key role in the activation of the innate immune system.
pan-FGFR inhibitor ABSK-121-NX: An orally bioavailable, small molecule pan-inhibitor of fibroblast growth factor receptor (FGFR) family proteins, with potential antineoplastic activity. Upon oral administration, pan-FGFR inhibitor ABSK-121 binds to and inhibits FGFR family proteins, including FGFR2 and FGFR3 gatekeeper, molecular brake, and activation loop mutations. This prevents FGFR-mediated signaling, and inhibits both tumor angiogenesis and proliferation of FGFR-overexpressing tumor cells. FGFR, a family of receptor tyrosine kinases upregulated in many tumor cell types, plays a key role in cellular proliferation, cell survival and angiogenesis.
pan-FGFR inhibitor LY2874455: An orally bioavailable pan-inhibitor of fibroblast growth factor receptor (FGFR) family proteins, with potential antineoplastic activity. Upon oral administration, FGFR inhibitor LY2874455 binds to and inhibits FGFR subtypes 1 (FGFR1), 2 (FGFR2), 3 (FGFR3) and 4 (FGFR4), which results in the inhibition of FGFR-mediated signal transduction pathways. This inhibits both tumor angiogenesis and proliferation of FGFR-overexpressing tumor cells. FGFR, a family of receptor tyrosine kinases upregulated in many tumor cell types, plays a key role in cellular proliferation, cell survival and angiogenesis.
pan-FLT3/Pan-BTK multi-kinase inhibitor CG-806: An orally bioavailable reversible, pan-inhibitor of both FMS-like tyrosine kinase 3 (FLT3; CD135; STK1; FLK2) and Bruton's tyrosine kinase (BTK; Bruton agammaglobulinemia tyrosine kinase), with potential antineoplastic activity. Upon oral administration, the pan-FLT3/pan-BTK multi-kinase inhibitor CG-806 targets, non-covalently binds to and inhibits the activity of both FLT3, including both wild-type (WT) FLT3 and FLT3-ITD (internal tandem duplications), tyrosine kinase domain (FLT3-TKD), and gatekeeper (FLT3-F691L) mutant forms, and BTK, including both the WT and its C481S mutant (BTK-C481S) form. This inhibits both uncontrolled FLT3-mediated and B-cell antigen receptor (BCR)-mediated signaling, respectively. This results in the inhibition of proliferation in tumor cells overexpressing FLT3 and BTK. In addition, CG-806 also inhibits, to a lesser degree, other oncogenic kinases, such as MET, RET, discoidin domain-containing receptor 2 (DDR2), Aurora kinase A, and interleukin-2-inducible T-cell kinase (ITK). FLT3, a class III receptor tyrosine kinase (RTK), is overexpressed or mutated in most B-lineage neoplasms and in acute myeloid leukemias (AMLs), and plays a key role in tumor cell proliferation. BTK, a member of the Src-related BTK/Tec family of cytoplasmic tyrosine kinases essential to BCR signaling, is overexpressed or mutated in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B lymphocytes.
pan-HER inhibitor FCN-411: An orally bioavailable pan-human epidermal growth factor receptors (EGFR; HER) tyrosine kinase inhibitor, with potential antineoplastic activity. Upon oral administration, pan-HER inhibitor FCN-411 targets, binds to and inhibits human epidermal growth factor receptors (HER) EGFR (HER1; ErbB1), HER2 (neu, ErbB-2), HER3 (ErbB-3) and HER4 (ErbB-4), and including EGFR activating and resistance mutations such as EGFR T790M/L858. This inhibits downstream signaling leading to the inhibition of proliferation of tumor cells that overexpress these receptors. EGFR family members play key roles in regulating cell proliferation and differentiation, and are overexpressed in many different tumor cell types.
pan-HER kinase inhibitor AC480: An orally bioavailable pan-HER tyrosine kinase inhibitor with potential antineoplastic activity. BMS-599626 inhibits human epidermal growth factor receptors (HER) HER1, HER2 and HER4, thereby inhibiting the proliferation of tumor cells that overexpress these receptors.
pan-HER/VEGFR2 receptor tyrosine kinase inhibitor BMS-690514: A pyrrolotriazine-based compound and a pan inhibitor of receptor tyrosine kinases with potential antineoplastic activity. Pan HER/VEGFR2 receptor tyrosine kinase inhibitor BMS-690514 binds to human epidermal growth factor receptors (EGFR) 1, 2 and 4 (HER1, HER2 and HER4) and vascular endothelial growth factor receptor 1, 2 and 3 (VEGFR-1, -2 and -3), all of which are frequently overexpressed by a variety of tumor types. Binding of this agent to these receptors may result in the inhibition of tumor cell proliferation; the inhibition of endothelial cell migration and proliferation and angiogenesis; and tumor cell death.
pan-KRAS inhibitor BGB-53038: An orally bioavailable inhibitor of KRAS mutations, with potential antineoplastic activity. Upon oral administration, pan-KRAS inhibitor BGB-53038 selectively targets, binds to and inhibits various forms of KRAS mutations, thereby inhibiting KRAS-dependent signaling. This inhibits the proliferation of and induces apoptosis in tumor cells in which KRAS is mutated. KRAS, a member of the RAS family of oncogenes, plays an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis. BGB-53038 has only weak inhibitory activity against NRAS and HRAS, which may reduce the risk of side effects.
pan-KRAS inhibitor BI 1701963: An orally available protein-protein interaction (PPI) inhibitor that targets the guanine nucleotide exchange factor Son of sevenless homolog 1 (SOS1), with potential antineoplastic activity. Upon oral administration, pan-KRAS inhibitor BI 1701963 selectively targets and binds to SOS1, thereby preventing the interaction of SOS1 with Kirsten rat sarcoma viral oncogene homolog (KRAS) in the guanosine diphosphate (GDP)-bound ‘off’ state, which is the inactivated state of KRAS. This abrogates the exchange of RAS-bound GDP for guanosine triphosphate (GTP) and prevents the formation of GTP-loaded KRAS, which is the activated ‘on’ state of KRAS. This prevents activation of downstream RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway by GTP-loaded KRAS. This inhibits mutant KRAS-dependent signaling and may inhibit growth and survival of KRAS-expressing tumor cells. KRAS is a member of the RAS family of oncogenes that is mutated in many cancer cell types. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell proliferation, survival, invasion, and metastasis. SOS1 regulates the KRAS GDP-GTP cycle and promotes nucleotide exchange and formation of ‘active’ KRAS-GTP.
pan-KRAS inhibitor PF-07934040: An orally bioavailable inhibitor of KRAS mutations, with potential antineoplastic activity. Upon oral administration, pan-KRAS inhibitor PF-07934040 targets, binds to and inhibits various forms of KRAS mutations, thereby inhibiting KRAS-dependent signaling. This inhibits the proliferation of and induces apoptosis in tumor cells in which KRAS is mutated. KRAS plays an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
pan-KRAS inhibitor PF-07985045: An orally bioavailable inhibitor of KRAS mutations, with potential antineoplastic activity. Upon oral administration, pan-KRAS inhibitor PF-07985045 targets, binds to and inhibits various forms of KRAS mutations, thereby inhibiting KRAS-dependent signaling. This inhibits the proliferation of and induces apoptosis in tumor cells in which KRAS is mutated. KRAS plays an important role in cell signaling, division and differentiation. Mutations of KRAS may induce constitutive signal transduction leading to tumor cell growth, proliferation, invasion, and metastasis.
pan-mutant-IDH1 inhibitor BAY1436032: An orally available pan-inhibitor of mutant forms of the metabolic enzyme isocitrate dehydrogenase type 1 (IDH1; IDH-1; IDH1 [NADP+] soluble), including forms with mutations of arginine 132 (IDH1(R132)), with potential antineoplastic activity. Upon administration, pan-mutant-IDH-1 inhibitor BAY-1436032 specifically inhibits the activity of IDH1 mutant forms, which prevents the formation of the oncometabolite 2-hydroxyglutarate (2HG) from alpha-ketoglutarate (a-KG). This prevents 2HG-mediated signaling and leads to both an induction of cellular differentiation and an inhibition of cellular proliferation in tumor cells expressing IDH1 mutant forms. IDH1 mutations, including IDH1(R132) mutations, are highly expressed in certain malignancies; they initiate and drive cancer growth by both blocking cell differentiation and catalyzing the formation of 2HG.
pan-mutant-selective PI3K-alpha inhibitor RLY-2608: An orally bioavailable, pan-mutant selective inhibitor of the class I phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) catalytic subunit alpha (phosphoinositide 3-kinase alpha; PIK3CA; PI3K p110alpha), with potential antineoplastic activity. Upon oral administration, pan-mutant selective PI3K-alpha inhibitor RLY-2608 selectively targets and allosterically binds to PIK3CA mutated forms, thereby preventing the activity of PIK3CA mutants. This prevents mutant PIK3CA-mediated activation of the PI3K/Akt (protein kinase B)/mammalian target of rapamycin (mTOR) pathway. This results in both apoptosis and growth inhibition in PIK3CA-mutant expressing tumor cells. By specifically targeting PIK3CA mutants, RLY-2608 may be more efficacious and less toxic than PI3K-alpha inhibitors that also inhibit the wild-type (WT) form. Dysregulation of the PI3K/Akt/mTOR pathway is often found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to chemo- and radio-therapy. PIK3CA, one of the most frequently mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K.
pan-mutant-selective PI3K-alpha inhibitor RLY-5836: An orally bioavailable, pan-mutant selective inhibitor of the class I phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) catalytic subunit alpha (phosphoinositide 3-kinase alpha; PIK3CA; PI3K p110alpha), with potential antineoplastic activity. Upon oral administration, pan-mutant-selective PI3K-alpha inhibitor RLY-5836 selectively targets and allosterically binds to PIK3CA mutated forms, thereby preventing the activity of PIK3CA mutants. This prevents mutant PIK3CA-mediated activation of the PI3K/Akt (protein kinase B)/mammalian target of rapamycin (mTOR) pathway. This results in both apoptosis and growth inhibition in PIK3CA mutant-expressing tumor cells. By specifically targeting PIK3CA mutants, RLY-5836 may be more efficacious and less toxic than PI3K-alpha inhibitors that also inhibit the wild-type (WT) form. Dysregulation of the PI3K/Akt/mTOR pathway is often found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to chemo- and radio-therapy. PIK3CA, one of the most frequently mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K.
pan-NOTCH protein-protein interaction inhibitor CB-103: An orally bioavailable protein-protein interaction (PPI) inhibitor that targets the assembly of the NOTCH transcription complex, with potential antineoplastic activity. Upon oral administration, pan-NOTCH PPI inhibitor CB-103 targets and inhibits the NOTCH transcriptional activation complex in the cell nucleus. This inhibits the expression of NOTCH target genes and prevents NOTCH signaling, which may inhibit the proliferation of tumor cells mediated by an overly-active Notch pathway. Overactivation of the Notch signaling pathway, often triggered by activating mutations, has been correlated with increased cellular proliferation and poor prognosis in certain tumor types.
pan-PI3K inhibitor CLR457: An orally bioavailable pan inhibitor of phosphatidylinositol-3-kinase (PI3K), with potential antineoplastic activity. Upon oral administration, pan-PI3K inhibitor CLR457 inhibits all of the PI3K kinase isoforms, which may result in apoptosis and growth inhibition in tumor cells overexpressing PI3K. Activation of the PI3K pathway promotes cell growth, survival, and resistance to both chemotherapy and radiotherapy.
pan-PI3K/mTOR inhibitor SF1126: A water soluble, small-molecule prodrug containing the pan-PI3K/mTOR inhibitor LY294002/SF1101 conjugated to the RGD-containing tetra-peptide SF1174 with potential antineoplastic and antiangiogenic activities. The targeting peptide SF1174 moiety of pan-PI3K/mTOR inhibitor SF1126 selectively binds to cell surface integrins and, upon cell entry, the agent is hydrolyzed to the active drug SF1101; SF1101 selectively inhibits all isoforms of phosphoinositide-3-kinase (PI3K) and other members of the PI3K superfamily, such as the mammalian target of rapamycin (mTOR) and DNA-PK. By inhibiting the PI3K signaling pathway, this agent may inhibit tumor cell and tumor endothelial cell proliferation and survival. Integrins are transmembrane cell adhesion proteins expressed on the surfaces of endothelial and tumor cells.
pan-PIM kinase inhibitor AZD1208: An orally available, small molecule inhibitor of PIM kinases with potential antineoplastic activity. Pan-PIM kinase inhibitor AZD1208 inhibits the activities of PIM1, PIM2 and PIM3 serine/threonine kinases, which may result in the interruption of the G1/S phase cell cycle transition, thereby causing cell cycle arrest and inducing apoptosis in cells that overexpress PIMs. The growth inhibition of several leukemia cell lines by this agent is correlated with the expression levels of PIM1, which is the substrate of STAT transcription factors. PIM kinases are downstream effectors of many cytokine and growth factor signaling pathways and are upregulated in various malignancies.
pan-PIM kinase inhibitor GDC-0570: An orally available small molecule pan-inhibitor of the PIM serine/threonine kinase family, with potential antineoplastic activity. Upon oral administration, pan-PIM kinase inhibitor GDC-0570 binds to and prevents the activation of the three PIM family kinases, PIM1, PIM2 and PIM3. This prevents the activation of PIM-mediated signaling pathways and inhibits proliferation in cells that overexpress PIMs. PIMs, constitutively active proto-oncogenic serine/threonine kinases upregulated in various types of cancers, play key roles in tumor cell proliferation and survival.
pan-RAF inhibitor JZP815: An orally bioavailable inhibitor of all members of the serine/threonine protein kinase Raf family, including A-Raf, B-Raf and C-Raf protein kinases, with potential antineoplastic activity. Upon oral administration, pan-RAF inhibitor JZP815 selectively binds to and inhibits the activity of wild-type and mutated forms of Raf, including B-Raf mutations, and B-Raf fusions. This prevents the activation of Raf-mediated signal transduction pathways, which may inhibit tumor cell growth. Oncogenic mutations in Raf plays a key role in the overactivation of the Ras-mitogen-activated protein kinase (MAPK) pathway and drives tumor cell proliferation and survival.
pan-Raf inhibitor KIN-2787: An orally available inhibitor of class I, II, and III B-Raf (BRAF) protein kinases, with potential antineoplastic activity. Upon administration, pan-Raf inhibitor KIN-2787 binds to and inhibits Class I, Class II, or Class III B-Raf mutations. This prevents B-Raf-mediated signal transduction pathways, which may lead to an inhibition of tumor growth in B-Raf mutant cells. B-Raf protein kinases play a key role in the RAF/MEK/ERK signaling pathway, which is often deregulated and mutated in human cancers, and plays a key role in tumor cell proliferation and survival.
pan-RAF inhibitor LY3009120: An orally available inhibitor of all members of the serine/threonine protein kinase Raf family, including A-Raf, B-Raf and C-Raf protein kinases, with potential antineoplastic activity. Upon administration, pan-RAF kinase inhibitor LY3009120 inhibits Raf-mediated signal transduction pathways, which may inhibit tumor cell growth. Raf protein kinases play a key role in the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival.
pan-RAF inhibitor QLH11906: An orally bioavailable inhibitor of all members of the serine/threonine protein kinase Raf family, including A-Raf, B-Raf and C-Raf protein kinases, with potential antineoplastic activity. Upon oral administration, pan-RAF kinase inhibitor QLH11906 binds to and inhibits the activity of Raf, including B-Raf mutated forms such as the B-Raf V600E mutation. This prevents the activation of Raf-mediated signal transduction pathways, which may inhibit tumor cell growth. Raf protein kinases play a key role in the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival. The valine to glutamic acid substitution at residue 600 accounts for the majority of BRAF gene mutations. The oncogenic product, BRAF(V600E) kinase, exhibits elevated activity that over-activates the MAPK signaling pathway.
pan-RAF inhibitor XP-102: An orally bioavailable, second-generation inhibitor of all members of the serine/threonine protein kinase Raf family, including A-Raf, B-Raf and C-Raf protein kinases, with potential antineoplastic activity. Upon administration, pan-RAF kinase inhibitor XP-102 specifically binds to the ATP binding site of the Raf kinase positioned in the inactive DFG-out conformation, and inhibits the activity of Raf, including B-Raf mutated forms such as the B-Raf V600E mutation. This prevents the activation of Raf-mediated signal transduction pathways, which may inhibit tumor cell growth. Raf protein kinases play a key role in the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival. The valine to glutamic acid substitution at residue 600 accounts for the majority of BRAF gene mutations. The oncogenic product, BRAF(V600E) kinase, exhibits elevated activity that over-activates the MAPK signaling pathway.
pan-RAF kinase inhibitor CCT3833: An orally available inhibitor of the serine/threonine protein kinase family Raf, including A-Raf, B-Raf and C-Raf, with potential antineoplastic activity. Upon administration, pan-RAF kinase inhibitor CCT3833 inhibits Raf-mediated signal transduction pathways, which may inhibit the proliferation of Raf-overexpressing tumor cells. Raf protein kinases play a key role in the RAF/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway, which is often dysregulated in human cancers and plays a key role in tumor cell proliferation and survival.
pan-RAF/MEK molecular glue NST-628: An orally bioavailable non-covalent non-degrading pan-RAF/mitogen-activated protein kinase kinase (MAP2K, MAPK/ERK kinase, or MEK) dual molecular glue, with potential antineoplastic activity. Upon oral administration, pan-RAF/MEK molecular glue NST-628 targets and glues A-RAF, B-RAF and C-RAF protein kinases with unphosphorylated MEK1, forming a stable and inactive RAF-MEK complex. This prevents the phosphorylation and activation of MEK by RAF, inhibits the activity of MEK, thereby preventing the activation of MEK-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. Oncogenic mutations in RAF plays a key role in the overactivation of the RAS-mitogen-activated protein kinase (MAPK) pathway and drives tumor cell proliferation and survival. MEK1/2 are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway that regulates cell growth. This pathway is often dysregulated in a variety of tumor cell types through BRAF, KRAS and NRAS mutations. NST-628 is able to cross the blood-brain barrier (BBB).
pan-selectin antagonist GMI-1070: A synthetic, glycomimetic molecule and pan-selectin antagonist, with potential use in a vaso-occlusive crisis. Upon administration, GMI-1070 prevents the interaction between leukocytes and the endothelium and may prevent cell activation and adhesion. By preventing selectin-mediated cell adhesion in sickle cell anemia, this agent may inhibit red blood cell-white blood cell interactions, normalize blood flow and reduce inflammation and vascular occlusive pain. GMI-1070 has the strongest antagonistic activity towards E-selectin but the incorporation of a sulfate-binding domain allows for interactions with P- and L-selectins. Selectins, containing lectin- and EGF-like domains, are a family of cell adhesion molecules implicated in inflammatory processes and cancer.
pan-TEAD inhibitor ISM6331: An orally bioavailable non-covalent small molecule inhibitor of the TEA domain (TEAD) family of transcription factors, including TEAD1, TEAD2, TEAD3 and TEAD4, with potential antineoplastic activity. Upon oral administration, pan-TEAD inhibitor ISM6331 reversibly binds to the TEAD palmitoylation site and inhibits TEAD, thereby disrupting the interaction between the transcription co-activators yes-associated protein 1 (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) and TEAD. This may inhibit YAP/TAZ-TEAD-promoted transcription of multiple genes involved in tumor cell proliferation, progression and survival, and may result in enhanced apoptosis in TEAD-dependent cancers. Hippo pathway alterations, as seen in tumors with neurofibromatosis type 2 (NF2)-deficiency, large tumor suppressor 1 (LATS1) and 2 (LATS2) mutations and YAP/TAZ fusions, lead to Hippo pathway activation, hyperactivation of YAP/TAZ and activation of TEAD. It plays a key role in cancer initiation, progression, and cancer cell resistance to various therapies.
pan-TRK inhibitor ICP-723: An orally bioavailable, selective pan-tropomyosin-related-kinase (tyrosine receptor kinase; TRK) inhibitor, with potential antineoplastic activity. Upon oral administration, pan-TRK inhibitor ICP-723 specifically targets and binds to TRK, TRK mutations and fusion proteins containing sequences from neurotrophic tyrosine receptor kinase (NTRK) types 1 (NTRK1; TrkA), 2 (NTRK2; TrkB), and 3 (NTRK3; TrkC). This inhibits neurotrophin-TRK interaction and TRK activation, thereby preventing the activation of downstream signaling pathways and resulting in both the induction of cellular apoptosis and the inhibition of cell growth in tumors that overexpress TRK and/or express NTRK fusion proteins. TRK, a family of receptor tyrosine kinases (RTKs) activated by neurotrophins, is encoded by NTRK family genes. The expression of either mutated forms of, or fusion proteins involving, NTRK family members results in uncontrolled TRK signaling, which plays an important role in tumor cell growth, survival, invasion and treatment resistance.
pan-TRK inhibitor ONO-7579: An orally bioavailable, selective pan-tropomyosin-related-kinase (tyrosine receptor kinase; TRK) inhibitor, with potential antineoplastic activity. Upon oral administration, ONO-7579 specifically targets and binds to TRK and fusion proteins containing sequences from neurotrophic tyrosine receptor kinase (NTRK) types 1 (NTRK1; TrkA), 2 (NTRK2; TrkB), and 3 (NTRK3; TrkC). This inhibits neurotrophin-TRK interaction and TRK activation, thereby preventing the activation of downstream signaling pathways and resulting in both the induction of cellular apoptosis and the inhibition of cell growth in tumors that overexpress TRK and/or express NTRK fusion proteins. TRK, a family of receptor tyrosine kinases (RTKs) activated by neurotrophins, is encoded by NTRK family genes. The expression of either mutated forms of, or fusion proteins involving, NTRK family members results in uncontrolled TRK signaling, which plays an important role in tumor cell growth, survival, invasion and treatment resistance.
Pan-TRK inhibitor ONO-7579: An orally bioavailable, selective pan-tropomyosin-related-kinase (tyrosine receptor kinase; TRK) inhibitor, with potential antineoplastic activity. Upon oral administration, ONO-7579 specifically targets and binds to TRK and fusion proteins containing sequences from neurotrophic tyrosine receptor kinase (NTRK) types 1 (NTRK1; TrkA), 2 (NTRK2; TrkB), and 3 (NTRK3; TrkC). This inhibits neurotrophin-TRK interaction and TRK activation, thereby preventing the activation of downstream signaling pathways and resulting in both the induction of cellular apoptosis and the inhibition of cell growth in tumors that overexpress TRK and/or express NTRK fusion proteins. TRK, a family of receptor tyrosine kinases (RTKs) activated by neurotrophins, is encoded by NTRK family genes.The expression of either mutated forms of, or fusion proteins involving, NTRK family members results in uncontrolled TRK signaling, which plays an important role in tumor cell growth, survival, invasion and treatment resistance.
pan-TRK inhibitor PBI-200: An orally bioavailable, brain-penetrant pan-tropomyosin-related-kinase (tyrosine receptor kinase; TRK) inhibitor, with potential antineoplastic activity. Upon oral administration, pan-TRK inhibitor PBI-200 specifically targets and binds to TRKs, mutated TRKs and fusion proteins containing sequences from neurotrophic tyrosine receptor kinase (NTRK) types 1 (NTRK1; TrkA), 2 (NTRK2; TrkB), and 3 (NTRK3; TrkC). This inhibits neurotrophin-TRK interaction and TRK activation, thereby preventing the activation of downstream signaling pathways and resulting in both the induction of cellular apoptosis and the inhibition of cell growth in tumors that overexpress TRK and/or express NTRK fusion proteins. TRK, a family of receptor tyrosine kinases (RTKs) activated by neurotrophins, is encoded by NTRK family genes. The expression of either mutated forms of, or fusion proteins involving, NTRK family members results in uncontrolled TRK signaling, which plays an important role in tumor cell growth, survival, invasion and treatment resistance.
pan-TRK/ROS1 dual inhibitor XZP-5955: An orally available dual inhibitor of the receptor tyrosine kinase c-ros oncogene 1 (ROS1) and the tropomyosin-related-kinase (tyrosine receptor kinase; TRK), with potential antineoplastic activity. Upon oral administration, pan-TRK/ROS1 dual inhibitor XZP-5955 targets, binds to and inhibits wild-type, point mutants and fusion proteins of ROS1 and TRK, including fusion proteins containing sequences from neurotrophic tyrosine receptor kinase (NTRK) types 1 (NTRK1; TrkA), 2 (NTRK2; TrkB), and 3 (NTRK3; TrkC). It specifically inhibits proliferation of tumor cells harboring certain TRK and ROS1 resistance mutations, such as TRKA G595R, TRKC G623R, TRKA G667C and ROS1 G2032R. Inhibition of these kinases leads to the disruption of downstream signaling pathways and the inhibition of cell growth of tumors in which these kinases are overexpressed, rearranged or mutated. TRK, a family of receptor tyrosine kinases (RTKs) activated by neurotrophins, is encoded by NTRK family genes. The expression of either mutated forms of, or fusion proteins involving, NTRK family members results in uncontrolled TRK signaling, which plays an important role in tumor cell growth, survival, invasion and treatment resistance. ROS1, overexpressed in certain cancer cells, plays a key role in cell growth and survival of cancer cells. XZP-5955 is able to penetrate the blood-brain barrier (BBB).
pan-variant KIT inhibitor THE-630: An orally bioavailable pan-inhibitor of the mutated forms of the tumor-associated antigen (TAA) receptor tyrosine kinase mast/stem cell factor receptor c-Kit (SCFR), with potential antineoplastic activity. Upon oral administration, pan-variant KIT inhibitor THE-630 targets, binds to and inhibits the activity of all known, clinically relevant KIT activating and resistance mutations in gastrointestinal stromal tumors (GIST). More specifically, THE-630 inhibits the primary activating mutations deletion in Ex11 (Ex11Del) and insertion in Ex9 (Ex9Ins); the secondary resistance mutations, including the ATP binding pocket mutants V654A and T670I and the activation loop mutants D816G/H, D820A/G, N822K, Y823D, and A829P. This inhibits KIT-mediated signaling and the proliferation of tumor cells that overexpress c-Kit mutations. c-Kit is mutated in various tumor cell types and plays a key role in the regulation of cellular proliferation and resistance to chemotherapy.
pan-VEGFR/TIE2 tyrosine kinase inhibitor CEP-11981: An orally bioavailable inhibitor of vascular endothelial growth factor receptor (VEGFR) and Tie2 receptor tyrosine kinases with potential antiangiogenic and antineoplastic activities. Pan-VEGFR/Tie2 tyrosine kinase inhibitor CEP-11981 selectively binds to VEGFR and Tie2 receptor tyrosine kinases, which may result in the inhibition of endothelial cell migration, proliferation and survival and the inhibition of tumor cell proliferation and tumor cell death. VEGFR and Tie2 are frequently overexpressed by a variety of tumor cell types and play crucial roles in the regulation of angiogenesis and the maintenance of tumor blood vessels. Tie2 (tyrosine kinase with immunoglobulin-like and EGF-like domains) is activated by angiopoietin-1 (Ang-1).
Pancrease: (Other name for: pancrelipase)
pancrelipase: A standardized enzyme concentrate containing the pancreatic enzymes, lipase, protease and amylase used in enzyme substitution therapy. Lipase, protease and amylase break down fat, protein, and starches, respectively in the small intestine, thereby promoting digestion. Pancrelipase is used to reduce malabsorption when the pancreas is unable to secrete sufficient amounts of these enzymes.
Panglobulin: (Other name for: therapeutic immune globulin)
Panhematin: (Other name for: therapeutic hemin)
panitumumab: A human IgG2kappa monoclonal antibody specific for the epidermal growth factor receptor (EGFR). Monoclonal antibody E7.6.3 binds to the EGFR, blocking the binding of epidermal growth factor and transforming growth factor alpha to EGFR-expressing cancer cells and ultimately inhibiting EGFR-dependent cell activation and proliferation.
panitumumab-IRDye800: An imaging agent composed of panitumumab, a humanized anti-epidermal growth factor receptor (EGFR) monoclonal antibody, conjugated to the near-infrared (NIR) fluorescent dye IRDye800, that can potentially be used for the imaging of EGFR-expressing tumors. Upon administration of panitumumab-IRDye800, the panitumumab moiety targets and binds to EGFR expressed on tumor cells. Upon fluorescence imaging of IRDye800, the tumor cells can be detected.
PankoMab-GEX: (Other name for: gatipotuzumab)
Panmycin: (Other name for: tetracycline hydrochloride)
panobinostat lactate: The lactate form of panobinostat, a pan histone deacetylase (HDAC) inhibitor, with potential antineoplastic activity. Upon administration, panobinostat selectively targets, binds to and inhibits HDAC, which induces hyperacetylation of core histone proteins. The accumulation of highly acetylated histones leads to chromatin remodeling, an altered pattern of gene expression, inhibition of tumor oncogene transcription and the selective transcription of tumor suppressor genes. This results in the inhibition of tumor cell division and the induction of tumor cell apoptosis. HDAC, upregulated in many tumor cell types, is an enzyme family that deacetylates histone proteins.
panobinostat nanoparticle formulation MTX110: A gold nanoparticle (GNP)-based formulation containing panobinostat, a pan histone deacetylase (HDAC) inhibitor, with potential antineoplastic activity. Upon intra-tumoral injection of MTX110, panobinostat is released from the formulation and selectively targets, binds to and inhibits histone deacetylase (HDAC), which induces hyperacetylation of core histone proteins. The accumulation of highly acetylated histones leads to chromatin remodeling, an altered pattern of gene expression, inhibition of tumor oncogene transcription and the selective transcription of tumor suppressor genes. This results in the inhibition of tumor cell division and the induction of tumor cell apoptosis. HDAC, upregulated in many tumor cell types, is an enzyme family that deacetylates histone proteins. Panobinostat is water insoluble and does not cross the blood-brain barrier (BBB) when administered orally or intravenously. MTX110 solubilizes panobinostat and can be directly injected into the brain, which bypasses the BBB and delivers high concentrations of panobinostat to the tumor, while minimizing systemic toxicity
Panretin: (Other name for: alitretinoin)
pantoprazole sodium: The sodium salt form of a substituted benzimidazole with proton pump inhibitor activity. Pantoprazole is a lipophilic, weak base that crosses the parietal cell membrane and enters the acidic parietal cell canaliculus where it becomes protonated, producing the active metabolite sulfenamide, which forms an irreversible covalent bond with two sites of the H+/K+-ATPase enzyme located on the gastric parietal cell, thereby inhibiting both basal and stimulated gastric acid production.
PANVAC-F: (Other name for: falimarev)
PANVAC-V: (Other name for: inalimarev)
Panwarfin: (Other name for: warfarin sodium)
Panzem: (Other name for: 2-methoxyestradiol)
Panzem NCD: (Other name for: 2-methoxyestradiol nanocrystal colloidal dispersion)
Panzyga: (Other name for: therapeutic immune globulin)
PAP/PSA-expressing arenaviral vectors HB-302/HB-301: An alternating, 2-vector replicating arenaviral combination agent composed of two genetically engineered replicating vectors: HB-301, which is based on the arenavirus lymphocytic choriomeningitis virus (LCMV), and HB-302, which is based on the arenavirus Pichinde virus (PICV), and both expressing the same transgenes encoding for the two prostate cancer-associated antigens prostatic acid phosphatase (PAP) and prostate specific antigen (PSA), with potential immunomodulating and antineoplastic activities. Upon intravenous administration, the PAP/PSA-expressing arenaviral vectors HB-302/HB-301 express PSA and PAP peptides and cause antibody-mediated and cytotoxic T-lymphocyte (CTL)-mediated immune responses against prostate cancer cells expressing PSA and PAP.
papaverine hydrochloride: The hydrochloride salt of the opiate alkaloid isolated from the plant Papaver somniferum and produced synthetically. As a direct-acting smooth muscle relaxant, papaverine is not closely related to the other opium alkaloids in structure or pharmacological actions; its mechanism of action may involve the non-selective inhibition of phosphodiesterases and direct inhibition of calcium channels. This agent also exhibits antiviral activity against respiratory syncytial virus, cytomegalovirus, and HIV.
para-toluenesulfonamide: A low-molecular-weight organic compound with potential antineoplastic activity. Upon intra-tumoral injection, para-toluenesulfonamide increases lysosomal membrane permeabilization (LMP) and the release of cathepsin B. Cytosolic cathepsin B released from lysosomes cleaves and activates proapoptotic B-cell lymphoma 2 (Bcl-2) family member BH3 interacting-domain death agonist (Bid) and poly [ADP-ribose] polymerase 1 (PARP-1), which may induce tumor cell death.
Paraflex: (Other name for: chlorzoxazone)
Paraplatin: (Other name for: carboplatin)
parathyroid hormone-related protein (1-36): A recombinant form of a mature, N-terminal secretory peptide derived from a parathyroid hormone-related protein (PTHrP) preprohormone through posttranslational endoproteolytic processing with vasodilating, myorelaxant, and parathyroid hormone (PTH)-like calciotropic activities. Expressed throughout the cardiovascular system, parathyroid hormone-related protein (1-36) [PTHrP (1-36)] was first identified as the PTH-like hypercalcemic factor of humoral hypercalcemia of malignancy; however, its sequence differs significantly from that of PTH (1-34) although both proteins share the same N-terminal end which accounts for the calciotropic activity. Both PTHrP (1-36) and PTH (1-34) bind to the type 1 parathyroid hormone receptor (PTH1R), a specific seven-transmembrane-helix-containing G protein-coupled receptor mainly located in bone and kidney cells.
parecoxib sodium: A water-soluble, injectable sodium salt form of parecoxib, an amide prodrug of the cyclooxygenase II (COX-2) selective, non-steroidal anti-inflammatory drug (NSAID) valdecoxib, with anti-inflammatory, analgesic, and antipyretic activities. Upon intravenous or intramuscular administration, parecoxib is hydrolyzed by hepatic carboxyesterases to its active form, valdecoxib. Valdecoxib selectively binds to and inhibits COX-2. This prevents the conversion of arachidonic acid into prostaglandins, which are involved in the regulation of pain, inflammation, and fever. This NSAID does not inhibit COX-1 at therapeutic concentrations and, therefore, does not interfere with blood coagulation.
PARG inhibitor ETX-19477: An orally bioavailable, small molecule inhibitor of poly (ADP-Ribose) (PAR) glycohydrolase (PARG), with potential antineoplastic activity. Upon oral administration, PARG inhibitor ETX-19477 targets, reversibly binds to and inhibits the activity of PARG, thereby inhibiting the hydrolysis of PAR chains by PARG. This attenuates DNA repair and induces mitotic arrest, ultimately leading to apoptosis of cancer cells. PARG, the only enzyme responsible for hydrolyzing PAR chains produced by poly (ADP-ribose) polymerase (PARP) 1, plays a key role in the resolution of PARP 1/2-dependent DNA damage repair.
PARG inhibitor IDE161: An orally bioavailable, small molecule inhibitor of poly (ADP-Ribose) (PAR) glycohydrolase (PARG), with potential antineoplastic activity. Upon oral administration, PARG Inhibitor IDE161 targets, binds to and inhibits the activity of PARG, thereby inhibiting the hydrolysis of PAR chains by PARG. This attenuates DNA repair and induces mitotic arrest, ultimately leading to apoptosis. PARG, the only enzyme responsible for hydrolyzing PAR chains produced by poly (ADP-ribose) polymerase (PARP) 1, plays a key role in the resolution of PARP 1/2-dependent DNA damage repair.
paricalcitol: A synthetic noncalcemic, nonphosphatemic vitamin D analogue. Paricalcitol binds to the vitamin D receptor and has been shown to reduce parathyroid hormone (PTH) levels. This agent also increases the expression of PTEN ('Phosphatase and Tensin homolog deleted on chromosome Ten'), a tumor-suppressor gene, in leukemic cells and cyclin-dependent kinase inhibitors, resulting in tumor cell apoptosis and tumor cell differentiation into normal phenotypes.
Parlodel: (Other name for: bromocriptine mesylate)
Parnate: (Other name for: tranylcypromine sulfate)
paromomycin sulfate: The sulfate salt form of paromomycin, a structural derivative of neomycin, an aminoglycoside antibiotic with amebicidal and bactericidal effects against predominantly aerobic gram-negative bacteria. Paromomycin binds specifically to the RNA oligonucleotide at the A site of bacterial 30S ribosomes, thereby causing misreading and premature termination of translation of mRNA and inhibition of protein synthesis followed by cell death.
paroxetine hydrochloride: The hydrochloride salt form of paroxetine, a phenylpiperidine derivative and a selective serotonin reuptake inhibitor (SSRI) with antidepressant and anxiolytic properties. Paroxetine binds to the pre-synaptic serotonin transporter complex resulting in negative allosteric modulation of the complex thereby blocking reuptake of serotonin by the pre-synaptic transporter. Inhibition of serotonin recycling enhances serotonergic function through serotonin accumulation in the synaptic cleft, resulting in long-term desensitization and downregulation of 5HT1 (serotonin) receptors and leading to symptomatic relief of depressive illness.
PARP 1/2 inhibitor NOV1401: An orally available small molecule inhibitor of the nuclear enzymes poly (ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon administration, NOV1401 selectively binds to PARP-1 and -2, thereby preventing PARP-1 and -2-mediated DNA repair. This promotes genetic instability and enhances the accumulation of single and double strand DNA breaks, ultimately leading to apoptosis. The PARP family of proteins catalyzes post-translational ADP-ribosylation of nuclear proteins and is activated by single-strand DNA (ssDNA) breaks.
PARP 1/2 inhibitor RP12146: An orally bioavailable, small molecule inhibitor of the nuclear enzymes poly (ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon oral administration, PARP 1/2 inhibitor RP12146 selectively binds to and inhibits PARP-1 and -2, thereby preventing PARP-1 and -2-mediated DNA repair. This promotes genetic instability and enhances the accumulation of single and double strand DNA breaks, ultimately leading to apoptosis. The PARP family of proteins catalyzes post-translational ADP-ribosylation of nuclear proteins and is activated by single-strand DNA (ssDNA) breaks.
PARP 1/2 inhibitor SC10914: An orally bioavailable inhibitor of the nuclear enzymes poly (ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon oral administration, PARP 1/2 inhibitor SC10914 selectively binds to and inhibits PARP-1 and -2, thereby preventing PARP-1 and -2-mediated DNA repair. This promotes genetic instability and enhances the accumulation of single and double strand DNA breaks, ultimately leading to apoptosis. The PARP family of proteins catalyzes post-translational ADP-ribosylation of nuclear proteins and is activated by single-strand DNA (ssDNA) breaks.
PARP 1/2 inhibitor TQB3823: An orally bioavailable, small molecule inhibitor of the nuclear enzymes poly (ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon oral administration, PARP 1/2 inhibitor TQB3823 selectively binds to and inhibits PARP-1 and -2, thereby preventing PARP-1 and -2-mediated DNA repair. This promotes genetic instability and enhances the accumulation of single and double strand DNA breaks, ultimately leading to apoptosis. The PARP family of proteins catalyzes post-translational ADP-ribosylation of nuclear proteins and is activated by single-strand DNA (ssDNA) breaks.
PARP inhibitor AZD2461: An orally bioavailable inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential antineoplastic activity. PARP inhibitor AZD2461 selectively binds to PARP and prevents PARP-mediated DNA repair of single strand DNA breaks via the base-excision repair pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability and eventually leads to apoptosis. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and is activated by single-strand DNA breaks.
PARP inhibitor CEP-9722: A small-molecule prodrug of CEP-8983, a novel 4-methoxy-carbazole inhibitor of the nuclear enzymes poly(ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon administration and conversion from CEP-9722, CEP-8983 selectively binds to PARP 1 and 2, preventing repair of damaged DNA via base excision repair (BER). This agent enhances the accumulation of DNA strand breaks and promotes genomic instability and apoptosis. CEP-8983 may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and can be activated by single strand breaks in DNA.
PARP inhibitor E7016: An inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential chemo- and/or radiosensitizing activity. PARP inhibitor E7016 selectively binds to PARP and prevents PARP-mediated DNA repair of single strand DNA breaks via the base-excision repair pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability and eventually leads to apoptosis. In addition, this agent may enhance the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapy and radiation therapy. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and is activated by single-strand DNA breaks.
PARP inhibitor NMS-03305293: An orally bioavailable inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) with potential antineoplastic activity. Upon administration, PARP inhibitor NMS-03305293 selectively binds to PARP and prevents PARP-mediated DNA repair of single-strand DNA breaks via the base-excision repair pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability and eventually leads to apoptosis. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and is activated by single-strand DNA breaks.
PARP-1/2 inhibitor ABT-767: An orally available inhibitor of the nuclear enzymes poly(ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon administration, ABT-767 selectively binds to PARP 1 and 2, thereby preventing repair of damaged DNA via the base excision repair (BER) pathway. This agent enhances the accumulation of DNA strand breaks and promotes genomic instability eventually leading to apoptosis. ABT-767 may enhance the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and can be activated by single strand DNA (ssDNA) breaks.
PARP/microtubule polymerization inhibitor AMXI-5001: An orally bioavailable, dual inhibitor of the nuclear enzymes poly (ADP-ribose) polymerase (PARP) 1 and 2 and microtubule polymerization, with potential antineoplastic activity. Upon oral administration, PARP/microtubule polymerization inhibitor AMXI-5001 selectively binds to and inhibits PARP-1 and -2, thereby preventing PARP-1 and -2-mediated DNA repair. This promotes genetic instability and enhances the accumulation of single and double strand DNA breaks, ultimately leading to apoptosis. In addition, the benzimidazole moiety of AMXI-5001 targets and binds to the colchicine-binding motif on tubulin, thereby inhibiting its polymerization into microtubules. This may interrupt microtubule dynamics, disrupt mitosis, lead to cell cycle arrest and induce tumor cell apoptosis. The PARP family of proteins catalyzes post-translational ADP-ribosylation of nuclear proteins and is activated by single-strand DNA (ssDNA) breaks. Microtubules play important roles in mitosis and cell division.
PARP/tankyrase inhibitor 2X-121: An orally available small molecule inhibitor of the nuclear enzymes poly (ADP-ribose) polymerase (PARP) 1 and 2, with potential antineoplastic activity. Upon administration, E7449 selectively binds to PARP 1 and 2, thereby preventing the repair of damaged DNA via the base excision repair (BER) pathway. This agent enhances the accumulation of single and double strand DNA breaks and promotes genomic instability eventually leading to apoptosis. PARP 1/2 inhibitor E7449 may enhance the cytotoxicity of DNA-damaging agents and of radiotherapy. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA.
PARP1 inhibitor ACE-86225106: An orally bioavailable inhibitor of nuclear enzyme poly(ADP-ribose) polymerase (PARP) 1, with potential antineoplastic activity. Upon oral administration, PARP1 inhibitor ACE-86225106 selectively binds to and inhibits the activity of PARP1, thereby preventing the repair of damaged DNA via the base excision repair (BER) pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability eventually leading to apoptosis. PARP1 catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and plays a key role in the repair of single strand DNA (ssDNA) breaks and double-strand breaks (DSBs).
PARP1 inhibitor GS-0201: An orally bioavailable inhibitor of nuclear enzyme poly(ADP-ribose) polymerase (PARP) 1, with potential antineoplastic activity. Upon oral administration, PARP1 inhibitor GS-0201 selectively binds to and inhibits the activity of PARP1, thereby preventing the repair of damaged DNA via the base excision repair (BER) pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability eventually leading to apoptosis. PARP1 catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and plays a key role in the repair of single strand DNA (ssDNA) breaks and double-strand breaks (DSBs).
PARP1 inhibitor HRS-1167: An orally bioavailable inhibitor of nuclear enzyme poly(ADP-ribose) polymerase (PARP) 1, with potential antineoplastic activity. Upon oral administration, PARP1 inhibitor HRS-1167 selectively targets, binds to and inhibits the activity of PARP1, thereby preventing the repair of damaged DNA via the base excision repair (BER) pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability eventually leading to apoptosis. PARP1 catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and plays a key role in the repair of single strand DNA (ssDNA) breaks and double-strand breaks (DSBs).
PARP1 inhibitor HS-10502: An orally bioavailable inhibitor of nuclear enzyme poly(ADP-ribose) polymerase (PARP) 1, with potential antineoplastic activity. Upon oral administration, PARP1 inhibitor HS-10502 selectively binds to and blocks the activity of PARP1, thereby preventing repair of damaged DNA via the base excision repair (BER) pathway. This agent enhances the accumulation of DNA strand breaks and promotes genomic instability eventually leading to apoptosis. HS-10502 may enhance the cytotoxicity of DNA-damaging agents and reverse tumor cell chemo- and radioresistance. PARP1 catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and plays a key role in the repair of single strand DNA (ssDNA) breaks and double-strand break (DSBs).
PARP1 inhibitor IMP1734: An orally bioavailable inhibitor of nuclear enzyme poly(ADP-ribose) polymerase (PARP) 1, with potential antineoplastic activity. Upon oral administration, PARP1 inhibitor IMP1734 selectively binds to and blocks the activity of PARP1, thereby preventing the repair of damaged DNA via the base excision repair (BER) pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability eventually leading to apoptosis. PARP1 catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and plays a key role in the repair of single strand DNA (ssDNA) breaks and double-strand breaks (DSBs).
PARP1 inhibitor SNV1521: An orally bioavailable inhibitor of nuclear enzyme poly(ADP-ribose) polymerase (PARP) 1, with potential antineoplastic activity. Upon oral administration, PARP1 inhibitor SNV1521 selectively targets, binds to and inhibits the activity of PARP1, thereby preventing the repair of damaged DNA via the base excision repair (BER) pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability eventually leading to apoptosis. PARP1 catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and plays a key role in the repair of single strand DNA (ssDNA) breaks and double-strand breaks (DSBs). SNV1521 is able to penetrate the central nervous system (CNS).
PARP7 inhibitor BY101921: An orally available inhibitor of the nuclear enzyme poly (ADP-ribose) polymerase (PARP) 7, with potential immunomodulating and antineoplastic activities. Upon oral administration, PARP7 inhibitor BY101921 targets, binds to, and inhibits the activity of PARP7, which restores type I interferon (IFN) signaling. This may lead to the induction of both innate and adaptive immune responses, and the inhibition of tumor growth and proliferation. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA.
Parsabiv: (Other name for: etelcalcetide)
parsaclisib: An inhibitor of the delta isoform of phosphoinositide-3 kinase (PI3K) with potential antineoplastic activity. Parsaclisib inhibits the delta isoform of PI3K and prevents the activation of the PI3K/AKT signaling pathway. This both decreases proliferation and induces cell death in PI3K-delta-overexpressing tumor cells. Unlike other isoforms of PI3K, PI3K-delta is expressed primarily in hematopoietic disease and cell lineages. The targeted inhibition of PI3K-delta is designed to preserve PI3K signaling in normal, non-neoplastic cells. PI3K, an enzyme often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.
parsatuzumab: A humanized IgG1 monoclonal antibody directed against the epidermal growth factor-like domain multiple 7 (EGFL7) with potential antineoplastic activity. Parsatuzumab binds to EGFL7, thereby preventing the activities of EGFL7 on endothelial cells and inhibiting the survival and migration of endothelial cells during angiogenesis. EGFL7, a vascular-restricted extracellular matrix protein which is upregulated during angiogenesis and which regulates vascular development, may be overexpressed on the cell surfaces of various solid tumor cell types.
partially engineered T-regulatory cell donor graft TRGFT-201: A T-regulatory (Treg) cell donor graft that has been partially engineered by depleting all the T cells and then enriching the graft with infusions of conventional T-cells, Tregs and CD34+ stem cells derived from peripheral blood from either related or unrelated matched donors, with potential immunomodulating activity. Upon administration of the partially engineered T-regulatory cell donor graft TRGFT-201 following myeloablation, the allograft may induce tolerance in patients undergoing allogeneic hematopoietic stem cell transplantation (AHSCT) as treatment for hematologic malignancies.
partially HLA-matched AdV/CMV/EBV-specific allogeneic T lymphocytes: Partially or closely human leukocyte antigen (HLA)-matched allogeneic cytotoxic T lymphocytes (CTLs), derived from cell lines, specifically reactive to the three human viruses adenovirus (AdV), cytomegalovirus (CMV) and Epstein-Barr virus (EBV), with potential antiviral activity. Upon infusion of the partially HLA-matched AdV/CMV/EBV-specific allogeneic T lymphocytes in immunocompromised patients or upon allogeneic hematopoietic stem cell transplantation (HSCT) in an immunodeficient recipient, these CTLs may kill AdV, CMV, and/or EBV-infected cells, and may prevent or reduce the severity of viral infections by these pathogens.
partially HLA-matched multiple TAA-specific allogeneic T lymphocytes: A preparation of partially human leukocyte antigen (HLA)-matched allogeneic T lymphocytes targeting multiple tumor-associated antigens (TAAs), with potential immunomodulating and antineoplastic activities. Upon administration, partially HLA-matched multiple TAA-specific allogeneic T lymphocytes target and kill tumor cells expressing these TAAs.
ParvOryx: (Other name for: parvovirus H-1)
parvovirus H-1: A replication-competent oncolytic parvovirus with potential antineoplastic activity. Upon infection of host cells, parvovirus H-1 preferentially replicates in tumor cells compared to healthy normal cells, thereby potentially resulting in tumor cell lysis and leading to an inhibition of tumor cell proliferation. In addition, H1-infected tumor cells strongly induce the release of the inducible heat shock protein 72 (Hsp72i), which chaperone tumor associated antigens in the H1-mediated tumor lysates and may activate antigen presenting cells (APCs), thereby leading to antitumor immune responses. Parvovirus H-1 does not cause any pathogenic effect in normal, healthy cells and is able to cross the blood brain barrier (BBB).
pasireotide: A synthetic long-acting cyclic peptide with somatostatin-like activity. Pasireotide activates a broad spectrum of somatostatin receptors, exhibiting a much higher binding affinity for somatostatin receptors 1, 3, and 5 than octreotide in vitro, as well as a comparable binding affinity for somatostatin receptor 2. This agent is more potent than somatostatin in inhibiting the release of human growth hormone (HGH), glucagon, and insulin.
pasotuxizumab: A recombinant T-cell engaging bispecific monoclonal antibody (BiTE) directed against human prostate specific membrane antigen (PSMA) and the CD3 epsilon subunit of the T cell receptor complex, with potential immunostimulating and antineoplastic activities. Pasotuxizumab possesses two antigen-recognition sites, one for PSMA, and one for the CD3 complex, a group of T cell surface glycoproteins that complex with the T cell receptor (TCR). This bispecific monoclonal antibody brings PSMA-expressing tumor cells and cytotoxic T lymphocytes (CTLs) together, which may result in the CTL-mediated cell death of PSMA-expressing cells. PSMA, a tumor associated antigen, is overexpressed on the surface of metastatic and hormone-refractory prostate cancer cells.
patent blue V dye: A synthetic dye with imaging and food coloring property. It is a sodium or calcium salt of [4-(alpha-(4-diethylaminophenyl)-5-hydroxy- 2,4-disulfophenyl-methylidene)-2,5-cyclohexadien-1-ylidene] diethylammonium hydroxide inner salt. Patent blue V dye is used in sentinel lymph node (SLN) technique to guide nodal dissection or other imaging procedures.
patidegib: An orally bioavailable, cyclopamine-derived inhibitor of the Hedgehog (Hh) pathway with potential antineoplastic activity. Specifically, patidegib binds to and inhibits the cell membrane-spanning G-protein coupled receptor SMO, which may result in the suppression of Hh pathway signaling and a decrease in tumor cell proliferation and survival. SMO is activated upon binding of Hh ligand to the cell surface receptor Patched (PTCH); inappropriate activation of Hh signaling and uncontrolled cellular proliferation may be associated with SMO mutations. The Hh signaling pathway plays an important role in proliferation of neuronal precursor cells in the developing cerebellum and other tissues.
patidegib topical gel: A topical gel containing patidegib, a cyclopamine-derived inhibitor of the Hedgehog (Hh) pathway, with potential antineoplastic activity. Upon topical application of the patidegib gel, patidegib binds to and inhibits the activity of the G-protein coupled receptor smoothened (SMO), thereby inhibiting Hh pathway signaling. This decreases proliferation and survival in tumor cells in which the Hh pathway is overactivated. Upregulated Hh signaling is associated with uncontrolled tumor cell proliferation. Topical application of patidegib allows for local anti-tumor activity while avoiding systemic exposure and unwanted systemic effects.
Patisiran: (Other name for: anti-transthyretin siRNA ALN-TTR02)
patritumab: A fully human monoclonal antibody directed against the membrane-bound receptor HER3 (ERBB3) with potential antineoplastic activity. Patritumab binds to and inhibits HER3 activation, which may result in inhibition of HER3-dependent PI3K/Akt signaling and so inhibition of cellular proliferation and differentiation. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in solid tumors, including breast, lung, and colorectal tumors of epithelial origin; it has no active kinase domain itself but is activated through heterodimerization with other members of the EGFR receptor family that do.
patritumab deruxtecan: An antibody-drug conjugate (ADC) composed of patritumab, a monoclonal antibody directed against the human epidermal growth factor receptor HER3 (ErbB3),linked to the topoisomerase I inhibitor DX 8951, a semisynthetic, water-soluble derivative of camptothecin, with potential antineoplastic activity. Upon administration of patritumab deruxtecan, the patritumab moiety targets and binds to HER3. After internalization, DX 8951 inhibits topoisomerase I activity by stabilizing the complex between topoisomerase I and DNA and inhibiting religation of DNA breaks, thereby inhibiting DNA replication and triggering apoptotic cell death. HER3, a member of the epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases, is frequently overexpressed in tumors.
patupilone: A compound isolated from the myxobacterium Sorangium cellulosum. Similar to paclitaxel, patupilone induces microtubule polymerization and stabilizes microtubules against depolymerization conditions. In addition to promoting tubulin polymerization and stabilization of microtubules, this agent is cytotoxic for cells overexpressing P-glycoprotein, a characteristic that distinguishes it from the taxanes. Epothilone B may cause complete cell-cycle arrest.
Pavabid: (Other name for: papaverine hydrochloride)
pavunalimab: An Fc-engineered bispecific antibody directed against the human negative immunoregulatory checkpoint receptors cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4) and lymphocyte activation gene 3 protein (LAG3; LAG-3; CD223), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, bavunalimab targets and binds to both CTLA-4 and LAG-3 expressed on T cells in the tumor microenvironment (TME). Both CTLA-4 and LAG-3 are inhibitory receptors and members of the immunoglobulin superfamily (IgSF); they are overexpressed by regulatory T cells (Tregs) in the TME where they downregulate T-cell activation and proliferation. Dual checkpoint blockade of CTLA-4 and LAG-3 with XmAb22841 may enhance T-cell activation and proliferation more than the blockade of either immune checkpoint receptor alone. The engineered Fc domain increases the stability and half-life of the antibody.
pavurutamab: A bispecific T-cell engager (BiTE) antibody composed of two single-chain variable fragments (scFv), one directed against the tumor-associated antigen (TAA) human B-cell maturation antigen (BCMA; TNFRSF17), fused to one that is directed against the CD3 antigen found on T-lymphocytes, with potential immunostimulating and antineoplastic activities. Upon administration of pavurutamab, this bispecific antibody binds to both CD3 on cytotoxic T-lymphocytes (CTLs) and BCMA found on BCMA-expressing tumor cells. This activates and redirects CTLs to BCMA-expressing tumor cells, which results in the CTL-mediated cell death of BCMA-expressing tumor cells. BCMA, a member of the tumor necrosis factor receptor superfamily that is specifically overexpressed on malignant plasma cells, plays a key role in promoting plasma cell survival.
paxalisib: A phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. paxalisib specifically inhibits PI3K in the PI3K/AKT kinase (or protein kinase B) signaling pathway, thereby inhibiting the activation of the PI3K signaling pathway. This may result in the inhibition of both cell growth and survival in susceptible tumor cell populations. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.
Paxil: (Other name for: paroxetine hydrochloride)
Paxil CR: (Other name for: paroxetine hydrochloride)
pazopanib hydrochloride: The hydrochloride salt of a small molecule inhibitor of multiple protein tyrosine kinases with potential antineoplastic activity. Pazopanib selectively inhibits vascular endothelial growth factor receptors (VEGFR)-1, -2 and -3, c-kit and platelet derived growth factor receptor (PDGF-R), which may result in inhibition of angiogenesis in tumors in which these receptors are upregulated.
pBCAR3 phosphopeptide-tetanus peptide vaccine: A vaccine composed of a phosphorylated peptide from the tumor-associated antigen breast cancer anti-estrogen resistance-3 (BCAR3) and a tetanus-derived peptide, with potential immunomodulating and antineoplastic activities. Upon administration of pBCAR3 phosphopeptide-tetanus peptide vaccine, the pBCAR3 phosphopeptide may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against phosphopeptide-containing tumor cells. The tetanus peptide serves as an immunoadjuvant and induces a helper T-cell response, which may help stimulate an immune response against the pBCAR3-expressing melanoma tumor cells. BCAR3 is upregulated in a variety of cancer cells.
pBCAR3/pIRS2-phosphopeptide-tetanus peptide vaccine: A vaccine composed of phosphorylated peptides from the tumor associated antigens breast cancer anti-estrogen resistance-3 (BCAR3) and insulin receptor substrate-2 (IRS2) and a tetanus-derived peptide, with potential immunomodulating and antineoplastic activities. Upon administration of pBCAR3/pIRS2 phosphopeptide-tetanus peptide vaccine, the pBCAR3/pIRS2 phosphopeptide may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing either phosphopeptide. The tetanus peptide serves as an immunoadjuvant and induces a helper T-cell response which may help stimulate an immune response against pBCAR3 and pIRS2-expressing melanoma tumor cells. BCAR3 and IRS2 are upregulated in a variety of cancer cells.
pbi-shRNA STMN1 lipoplex: A proprietary RNA interference construct consisting of bifunctional short hairpin RNAs (shRNA) against human stathmin 1 (STMN1) encapsulated in the cationic bilamellar invaginated vesicle lipoplex (LP) with potential antineoplastic activity. pbi-shRNA STMN1 LP contains 2 stem-loop structures encoded by a plasmid vector. Upon intratumoral administration, one shRNA unit with a perfectly matched sequence renders the suppression of STMN1 mRNA translation (mRNA sequestration and cleavage-independent degradation) while the other unit with an imperfectly matched sequence renders STMN1 mRNA degradation via RNase H-like cleavage (cleavage-dependent mRNA silencing). The suppression of STMN1 expression in tumor cells results in a reduction of tumor cell proliferation. STMN1, a ubiquitous cytosolic phosphoprotein and tubulin modulator that plays a key role in mitosis, is overexpressed in a variety of tumors and correlates with poor prognosis.
PCNA inhibitor AOH1996: An orally bioavailable, small molecule inhibitor of proliferating cell nuclear antigen (PCNA), with potential chemo-sensitizing and antineoplastic activities. Upon oral administration, PCNA inhibitor AOH1996 penetrates cells and targets and binds to PCNA, preventing the binding of PCNA's interacting proteins to PCNA. This disrupts the interactions between PCNA and these proteins and may result in DNA replication stress and inhibition of DNA repair, which may enhance the efficacy of some antineoplastic agents and induce apoptosis. PCNA is a scaffold protein involved in multiple cellular processes via its interactions with many proteins.
PCV regimen: A regimen consisting of procarbazine, lomustine and vincristine used for the treatment of gliomas.
PD-1 knockout autologous T lymphocytes: A population of engineered autologous T lymphocytes in which the gene encoding for the programmed cell death protein 1 (PDCD-1) is deleted, with potential immunomodulating activity. Following collection of peripheral blood lymphocytes and selection of T cells, the PDCD-1 gene was knocked out and the T cells were expanded. Upon reinfusion of the PDCD-1 knockout T lymphocytes, these T cells target and lyse cancer cells. The PDCD-1 protein, found on activated T cells and often overexpressed on T cells in cancer patients, negatively regulates T-cell activity; it plays a key role in immune evasion and prevents tumor cell lysis. PDCD-1 knockout enhances cytotoxicity and T-cell-mediated anti-tumor immune responses.
PD-1 knockout EBV-specific cytotoxic T lymphocytes: A preparation of Epstein-Barr virus (EBV) reactive cytotoxic T lymphocytes (CTLs) in which the programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1) gene is deleted, with potential immunomodulating activity. Upon administration of the PD-1 knockout EBV-specific CTLs, these CTLs target and induce selective toxicity in EBV-positive cancer cells. This results in cell lysis and inhibition of cancer cell proliferation. Expression of PD-1, an inhibitory receptor expressed on activated T cells, plays a key role in CTL suppression, T-cell exhaustion and CTL apoptosis. PD-1 knockout abrogates T-cell exhaustion and increases T-cell activity and cytotoxicity. EBV, a ubiquitous human herpesvirus, is associated with various cancer cell types.
PD-1 targeted IL-2 mutein fusion protein KY-0118: A fusion protein comprised of a human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279)-targeting moiety linked to an interleukin-2 (IL-2) mutein, with potential immunostimulating and antineoplastic activities. Upon administration of PD-1-targeted IL-2 mutein fusion protein KY-0118, the PD-1 targeting moiety targets and binds to PD-1 expressed on tumor-infiltrating lymphocytes (TILs) and inhibits PD-1-mediated downregulation of T-cell activation and proliferation. The IL-2 mutein moiety activates IL-2 cytokine signaling. This stimulates a local immune response and activates natural killer (NK) cells and cytotoxic T cells. This may enhance the activity of neoantigen specific T cells and potentiates T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity.
PD-1-directed probody CX-188: A probody composed of a monoclonal antibody directed against the negative immunoregulatory human cell surface receptor, programmed cell death protein 1 (PD-1; PDCD1; CD279), linked to a proprietary masking peptide that covers the active antigen binding site of the antibody through a protease-cleavable linker, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of PD-1-directed probody CX-188, the masking peptide is cleaved by tumor-associated proteases within the tumor microenvironment (TME). Protease-mediated removal of the linker enables binding of the unmasked monoclonal antibody moiety to PD-1, thereby disrupting PD-1 signaling. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity. Tumor-associated proteases are present in high concentrations and aberrantly activated in the TME.
PD-1-targeted IL-15 mutein fusion protein PF-07209960: A fusion protein composed of a moiety targeting the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) fused to a mutein of the cytokine interleukin-15 (IL-15), with potential immune checkpoint inhibitory, immunomodulating and antineoplastic activities. Upon administration of PD-1-targeted IL-15 mutein fusion protein PF-07209960, the PD-1 targeting moiety specifically targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. The IL-15 mutein moiety binds to the IL-15 receptor and activates IL-15 cytokine signaling. This stimulates the proliferation of natural killer (NK) cells, cytotoxic T lymphocytes (CTLs) and memory T cells locally in the tumor microenvironment (TME), and induces an anti-tumor immune response. This may increase tumor cell killing and decrease tumor cell proliferation. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity. IL-15 regulates CD8+ T- and NK-cell development, activation and proliferation.
PD-1-targeted IL-2 variant antibody fusion protein RO7284755: A recombinant fusion protein comprised of an antibody directed against the human negative immunoregulatory checkpoint receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) linked to an engineered, variant form of interleukin-2 (IL-2v), with potential immunostimulating and antineoplastic activities. Upon administration of PD-1-targeted IL-2v antibody fusion protein RO7284755, the antibody moiety specifically targets and binds to PD-1 expressed on tumor-infiltrating lymphocytes (TILs) and inhibits the PD-1-mediated downregulation of T-cell activation and proliferation. The IL-2 moiety may stimulate a local immune response and activate natural killer (NK) cells and cytotoxic T cells. This may enhance the activity of neoantigen specific T cells and potentiates T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands, programmed cell death-1 ligand 1 (PD-L1; B7-H1; CD274) and 2 (PD-L2); it plays an important role in tumor evasion from host immunity. IL-2v cannot bind to IL-2 receptor-alpha (CD25, IL2Ra) and does not activate regulatory T cells (Tregs).
PD-L1 inhibitor ABSK043: An orally available, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor ABSK043 specifically targets and binds to PD-L1 expressed on tumor cells, leading to internalization and preventing the binding to and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.
PD-L1 inhibitor BPI-371153: An orally bioavailable, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor BPI-371153 specifically targets and binds to PD-L1 expressed on tumor cells, thereby preventing the binding to and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.
PD-L1 inhibitor GS-4224: An orally available, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory, anti-viral and antineoplastic activities. Upon administration, PD-L1 inhibitor GS-4224 specifically targets PD-L1 expressed on tumor cells preventing the binding and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. It may also enhance hepatitis B virus (HBV)-specific CD8+ T-cell function, thereby killing HBV-infected cells. PD-L1, a transmembrane protein expressed on activated T cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells. It is also upregulated in HBV-positive patients and contributes to immune dysfunction against HBV infection.
PD-L1 inhibitor INCB086550: An orally available, small molecule inhibitor of the immunosuppressive ligand, programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, PD-L1 inhibitor INCB086550 specifically targets PD-L1 expressed on tumor cells preventing the binding and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.
PD-L1 inhibitor INCB099280: An orally bioavailable, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor INCB099280 specifically targets and binds to PD-L1 expressed on tumor cells, thereby preventing the binding to and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.
PD-L1 inhibitor INCB099318: An orally available, small molecule inhibitor of the immunosuppressive ligand programmed cell death-1 ligand 1 (PD-L1; cluster of differentiation 274; CD274), with potential immune checkpoint inhibitory and antineoplastic activities. Upon oral administration, PD-L1 inhibitor INCB099318 specifically targets and binds to PD-L1 expressed on tumor cells, thereby preventing the binding and subsequent activation of its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This reverses T-cell inactivation caused by PD-L1/PD-1 signaling, increases T-cell expansion and enhances the cytotoxic T-lymphocyte (CTL)-mediated anti-tumor immune response against PD-L1-expressing tumor cells. PD-L1, a transmembrane protein expressed on activated T cells, is overexpressed in some cancer types and plays a significant role in immune evasion by tumor cells.
PD-L1 peptide vaccine: A vaccine composed of a peptide derived from the tumor-associated antigen (TAA) and immune checkpoint molecule programmed cell death-1 ligand 1 (PD-L1) combined with the immunoadjuvant montanide ISA-51, with potential immunomodulating and antineoplastic activities. Vaccination with PD-L1 peptide vaccine may activate the immune system to induce an immune response against PD-L1-expressing cells. This may increase and restore the proliferation and activation of various immune cells, including cytotoxic T lymphocytes (CTLs), and may eradicate PD-L1-expressing tumor cells. PD-L1 is overexpressed on many human cancer cell types as well as on antigen presenting cells (APCs) and immunosuppressive cells in the tumor micro-environment (TME), such as regulatory T cells (Tregs). PD-L1 binding to its cognate receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) on T cells suppresses the immune system and results in increased immune evasion and decreased CTL activation. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.
PD-L1/4-1BB/HSA trispecific fusion protein NM21-1480: A recombinant, trispecific monovalent antibody-based molecule targeting the human programmed death-ligand 1 (PD-L1), 4-1BB (CD137; tumor necrosis factor receptor superfamily member 9; TNFRSF9) and human serum albumin (HSA), with potential checkpoint inhibitory, immunostimulating and antineoplastic activities. PD-L1/4-1BB/HSA trispecific fusion protein NM21-1480 consists of three monovalent antibody Fvs specific for PD-L1, HSA and 4-1BB fused in a single chain. Upon administration, PD-L1/4-1BB/HSA trispecific fusion protein NM21-1480 simultaneously targets and binds to a membrane-distal epitope of 4-1BB, which is expressed on a variety of leukocyte subsets including activated T-lymphocytes, and PD-L1 expressed on tumor cells. The simultaneous binding to PD-L1 enables clustering of 4-1BB and thereby allows for conditional stimulation of 4-1BB signaling in the tumor microenvironment (TME) only upon binding to PD-L1 on tumor cells. 4-1BB activation results in T-cell stimulation and enhances T-lymphocyte-mediated anti-tumor activity. At the same time, NM21-1480 prevents PD-L1 from binding to and activating its receptor, programmed cell death 1 (PD-1; PDCD1; CD279; programmed death-1). This abrogates T-cell inhibition, activates antigen-specific T-lymphocytes and enhances cytotoxic T-cell-mediated tumor cell lysis, which may lead to a reduction in tumor growth. PD-L1 binding to PD-1 on activated T cells inhibits the expansion and survival of CD8-positive T cells, suppresses the immune system and results in immune evasion. 4-1BB, a surface glycoprotein of the tumor necrosis factor receptor superfamily, is an inducible costimulatory receptor that plays a key role in T-cell proliferation, survival and cytolytic activity. HSA fusion prolongs the half-life of NM21-1480. The conditional activation of 4-1BB signaling prevents systemic T-cell activation and lowers toxicity.
PD-L1/IDO peptide vaccine IO102-103: A peptide vaccine composed of IO103, a peptide vaccine derived from the tumor-associated antigen (TAA) programmed cell death-1 ligand 1 (PD-L1), IO102, the 21-mer peptide vaccine derived from the immunomodulatory enzyme indoleamine 2,3-dioxygenase (IDO), and the immunoadjuvant montanide ISA-51, with potential immunomodulating and antineoplastic activities. Vaccination with the PD-L1/IDO peptide vaccine IO102-103 may activate the immune system to induce an immune response against PD-L1 and IDO-expressing cells. This may increase and restore the proliferation and activation of various immune cells, including cytotoxic T lymphocytes (CTLs), and may eradicate PD-L1 and IDO-expressing tumor cells through a CTL-mediated immune response. PD-L1 is overexpressed on many human cancer cell types. PD-L1 binding to its cognate receptor programmed cell death protein 1 (PD-1; PDCD1; CD279) on T cells suppresses the immune system and results in increased immune evasion and decreased CTL activation. IDO, a cytosolic enzyme responsible for tryptophan catabolism and conversion of tryptophan into kynurenine, is overexpressed by a variety of tumor cell types and antigen presenting cells (APCs) and plays an important role in immunosuppression mainly through suppression of CTL activation; tryptophan depletion inhibits T-lymphocyte proliferation and activation, and suppresses the immune system. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.
PD-L1/PD-L2 peptide-Montanide vaccine: A vaccine composed of peptides derived from the immune checkpoint molecules, programmed death ligand 1 (PD-L1) and programmed death ligand 2 (PD-L2), combined with the immunoadjuvant montanide ISA-51, with potential immunomodulating and antineoplastic activities. Vaccination with PD-L1/PD-L2 peptide-montanide vaccine may stimulate an immune response against PD-L1 and PD-L2 expressing cells. This may enhance T-cell proliferation, cytokine production, and T-cell mediated cytolysis. Binding of programmed cell death protein 1 (PD-1; PDCD1; CD279) by its ligands, PD-L1 and PD-L2, results in downregulation of T-cell responses and enhanced immune evasion. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.
PD-L1/PD-L2/VISTA antagonist CA-170: An orally bioavailable small molecule inhibitor of the immune checkpoint regulatory proteins programmed cell death ligand-1 (PD-L1; B7-H1; CD274), PD-L2, and V-domain immunoglobulin (Ig) suppressor of T-cell activation (VISTA; programmed death 1 homolog; PD1H; PD-1H), with potential negative immune checkpoint regulatory and antineoplastic activities. Upon oral administration, PD-L1/PD-L2/VISTA antagonist CA-170 targets and binds to PD-L1, PD-L2 and VISTA. This inhibits PD-L1/PD-L2/VISTA-mediated signaling, abrogates the PD-L1-, PD-L2- and VISTA-induced suppression of T-lymphocyte immune responses, enhances cytotoxic T-cell proliferation and activation against tumor cells, increases cytokine production by T-cells, and inhibits tumor cell growth. PD-L1, PD-L2 and VISTA, negative checkpoint molecules of immune activation, play key roles in the suppression of T-cell functions.
PD-L2 peptide-Montanide vaccine: A vaccine composed of a peptide derived from the immune checkpoint molecule programmed death ligand 2 (PD-L2) combined with the immunoadjuvant montanide ISA-51, with potential immunomodulating and antineoplastic activities. Vaccination with PD-L2 peptide-montanide vaccine may mount an immune response against PD-L2 expressing cells. This may enhance T-cell proliferation, cytokine production, and T-cell mediated cytolysis. PD-L2 binding to its cognate receptor, programmed cell death protein 1 (PD-1; PDCD1; CD279), downregulates T-cell responses and enhances immune evasion. Montanide ISA-51, also known as incomplete Freund's adjuvant or IFA, is a stabilized water-in-oil emulsion adjuvant containing mineral oil with mannide oleate added as a surfactant that non-specifically stimulates cell-mediated immune responses to antigens.
PDK1 inhibitor AR-12: An orally bioavailable, small-molecule, celecoxib-derived inhibitor of phosphoinositide-dependent kinase-1 (PDK1) with potential antineoplastic activity. Devoid of any COX inhibiting activity, PDK1 inhibitor AR-12 binds to and inhibits the phosphorylation of 3-phosphoinositide-dependent kinase-1 (PDK-1).; subsequently, the phosphorylation and activation of the serine/threonine protein kinase Akt (protein kinase B or PKB) is inhibited, which may result in inhibition of the PI3K/Akt signaling pathway, inhibition of tumor cell proliferation, and the induction of tumor cell apoptosis. In addition, this agent appears to induce the activity of protein kinase R-like endoplasmic reticulum kinase (PERK), which plays a key role in the endoplasmic reticulum stress pathway. Activation and dysregulation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.
pDNA-encoding Emm55 autologous cancer cell vaccine IFx-Hu2.0: A whole cell cancer vaccine composed of irradiated autologous whole tumor cells that are transfected, ex vivo, with a plasmid DNA encoding the highly immunogenic Streptococcus pyogenes (S. pyogenes) bacterial antigen Emm55, with potential immunostimulating and antineoplastic activities. Upon intralesional administration of IFx-Hu2.0, the tumor cells expressing the Emm55 bacterial antigen on their cell surface are taken up and processed by antigen-presenting cells (APCs), thereby presenting both the Emm55 and the patient-specific tumor-associated antigens (TAAs) to the immune system. This activates the immune system to elicit a tumor antigen-specific cytotoxic T-lymphocyte (CTL)-mediated immune response against the tumor cells expressing the TAAs.
PE/HPV16 E7/KDEL fusion protein/GPI-0100 TVGV-1: A vaccine composed of a lyophilized fusion protein consisting of a peptide sequence of human papillomavirus type 16 (HPV16) E7 nuclear protein fused to the Pseudomonas aeruginosa exotoxin A (PE) and an endoplasmic reticulum (ER) retention signal (KDEL) combined with the immunoadjuvant GPI-0100, a semi-synthetic dodecylamide saponin derivative, with potential immunomodulating and antineoplastic activities. Upon administration of PE/HPV16 E7/KDEL fusion protein/GPI-0100 TVGV-1, the PE moiety of the fusion protein targets and binds to CD91 (Prolow-density lipoprotein receptor-related protein 1; LRP1) expressed on a variety of cells, including antigen-presenting cells (APCs) such as dendritic cells (DCs), which facilitates the internalization, through endocytosis, of TVGV-1. Following endocytosis, this agent is proteolytically cleaved by the proteasome and the epitopes from the HPV16 E7 protein become bound to major histocompatibility complex class I (MHC-I) molecules and are presented on the DC-cell surface. This facilitates a cytotoxic T-lymphocyte (CTL)-mediated immune response against HPV16 E7 expressing-tumor cells. KDEL targets the fusion protein to the ER which increases this agent's potential to be bound by MHC-I molecules and increases the immune response against HPV16 E7-expressing cancer cells. GPI-0100 acts as an adjuvant for vaccines to improve the immunogenicity of proteins.
PEB regimen: A chemotherapy regimen consisting of bleomycin, etoposide and cisplatin used for the treatment of pediatric germ cell tumors (GCT). In the PEB regimen, the pediatric patients receive bleomycin once per cycle and do not receive weekly bleomycin during the weeks between cycles (every 21 days); in the adult BEP regimen, patients receive weekly bleomycin.
PectaSol-C: (Other name for: modified citrus pectin supplement)
Pedi-Vit-A: (Other name for: vitamin A compound)
PediaBerry: (Other name for: powdered mixed berry extract supplement)
PEDIARIX: (Other name for: diphtheria toxoid/tetanus toxoid/acellular pertussis adsorbed, recombinant hepatitis B/inactivated poliovirus vaccine combined)
PediaSure: (Other name for: nutritional supplement drink (pediatric))
PedvaxHIB: (Other name for: Haemophilus influenzae b vaccine)
PEG-3350/sodium sulfate/sodium chloride/potassium chloride/sodium ascorbate/ascorbic acid-based laxative: A preparation containing the nonabsorbable polymer polyethylene glycol (PEG or macrogol) 3350 and sodium sulfate, sodium chloride, potassium chloride, sodium ascorbate and ascorbic acid with laxative activity. Upon oral administration, the PEG-3350, sodium sulfate, sodium chloride, potassium chloride, sodium ascorbate and ascorbic acid-based laxative promotes the retention of water in the bowel. This increases the water content of stool, which results in increased gastrointestinal motility and evacuation of colonic contents. This results in a complete cleansing of the colon. Compared to the 4 liter PEG-3350-based preparations, this PEG-based laxative is a low volume (2 liter) preparation, which improves patients’ tolerance.
PEG-based laxative NER1006: A preparation containing the nonabsorbable polymer polyethylene glycol (PEG or macrogol) 3350 with laxative activity. Upon oral administration, the PEG-3350-based laxative NER1006 promotes the retention of water in the bowel. This increases both the water content and volume of stool, which results in increased gastrointestinal motility and the evacuation of colonic contents leading to a complete cleansing of the colon. Compared to the 4 liter PEG-3350-based preparations, this PEG-based laxative is a low volume (2 liter) preparation, which may improve tolerance.
PEG-conjugated TLR7/8 agonist NKTR-262: A formulation composed of an agonist of toll-like receptor (TLR) type 7 and 8 (TLR7/8) that is attached to polyethylene glycol (PEG) via a hydrolyzable glycine linker, with potential immunostimulating and antitumor activities. Upon intratumoral (IT) administration, TLR7/8 agonist NKTR-262 binds to and activates TLR7 and 8, thereby activating TLR7/8-mediated pathways. This stimulates the maturation and activation of antigen-presenting cells (APCs), including dendritic cells (DCs). Activation of DCs results in the production of pro-inflammatory cytokines, and the activation of cytotoxic T-lymphocyte (CTL)- and B-lymphocyte-mediated immune responses against tumor-associated antigens (TAAs), which lead to tumor cell lysis. TLR7 and 8, members of the TLR family, play fundamental roles in the activation of the innate immune system, myeloid cell responses and tumor antigen presentation. Pegylation of the TLR7/8 agonist enhances retention of this agent in the tumor microenvironment (TME), provides local sustained release of the TLR7/8 agonist, increases efficacy and reduces systemic exposure compared to the administration of the naked TLR7/8 agonist alone.
PEG-interleukin-2: A complex of polyethylene glycol conjugated with human recombinant cytokine interleukin-2 (IL-2) with antineoplastic activity. PEG-interleukin-2 induces natural killer (NK) cell activity and the production of interferon-gamma (IFN-gamma), and enhances T cell-mediated cytotoxicity. Pegylation of IL-2 protects the cytokine from degradation.
PEG-modified/site-mutated IL-2 SHR-1916: A polyethylene glycol (PEG)-modified and site-mutated form of the cytokine interleukin-2 (IL-2), with potential immunopotentiating and antineoplastic activities. Upon administration, PEG-modified/site-mutated IL-2 SHR-1916 activates the Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway. This induces the selective proliferation of CD8+ T cells and natural killer (NK) cells, enhances tumor cell killing and decreases tumor cell proliferation. Pegylation of IL-2 protects the cytokine from degradation.
PEG-PEI-cholesterol lipopolymer-encased IL-12 DNA plasmid vector IMNN-001: A nanoparticle-based formulation composed of a non-viral plasmid DNA vector encoding the human pro-inflammatory cytokine interleukin-12 (IL-12) encapsulated in a biodegradable, biocompatible lipoplex composed of polyethylene glycol (PEG), polyethylenimine (PEI), and cholesterol, with potential immunoactivating and antineoplastic activities. Upon intraperitoneal (IP) delivery of the PEG-PEI-cholesterol lipopolymer-encased IL-12 DNA plasmid vector IMNN-001, the lipoplex is endocytosed by nearby cells, and the plasmid DNA is transported into the nucleus, which leads to local expresssion of IL-12. In turn, the increased IL-12 production at the tumor site activates the immune system by promoting the activation of natural killer cells (NKs), inducing secretion of interferon-gamma (IFN-g) and promoting cytotoxic T-cell responses against tumor cells.
PEG4000/simethicone/sodium sulphate/sodium bicarbonate/electrolytes oral solution: A powder for orF3:J23tion containing polyethylene glycol (PEG) 4000 (macrogol 4000), simethicone, sodium sulphate, sodium bicarbonate, and electrolytes, with laxative and bowel cleansing activities. Upon oral administration, macrogol 4000-based oral osmotic laxative promotes the retention of water in the bowel, thereby increasing the water content of stool, which results in increased gastrointestinal (GI) motility, accelerated stool transit time and evacuation of colonic contents.
pegargiminase: An agent consisting of the arginine-degrading enzyme arginine deiminase combined with polyethylene glycol (20,000 MW) (ADI-PEG 20) with potential antineoplastic activity. Upon administration, pegargiminase breaks down the amino acid arginine into citrulline. Although arginine is a nonessential amino acid for normal human cells, certain cancer cells are autotrophic for arginine and need arginine in order to survive. Depletion of arginine may lead to an inhibition of cellular proliferation in those cancer cells. ADI is coupled to PEG in order to enhance this agent's half-life.
pegaspargase: A complex of polyethylene glycol conjugated with L-asparaginase. Asparaginase hydrolyzes L-asparagine to L-aspartic acid and ammonia, thereby depleting these cells of asparagine and blocking protein synthesis and tumor cell proliferation, especially in the G1 phase of the cell cycle. The agent also induces apoptosis in tumor cells. Pegylation decreases the enzyme's antigenicity. Asparagine is critical to protein synthesis in leukemic cells, which cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase.
PEGASYS: (Other name for: peginterferon alfa-2a)
pegcetacoplan: A pegylated peptide inhibitor of human complement components C3 and C3b, with potential use as a treatment for various diseases in which excessive complement activation plays a key role, including paroxysmal nocturnal hemoglobinuria (PNH), geographic atrophy (GA), cold agglutinin disease (CAD), and C3 glomerulopathy (C3G). Upon administration, pegcetacoplan selectively binds to C3 and C3b and inhibits their activities. This prevents complement pathway activation, and inhibits complement-mediated inflammation and cell lysis. Excessive complement activation plays a key role in various inflammatory and autoimmune diseases, and leads to tissue destruction. C3 is a key component of the complement system, and the complement system is an integral component of the innate immune response.
pegcrisantaspase: A recombinant, pegylated form of Erwinia asparaginase (crisantaspase), derived from the bacterium Erwinia chrysanthemi and genetically engineered to be produced in Pseudomonas fluorescens, with potential antineoplastic activity. Pegcrisantaspase hydrolyzes L-asparagine to L-aspartic acid and ammonia. This depletes cancer cells of asparagine, which blocks protein synthesis and tumor cell proliferation. Asparagine is critical to protein synthesis in cancer cells, which cannot synthesize this amino acid due to the absence of the enzyme asparagine synthase. Pegcrisantaspase can be used as an alternative in patients who are hypersensitive to Escherichia (E.) coli-derived asparaginase products.
pegdinetanib: A highly specific, synthetic peptide vascular endothelial growth factor receptor-2 (VEGFR-2) antagonist with potential antiangiogenic activity. Derived from human fibronectin with a proprietary protein engineering process, pegdinetanib may block the activation of VEGFR-2 by all known activating ligands, thereby inhibiting the growth of new tumor blood vessels.
pegenzileukin: A pegylated recombinant, engineered variant of cytokine interleukin-2 (IL-2; IL2) where novel amino acid is encoded in the IL-2 gene that is leveraged for use in site-specific pegylation, with potential immunostimulating activity. Upon administration of pegenzileukin, the IL-2 variant moiety binds to dimers containing the IL-2 receptor beta and gamma chains (IL2Rbg; IL2Rbetagamma) on immune cells, such as cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells, thereby activating these cells and inducing their expansion. It also induces the expression of certain cytotoxic cytokines, such as interferon-gamma (IFNg) and transforming growth factor-beta (TGFb). The specific induction of T-cell-mediated cytotoxic immune responses against tumor cells causes tumor cell destruction. The addition of the novel amino acid and the concurrent pegylation prevents the binding of the IL-2 moiety to the IL-2 receptor alpha chain (IL2Ra), thereby blocking the IL2Ra-mediated activation of CD4-positive regulatory and immunosuppressive T cells (Tregs). Since it cannot bind to IL2Ra expressed on innate lymphoid cells in the vascular endothelium, pegenzileukin prevents IL-2-mediated recruitment and activation of eosinophils, and inhibits the induction of eosinophil-mediated vascular leak syndrome (VLS). Pegylation also extends the half-life of pegenzileukin. Compared to recombinant IL-2, pegenzileukin allows for increased IL-2Rbg binding and proliferation of CTLs without stimulating the toxicity caused by binding to IL-2Ra.
pegfilgrastim: A long-acting pegylated form of a recombinant therapeutic agent which is chemically identical to or similar to an endogenous human granulocyte colony-stimulating factor (G-CSF). Produced endogenously by monocytes, fibroblasts, and endothelial cells, G-CSF binds to and activates specific cell surface receptors, stimulating neutrophil progenitor proliferation and differentiation and selected neutrophil functions. Conjugation of the cytokine with a branched polyethylene glycol molecule (pegylation) significantly increases its therapeutic half-life.
pegfilgrastim anti-neutropenic factor: A long-acting, engineered and pegylated version of human granulocyte-colony stimulating factor (G-CSF), with potential hematopoietic activity. Similar to G-CSF, pegfilgrastim anti-neutropenic factor (ANF) binds to and activates specific cell surface receptors, and stimulates neutrophil progenitor proliferation and differentiation. Therefore, this agent may prevent the duration and incidence of chemotherapy-induced neutropenia. Compared to filgrastim, the conjugation with a branched polyethylene glycol molecule reduces renal clearance and increases its plasma half-life.
pegfilgrastim biosimilar LA-EP2006: A biosimilar of pegfilgrastim, a long-acting pegylated form of recombinant human granulocyte colony-stimulating factor (G-CSF) filgrastim, with hematopoietic activity. In a similar manner to G-CSF, pegfilgrastim biosimilar LA-EP2006 binds to and activates specific cell surface receptors, stimulating neutrophil progenitor proliferation and differentiation and selected neutrophil functions. Therefore, this agent may prevent the incidence and shorten the duration of chemotherapy-induced neutropenia. Conjugation of the cytokine with a branched polyethylene glycol molecule significantly increases this agent's therapeutic half-life compared to filgrastim.
pegilodecakin: A covalent conjugate of recombinant human interleukin-10 (IL-10) and polyethylene glycol (PEG), with potential anti-fibrotic, anti-inflammatory, immunomodulating and antineoplastic activities. Upon subcutaneous administration, pegilodecakin may activate cell-mediated immunity against cancer cells by stimulating the differentiation and expansion of tumor specific cytotoxic CD8+ T cells. This agent may also lower serum cholesterol levels and reduce atherosclerotic plaques by inhibiting the synthesis of pro-inflammatory cytokines, such as Interferon-gamma, IL-2, IL-3, TNF-alpha, and GM-CSF. The PEG moiety inhibits proteolytic breakdown and clearance of AM0010, which prolongs its half-life, extends the duration of its therapeutic effects and allows less frequent dosing.
peginterferon alfa-2a: A covalent conjugate of recombinant interferon alfa, subtype 2a, and polyethylene glycol (PEG), used as an antiviral and antineoplastic agent. The biological activity of this agent is derived from its interferon alpha-2a protein moiety. Interferons alfa bind to specific cell-surface receptors, leading to the transcription and translation of genes whose protein products mediate antiviral, antiproliferative, anticancer and immune-modulating effects. The PEG moiety lowers the clearance of interferon alpha-2a, thereby extending the duration of its therapeutic effects, but may also reduce interferon-mediated stimulation of an immune response.
peginterferon alfa-2b: A covalent conjugate of recombinant interferon alpha, subtype 2b, and polyethylene glycol (PEG), used as an antiviral and antineoplastic agent. The biological activity of this agent is derived from its interferon alpha-2b protein moiety. Interferons alfa bind to specific cell-surface receptors, leading to the transcription and translation of genes whose protein products mediate antiviral, antiproliferative, anticancer, and immune-modulating effects. The PEG moiety lowers the clearance of interferon alpha-2b, thereby extending the duration of its therapeutic effects, but may also reduce the interferon-mediated stimulation of an immune response.
pegipanermin: A pegylated, human, engineered dominant-negative tumor necrosis factor (TNF; TNF-alpha) variant devoid of TNF receptor-binding activity, with potential anti-inflammatory activity. Upon administration, pegipanermin forms heterotrimers with native soluble TNF (sTNF) but not membrane-bound transmembrane TNF (tmTNF). This prevents the binding of sTNF with TNF receptors and inhibits sTNF pro-inflammatory signaling, thereby reducing inflammation. TNF, a pro-inflammatory cytokine, is upregulated in various diseases and in cytokine storm. sTNF signaling, primarily via TNF receptor 1 (TNFR1; CD120a; p55/p60), may be responsible for exacerbation of existing inflammatory response while tmTNF signaling, primarily via TNF receptor 2 (TNFR2; CD120b; p75/p80), plays an important role in immune system development and cell survival.
pegloticase: A recombinant modified mammalian urate oxidase (uricase) conjugated to monomethoxypolyethylene glycol (mPEG), that can be used to lower serum uric acid. Upon intravenous infusion, pegloticase catalyzes the oxidation of uric acid to allantoin, thereby lowering serum uric acid. Allantoin is an inert and water-soluble purine metabolite; it is readily eliminated, primarily by renal excretion.
pegol sihematide: A synthetic peptide derived from erythropoietin (EPO) linked to polyethylene glycol (PEG), with erythropoietic stimulating activity. Upon administration, pegol sihematide binds to and activates EPO receptors on the surface of erythroid progenitor cells in the bone marrow resulting in their differentiation and proliferation. This increases the production of red blood cells and prevents anemia. Pegylation increases this agent's blood circulation time.
pegsitacianine: A micellar polymer tracer labeled with the near-infrared (NIR) fluorescent imaging dye indocyanine green (ICG), with potential fluorescent imaging activity. Upon administration, pegsitacianine accumulates in tumor tissue. The micelles dissociate and subsequently fluoresce upon exposure to the acidic conditions of the tumor microenvironment (TME), allowing the visualization of tumors using infrared-based cameras.
pegteograstim: An analogue of pegfilgrastim, a recombinant, pegylated form of endogenous human granulocyte colony-stimulating factor (G-CSF), with hematopoietic activity. Similar to endogenous G-CSF, this agent binds to and activates specific cell surface receptors, and stimulates neutrophil progenitor proliferation, differentiation and selected neutrophil functions. Pegteograstim may prevent and shorten the duration of chemotherapy-induced neutropenia (CIN). Pegylation of teograstim increases the half-life of this agent.
pegtomarginase: A genetically modified form of human enzyme arginase (ARG) site-specifically linked with a linear 20 kDa polyethylene glycol (PEG), with potential arginine depleting and antineoplastic activities. Upon intravenous administration of pegtomarginase, arginase metabolizes the amino acid arginine to ornithine and urea, thereby lowering blood arginine levels. This normalizes blood arginine levels in patients with arginase deficiency and prevents hyperargininemia. As many cancer types lack the ability to synthesize arginine due to deficient expression of certain metabolic enzymes of the urea cycle and are dependent on extracellular arginine uptake for their proliferation, depriving cancer cells of arginine inhibits their proliferation. In normal, healthy cells, arginine is synthesized intracellularly by metabolic enzymes of the urea cycle, including ornithine transcarbamylase (OTC), argininosuccinate synthase (ASS), and argininosuccinate lyase (ASL), and they are not dependent on extracellular arginine for survival. Pegylation improves blood circulation times of this agent.
pegvisomant: A pegylated, recombinant, human growth hormone (GH) structural analog with GH receptor antagonist activity. As a GH analog, the structure of pegvisomant is similar to that of native GH with the exception of 9 amino acid substitutions. Pegvisomant selectively binds to GH receptors on cell surfaces, interfering with endogenous GH receptor binding and so GH signal transduction. Inhibition of GH signal transduction results in decreased serum concentrations of insulin-like growth factor-I (IGF-I), and other GH-responsive serum proteins, including IGF binding protein-3 (IGFBP-3) and the acid-labile subunit (ALS), and may inhibit the growth of cancers in which IGF-1 is upregulated.
pegylated CD25/CD122-selective interleukin-2 mutein STK-012: A pegylated, engineered variant form of the human cytokine interleukin 2 (IL-2; IL2), with selective binding affinity for IL-2 receptor subunit alpha (IL-2Ralpha; CD25) and beta (IL-2Rbeta; CD122), with potential immunoregulatory and antineoplastic activities. Upon administration, pegylated CD25/CD122-selective IL-2 mutein STK-012 targets and binds to CD25 and CD122 on antigen-activated effector T cells and activates CD25/CD122-mediated signaling. This activates cytotoxic T lymphocytes (CTLs), enhances T-cell-mediated tumor cell killing and decreases tumor cell proliferation. STK-012 does not activate peripheral natural killer (NK) and naive T cells, thereby circumventing the exacerbation of vascular leak syndrome (VLS) and other NK cell-mediated adverse effects associated with recombinant IL-2. CD25 and CD122 are highly expressed in antigen-activated and tumor-specific T cells.
pegylated deoxycytidine analogue DFP-14927: A pegylated formulation containing DFP-10917, an analogue of the nucleoside deoxycytidine, with potential antineoplastic activity. Upon administration, the pegylated deoxycytidine analogue DFP-14927 is incorporated into the DNA of rapidly proliferating cells, such as tumor cells, and directly inhibits the activity of DNA polymerase, which results in the inhibition of DNA replication and cell cycle arrest, DNA fragmentation, and tumor cell apoptosis.
pegylated granulocyte colony stimulating factor MAXY-G34: A long-acting, pegylated recombinant variant of human granulocyte colony-stimulating factor (G-CSF) with immunomodulating activity. Pegylated granulocyte colony stimulating factor MAXY-G34 contains multiple non-naturally occurring lysines that have been introduced into alpha helixes of wild type human G-CSF as pegylation sites; other naturally occurring lysine residues have been removed to prevent pegylation and the variant G-CSF is pegylated with methoxypolyethylene glycol succinimidyl propionate (mPEG SPA) at three amino acid residues. Similar to endogenous G-CSF, this agent binds to and activates specific cell surface receptors, stimulating neutrophil progenitor proliferation and differentiation and selected neutrophil functions. A difference in the degree of pegylation may account for the extended half-life of this agent compared to pegfilgrastim which is pegylated at only one amino acid residue.
pegylated IL-2 8MW2311: A polyethylene glycol (PEG)-conjugated form of the cytokine interleukin-2 (IL-2), with potential immunopotentiating and antineoplastic activities. Upon administration, pegylated IL-2 8MW2311 activates the Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway. This induces the proliferation of CD8+ T cells, enhances tumor cell killing and decreases tumor cell proliferation. Pegylation of IL-2 protects the cytokine from degradation.
pegylated interferon alfa: A covalent conjugate of recombinant interferon alpha and polyethylene glycol (PEG), used as an antiviral and antineoplastic agent. The biological activity of this agent is derived from its interferon alpha protein moiety. Interferons alfa bind to specific cell-surface receptors, leading to the transcription and translation of genes whose protein products mediate antiviral, antiproliferative, anticancer, and immune-modulating effects. The PEG moiety lowers the clearance of interferon alpha, thereby extending the duration of its therapeutic effects, but may also reduce interferon-mediated stimulation of an immune response.
pegylated liposomal doxorubicin hydrochloride: A liposome-encapsulated preparation of the hydrochloride salt of the anthracycline antineoplastic antibiotic doxorubicin. Doxorubicin intercalates between DNA base pairs, thereby hinders the movement of replication machinery along DNA strands, as well as blocks the activity of topoisomerase II during replication. As a result, this agent causes DNA adducts formation, renders single- and double-stranded DNA breakages that induce DNA repair and or apoptotic processes. Doxorubicin also generates reactive oxygen species that leads to cytotoxicity secondary to lipid peroxidation of cell membrane lipids. Liposomal delivery of doxorubicin HCl improves drug penetration into tumors and decreases drug clearance, thereby increasing the duration of therapeutic drug effects. A liposomal formulation of doxorubicin also modulates toxicity, specifically the cardiac effects commonly seen with anthracycline antitumor drugs.
pegylated liposomal irinotecan: A formulation of polyethylene glycol (PEG)-modified liposomes encapsulating the semisynthetic derivative of camptothecin irinotecan, with antineoplastic activity. As a prodrug, irinotecan is converted to the biologically active metabolite 7-ethyl-10-hydroxy-camptothecin (SN-38) by a carboxylesterase-converting enzyme. In turn, SN-38 inhibits topoisomerase I activity by stabilizing the cleavable complex of topoisomerase I and DNA, resulting in DNA breaks. This results in an inhibition of DNA replication and an induction of apoptosis. Pegylated liposomal delivery of irinotecan improves drug penetration into tumors and decreases drug clearance, thereby increasing the duration of exposure while lowering systemic toxicity.
pegylated liposomal mitomycin C lipid-based prodrug: A pegylated liposomal formulation comprised of a lipophilic prodrug of the antineoplastic antibiotic mitomycin C containing a cleavable disulfide bond (PL-MLP), with potential antineoplastic activity. Upon administration of the pegylated liposomal mitomycin C lipid-based prodrug, the MLP moiety becomes activated upon thiolysis at the tumor site, thereby releasing mitomycin C. Bioreduced mitomycin C generates oxygen radicals, alkylates DNA, and produces interstrand DNA cross-links, thereby inhibiting DNA synthesis. The thiolytic environment and upregulated expression of thioredoxins at the tumor site allow for the activation and release of mitomycin C. This prodrug formulation allows for greater circulation time, less systemic toxicity and increased accumulation of mitomycin C at the tumor site.
pegylated liposomal mitoxantrone hydrochloride: A pegylated liposomal mitoxantrone formulation composed of the hydrochloride salt form of the anthracenedione antibiotic mitoxantrone encapsulated within pegylated small unilamellar vesicles (SUVs), with potential antineoplastic activity. Upon intravenous administration, mitoxantrone intercalates into and forms crosslinks with DNA, thereby disrupting DNA and RNA replication. This agent also binds to topoisomerase II, which both results in DNA strand breaks and prevents DNA synthesis. This leads to the induction of apoptosis in rapidly dividing cancer cells. The pegylated liposomal formulation improves drug penetration into tumors and decreases drug clearance, thereby increasing drug circulation and therapeutic efficacy while lowering toxic effects.
pegylated orthogonal IL-2 STK-009: A polyethylene glycol (PEG)-conjugated mutein form of the cytokine interleukin-2 (IL-2), with potential and specific activity on enhancing proliferation, survival and anti-tumor activity of engineered orthoIL-2Rb-expressing CAR T cells. Upon subcutaneous administration, pegylated orthogonal (ortho) IL-2 STK-009 specifically targets and binds to mutated orthoIL-2Rbeta (hoRbeta; hoRb) that is specifically expressed on certain engineered CAR T cells. This induces selective proliferation, survival, and cytotoxic function of orthoIL-2Rbeta-expressing CAR T cells, which enhances tumor cell killing and decreases tumor cell proliferation. Pegylation of IL-2 protects the cytokine from degradation. STK-009 does not bind to the wild type (WT) IL-2b receptor and does not activate IL-2-mediated signaling in bystander T and NK cells, thereby limiting systemic toxicity.
pegylated recombinant human arginase I BCT-100: A recombinant human arginase I (liver arginase) covalently attached, via a succinamide propionic acid (SPA) linker, to a polyethylene glycol (PEG) of molecular weight 5,000 [rhArg-peg(5,000mw)] with potential antineoplastic activity. Upon intravenous administration of pegylated recombinant human arginase I BCT-100, arginase metabolizes the amino acid arginine to ornithine and urea, depleting intracellular arginine, which may inhibit proliferation of cells that are auxotrophic for arginine such as hepatocellular carcinoma (HCC) cells. This agent may also work synergistically with various cytotoxic agents.
pegylated recombinant human hyaluronidase PH20: A pegylated formulation of a recombinant form of human hyaluronidase with potential antitumor activity. Upon intravenous administration, pegylated recombinant human PH20 degrades hyaluronic acid (HA) coating tumor cells, which may result in the inhibition of tumor cell growth. In addition, the degradation of HA may result in a lowering of the interstitial fluid pressure (IFP), allowing better penetration of chemotherapeutic agents into the tumor bed. HA is a glycosaminoglycan found in the extracellular matrix (ECM) that is frequently overproduced by various tumor cell types. The presence of HA in tumors correlates with increased tumor cell growth, metastatic potential, tumor progression, increased resistance to chemotherapeutic agents, and an elevation in tumor IFP.
pegylated SN-38 conjugate PLX038: A pegylated conjugate of SN-38 (7-ethyl-10-hydroxy-camptothecin), a biologically active metabolite of the prodrug irinotecan, with potential antineoplastic activity. Upon administration, the proprietary linker slowly releases SN-38 from the pegylated SN-38 conjugate PLX038. SN-38 binds to and inhibits topoisomerase I by stabilizing the cleavable complex between topoisomerase I and DNA, resulting in DNA breaks, inhibition of DNA replication, and apoptosis. Compared with irinotecan, this formulation allows higher accumulation in solid tumors due to its nanoparticle size and long half-life.
pegylated TOP1 inhibitor PEEL-224: A pegylated camptothecin derivative, with potential antineoplastic activity. Upon administration of pegylated TOP1 inhibitor PEEL-224, camptothecin reaches the tumor cells and selectively stabilizes covalent topoisomerase I-DNA complexes, which results in single-stranded and double-stranded DNA breaks, the inhibition of DNA replication, and the induction of apoptosis. Pegylation allows for increases in half-life and the exposure time for tumor cells, while decreasing both blood plasma concentrations and exposure to off-target organs. This may increase efficacy and reduce systemic toxicities.
pegzerepoetin alfa: A pegylated form of recombinant human erythropoietin, a glycosylated protein naturally produced in the kidney that stimulates erythrocyte production in the bone marrow. Pegzerepoetin alfa may reverse anemias induced by cancer therapy.
pegzilarginase: A recombinant modified form of the human enzyme arginase 1 (ARG1), in which cobalt is substituted for manganese as a cofactor, covalently attached to polyethylene glycol (PEG), with potential arginine degrading and antineoplastic activities. Upon intravenous administration of pegzilarginase, ARG1 metabolizes the amino acid arginine to ornithine and urea, thereby lowering blood arginine levels. This normalizes blood arginine levels in patients with ARG1 deficiency and prevents hyperargininemia. This also inhibits the proliferation of cancer cells that are dependent on extracellular arginine uptake for their proliferation. In normal, healthy cells, arginine is synthesized intracellularly by the enzymes ornithine transcarbamylase (OTC), argininosuccinate synthase (ASS), and argininosuccinate lyase (ASL); thus they are not dependent on extracellular arginine for survival. In cancer cells these enzymes are disabled; therefore, this agent may inhibit proliferation and survival of these cells by depleting extracellular arginine. Pegylation improves blood circulation times and cobalt substitution increases the catalytic activity of ARG1.
pelabresib anhydrous: The anhydrous form of pelabresib, a small molecule inhibitor of the Bromodomain and Extra-Terminal (BET) family of proteins, with potential antineoplastic activity. Upon administration, pelabresib binds to the acetylated lysine recognition motifs on the bromodomain of BET proteins, thereby preventing the interaction between the BET proteins and acetylated histone peptides. This disrupts chromatin remodeling and gene expression. Prevention of the expression of certain growth-promoting genes may lead to an inhibition of tumor cell growth. Characterized by a tandem repeat of two bromodomains at the N-terminus, the BET proteins (BRD2, BRD3, BRD4 and BRDT) are transcriptional regulators that play an important role during development and cellular growth.
pelareorep: An isolate of the oncolytic, human wild-type serotype 3 Dearing (T3D) strain of the double-stranded RNA virus reovirus (Respiratory Enteric Orphan virus), with potential oncolytic activity. Upon administration, pelareorep is able to replicate specifically in cancer cells bearing an activated Ras pathway. This induces apoptosis in Ras-activated tumor cells and subsequently frees progeny viral particles to infect, replicate in and induce cell death of surrounding cancer cells. In addition, viral replication causes the activation of innate and adaptive immune responses, causing a natural killer (NK)-cell-mediated and a cytotoxic T-cell (CTL)-mediated killing of tumor cells, respectively. Ras-activated tumor cells are deficient in their ability to trigger the antiviral response mediated by the host cellular protein, double-stranded RNA-dependent protein kinase (PKR).
pelcitoclax: A Bcl-2 homology (BH)-3 mimetic and selective inhibitor of the anti-apoptotic proteins B-cell lymphoma 2 (Bcl-2) and Bcl-XL, with potential pro-apoptotic and antineoplastic activities. Upon administration, pelcitoclax specifically binds to and inhibits the activity of the pro-survival proteins Bcl-2 and Bcl-XL. This restores apoptotic processes and inhibits cell proliferation in Bcl-2/Bcl-XL-dependent tumor cells. Bcl-2 and Bcl-XL, proteins belonging to the Bcl-2 family that are overexpressed in many cancers, play an important role in the negative regulation of apoptosis; tumor expression is associated with increased drug resistance and cancer cell survival.
pelecopan: An orally bioavailable inhibitor of complement factor D (FD; CFD), a serine protease that cleaves complement factor B, with potential complement system inhibiting activity. Upon oral administration, pelecopan targets, binds to and blocks the activity of FD, thereby inhibiting the cleavage of complement factor B into Ba and Bb in the alternative pathway of the complement cascade. This inhibits FD-mediated signaling and the activation of the alternative complement pathway (ACP), blocks complement-mediated hemolysis in paroxysmal nocturnal hemoglobinuria (PNH) and prevents ACP-induced tissue damage. FD plays a key role in the activation of the ACP.
pelitinib: A 3-cyanoquinoline pan-ErbB tyrosine kinase inhibitor with potential antineoplastic activity. Pelitinib irreversibly binds covalently to epidermal growth factor receptors (EGFR) ErbB-1, -2 and -4, thereby inhibiting receptor phosphorylation and signal transduction and resulting in apoptosis and suppression of proliferation in tumor cells that overexpress these receptors.
pelitrexol: A water soluble antifolate with anti-proliferative activity. Pelitrexol inhibits activity of glycinamide ribonucleotide formyltransferase (GARFT), the first folate-dependent enzyme of the de novo purine synthesis pathway essential for cell proliferation. Enzyme inhibition reduces the purine nucleotides pool required for DNA replication and RNA transcription. As a result, this agent causes cell cycle arrest in S-phase, and ultimately inhibits tumor cell proliferation.
Pemazyre: (Other name for: pemigatinib)
pembrolizumab: A humanized monoclonal immunoglobulin (Ig) G4 antibody directed against human cell surface receptor PD-1 (programmed death-1 or programmed cell death-1) with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, pembrolizumab binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T cells, and blocks the binding to and activation of PD-1 by its ligands, which results in the activation of T-cell-mediated immune responses against tumor cells. The ligands for PD-1 include programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on APCs. Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity.
pembrolizumab/quavonlimab MK-1308A: A combination formulation containing fixed doses of the two monoclonal antibodies pembrolizumab and quavonlimab, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration of pembrolizumab/quavonlimab MK-1308A, pembrolizumab, a monoclonal antibody directed against the human cell surface receptor PD-1 (programmed death-1 or programmed cell death-1), targets and binds to PD-1, an inhibitory signaling receptor expressed on the surface of activated T cells, and blocks the binding to and activation of PD-1 by its ligands, which results in the activation of T-cell-mediated immune responses against tumor cells. The ligands for PD-1 include programmed cell death ligand 1 (PD-L1), overexpressed on certain cancer cells, and programmed cell death ligand 2 (PD-L2), which is primarily expressed on antigen presenting cells (APCs). Activated PD-1 negatively regulates T-cell activation and plays a key role in in tumor evasion from host immunity. Quavonlimab, a monoclonal antibody directed against the human T-cell-expressed receptor cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; CTLA-4), targets and binds to CTLA4 expressed on T cells and inhibits the CTLA4-mediated downregulation of T-cell activation. This leads to a cytotoxic T-lymphocyte (CTL)-mediated immune response against cancer cells. CTLA4, an inhibitory receptor and member of the immunoglobulin superfamily, plays a key role in the downregulation of the immune system.
pemetrexed disodium: The disodium salt of a synthetic pyrimidine-based antifolate. Pemetrexed binds to and inhibits the enzyme thymidylate synthase (TS) which catalyses the methylation of 2'-deoxyuridine-5'-monophosphate (dUMP) to 2'-deoxythymidine-5'-monophosphate (dTMP), an essential precursor in DNA synthesis.
Pemfexy: (Other name for: pemetrexed disodium)
pemigatinib: An orally bioavailable inhibitor of the fibroblast growth factor receptor (FGFR) types 1, 2, and 3 (FGFR1/2/3), with potential antineoplastic activity. Pemigatinib binds to and inhibits FGFR1/2/3, which may result in the inhibition of FGFR1/2/3-related signal transduction pathways. This inhibits proliferation in FGFR1/2/3-overexpressing tumor cells. FGFR, a family of receptor tyrosine kinases upregulated in many tumor cell types, plays a key role in cellular proliferation, migration, and survival.
Pen-Vee: (Other name for: penicillin V potassium)
penclomedine: A synthetic derivative of pyrimidine with antineoplastic activity. Penclomedine alkylates and crosslinks DNA, resulting in DNA strand breaks and inhibition of DNA and RNA synthesis. This agent is more active against tumor cells that are defective in p53 function.
penicillamine: A beta dimethyl analog of the amino acid cysteine. As a degradation product of penicillin antibiotics, penicillamine chelates with heavy metals and increases their urinary excretion. Possessing antineoplastic properties, penicillamine induces apoptosis by a p53-mediated mechanism and inhibits angiogenesis by chelating with copper, a cofactor for angiogenesis.
penicillin V potassium: The potassium salt of penicillin V, a member of the penicillin antibiotic family with broad-spectrum bactericidal activity. Penicillin V binds to and inactivates penicillin-binding proteins (PBPs), enzymes located on the inner membrane of the bacterial cell wall, resulting in the weakening of the bacterial cell wall and cell lysis. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity.
penpulimab-kcqx: A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, penpulimab targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.
Pentam: (Other name for: pentamidine isethionate)
pentamethylmelamine: A principal metabolite of hexamethylmelamine with antineoplastic activity. Pentamethylmelamine alkylates DNA and other macromolecules and forms DNA intrastrand and DNA-protein crosslinks, thereby preventing DNA replication.
pentamidine: A synthetic derivative of amidine with antiprotozoal and antifungal activities. Although the precise mode of action of pentamidine is unclear, it appears to interact directly with the pathogen genome by binding to AT-rich regions of duplex DNA and the minor groove of DNA, thereby interfering with DNA replication.
pentamidine isethionate: A synthetic amidine derivative, Pentamidine Isethionate is an antiprotozoal and antifungal agent that appears to interact with the minor groove of AT-rich DNA regions of the pathogen genome, interfering with DNA replication and function. It is effective in the treatment of trypanosomiasis, leishmaniasis, some fungal infections, and Pneumocystis carinii pneumonia in HIV-infected patients.
Pentasa: (Other name for: mesalamine)
pentavalent KLH conjugate vaccine: A pentavalent vaccine comprised of the epitope antigens of the ganglioside lactones GD2L and GD3L, Globo H hexasaccharide 1 (Globo H), fucosyl GM1 and N-propionylated polysialic acid conjugated with the immunostimulant keyhole limpet hemocyanin (KLH), with potential immunostimulating and antineoplastic activity. Vaccination with the pentavalent KLH conjugate vaccine may induce production of IgG and IgM antibodies as well as an antibody-dependent cell-mediated cytotoxicity (ADCC) against tumors expressing any of these antigens. The antigens included in the pentavalent KLH conjugate vaccine are upregulated in a variety of cancer cells. KLH, a natural protein isolated from the marine mollusk keyhole limpet, is an immunostimulant carrier protein.
pentetic acid calcium: The calcium salt of pentetic acid, a synthetic chelating agent related to the chelating agent ethylenediaminetetraacetic acid (EDTA). Pentetic acid chelates with the metallic radioisotopic moieties of unbound, extracellular radioimmunotherapeutic agents, resulting in higher specific tumor cell binding of radioimmunotherpeutic agents; this results in improved tumor cell radiocytotoxicity and the sparing of normal cells and tissues from the radiocytotoxic effects of these agents.
pentosan polysulfate sodium: The sodium salt of a semisynthetic heparin-like glucosaminoglycan. Although its mechanism of action is unknown, pentosan polysulfate may act as a buffer to control cell permeability by preventing irritating solutes from reaching cells coated with it. Administered orally, excreted pentosan polysulfate adheres to the urinary bladder wall, preventing irritants from entering bladder cells and the development or progression of interstitial cystitis (IC), a complication of some chemotherapies. This agent also exhibits anticoagulant and fibrinolytic properties.
pentostatin: A purine nucleotide analogue antibiotic isolated from the bacterium Streptomyces antibioticus. Also known as 2'-deoxycoformycin, pentostatin binds to and inhibits adenine deaminase (ADA), an enzyme essential to purine metabolism; ADA activity is greatest in cells of the lymphoid system with T-cells having higher activity than B-cells and T-cell malignancies higher ADA activity than B-cell malignancies. Pentostatin inhibition of ADA appears to result in elevated intracellular levels of dATP which may block DNA synthesis through the inhibition of ribonucleotide reductase. This agent may also inhibit RNA synthesis and may selectively deplete CD26+ lymphocytes.
pentoxifylline: A methylxanthine derivative with hemorrheologic and immunomodulating properties. Pentoxifylline inhibits phosphodiesterase, resulting in increased levels of cyclic adenosine monophosphate (cAMP) in erythrocytes, endothelium, and the surrounding tissues. This leads to vasodilation, improves erythrocyte flexibility, and enhances blood flow. In addition, the increased level of cAMP in platelets inhibits platelet aggregation, which may contribute to a reduction in blood viscosity. This agent also inhibits production of tumor necrosis factor-alpha and interferon-gamma, while it induces Th2-like (T-helper 2) cytokine production, thereby inhibiting Th1-mediated (T-helper 1) inflammatory and autoimmune responses.
PEOX-based polymer encapsulated paclitaxel FID-007: A nanoparticle-based formulation composed of the poorly water-soluble paclitaxel encapsulated within branched polymers composed of polyethyloxazoline (PEOX), with potential antineoplastic activity. Upon injection of the PEOX-based polymer encapsulated paclitaxel FID-007, the nanoparticles accumulate at the tumor site, due to the unique characteristics of the tumor vasculature, while avoiding normal, healthy tissue. Once the paclitaxel is released, it binds to tubulin inside tumor cells and inhibits the disassembly-assembly dynamics of microtubules, resulting in cell cycle arrest and cell death. Compared to the administration of paclitaxel alone, this formulation increases paclitaxel's solubility and enhances its tumor tissue penetration and efficacy, while avoiding systemic exposure, which minimizes its toxicity.
PEP-3-KLH conjugate vaccine: A cancer vaccine consisting of PEP-3, a synthetic peptide encompassing a tumor-specific mutated segment of the epidermal growth factor receptor type vIII (EGFRvIII), conjugated to the naturally-occuring immunoadjuvant keyhole limpet hemocyanin (KLH) with potential immunostimulating and antineoplastic activities. Upon administration, PEP-3-KLH conjugate vaccine may induce a cytotoxic immune response against tumor cells that overexpress EGFRvIII; this antitumoral immune response may involve antibody-dependent cellular cytotoxicity (ADCC).
PEP-CMV vaccine: A peptide vaccine derived from cytomegalovirus (CMV) antigens with potential immunostimulating activity. Intradermal administration of the PEP-CMV vaccine may stimulate the immune system to mount a specific helper and cytotoxic T-lymphocyte (CTL) response against CMV-infected tumor cells. Infection with the herpesvirus CMV may play a significant role in tumor cell initiation and progression as well as chemoresistance.
Pepaxto: (Other name for: melphalan flufenamide hydrochloride)
Pepcid: (Other name for: famotidine)
Pepcid AC: (Other name for: famotidine)
pepinemab: A humanized IgG4 monoclonal antibody against the semaphorin 4D (SEMA4D; CD100) with potential immunomodulating and antineoplastic activities. Upon administration, pepinemab binds to and neutralizes SEMA4D, thereby preventing binding of SEMA4D to its receptor plexin-B1 (PLXNB1). By blocking the interaction of SEMA4D and PLXNB1, pepinemab may cause an inhibition of endothelial cell activation and migration, eventually leading to an inhibition of angiogenesis and tumor cell proliferation. Semaphorin 4D, a large cell surface antigen found on the resting T-cell and overexpressed in a variety of tumor cell types, plays an important role in vascular growth, tumor progression, invasion and immune cell regulation.
peplomycin: A semisynthetic analog of Bleomycin, a mixture of several basic glycopeptide antineoplastic antibiotics isolated from the fungus Streptomyces verticillus. Peplomycin forms complexes with iron that reduce molecular oxygen to superoxide and hydroxyl radicals that cause single- and double-stranded breaks in DNA. This agent appears to show greater antitumor activity than bleomycin; its use is limited due to pulmonary toxicity.
peposertib: An orally bioavailable inhibitor of DNA-dependent protein kinase (DNA-PK) with potential antineoplastic activity, and potential sensitizing and enhancing activities for both chemo- and radiotherapies. Upon administration, peposertib binds to and inhibits the activity of DNA-PK, thereby interfering with the non-homologous end joining (NHEJ) process and preventing repair of DNA double strand breaks (DSBs) caused by ionizing radiation or chemotherapeutic treatment. This increases chemo- and radiotherapy cytotoxicity and leads to enhanced tumor cell death. The enhanced ability of tumor cells to repair DSBs plays a major role in the resistance of tumor cells to chemo- and radiotherapy; DNA-PK plays a key role in the NHEJ pathway and DSB repair.
peppermint oil: The essential oil extracted from the leaves of Mentha x piperita. Peppermint oil is used for its aromatic properties and as a flavoring and to treat illnesses of the digestive and respiratory system as well as pain.
peppermint oil-containing enteric-coated microspheres: A formulation composed of enteric-coated, sustained-release (SR) microspheres containing ultrapurified peppermint oil (Mentha piperita), a naturally-occurring carminative herb containing monoterpene compounds, with potential calming, anti-bacterial, anti-inflammatory, analgesic and anti-spasmodic activities. Upon oral administration of the peppermint oil-containing enteric-coated microspheres, the formulation allows for an initial quick release of peppermint oil in the small intestine and after that it is released throughout the small intestine over an extended period of time from the individual microspheres. The L-menthol in this formulation targets and blocks calcium channels in smooth muscle in the small intestine, thereby producing an anti-spasmodic effect on the gastrointestinal tract (GI). This allows for relaxation of smooth muscle and helps calm uncontrolled spasms. This may normalize digestion, decrease pain and discomfort, prevents cramping, bloating, diarrhea and constipation. L-menthol's kappa opioid agonist activity may further reduce abdominal pain and cramping. Through its anti-microbial effect, L-menthol may promote bacterial balance in the small intestine. The anti-inflammatory activity of L-menthol prevents inflammation associated with gut mucosal barrier disruption. Additionally, this formulation contains fiber and amino acids, which may further improve the integrity of the mucosal barrier.
Peptamen: (Other name for: enzymatically hydrolyzed whey protein-based nutritional supplement)
peptide drug conjugate OPD5: A peptide-drug conjugate (PDC) composed of a peptide conjugated, via an aminopeptidase-targeting linkage, to an as of yet undisclosed alkylating agent, with potential antineoplastic activity. Upon administration, PDC OPD5 is hydrolyzed by peptidases to release the alkylating agent, thereby allowing for specific accumulation of the agent in aminopeptidase-positive tumor cells. This may result in the inhibition of DNA and/or RNA synthesis and the induction of apoptosis, thereby inhibiting tumor cell proliferation. Peptidases are overexpressed by certain cancer cells.
peptidoglycan complex of spirulina K-001: An orally bioavailable preparation of peptidoglycan derived from the fermentation product of the marine microorganism spirulina, with potential immunomodulating and antineoplastic activities. Upon oral administration, peptidoglycan complex of spirulina K-001 may activate the innate immune system. This may re-activate the immune system to exert an antitumor immune response.
Pepto Bismol: (Other name for: bismuth subsalicylate)
Pepto-Bismol: (Other name for: bismuth subsalicylate)
perampanel: An orally active, non-competitive, and selective alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor antagonist, with anti-epileptic activity. Although the mechanism of action through which perampanel exerts its antiepileptic effect has not been fully elucidated, this agent antagonizes the AMPA subtype of the excitatory glutamate receptor found on postsynaptic neurons in the central nervous system (CNS). This antagonistic action prevents AMPA receptor activation by glutamate and results in the inhibition of neuronal excitation, repetitive neuronal firing, and the stabilization of hyper-excited neural membranes. Glutamate, the primary excitatory neurotransmitter in the CNS, plays an important role in various neurological disorders caused by neuronal hyperexcitation.
Percocet: (Other name for: oxycodone/acetaminophen)
Perdolat: (Other name for: penicillamine)
peretinoin: An orally available, acyclic retinoid with potential antineoplastic and chemopreventive activities. Peretinoin binds to and activates nuclear retinoic acid receptors (RAR), which in turn recruit coactivator proteins and promote, with other transcriptional complexes, the transcription of target genes. As a result, this agent may modulate the expression of genes involved in the regulation of cell proliferation, cell differentiation, and apoptosis of both normal and tumor cells.
perflenapent emulsion: An oil-in-water nano-emulsion composed of the perfluorocarbon perflenapent, that has oxygen-carrying capacity, can be used as a contrast agent and has potential antihypoxic and radiosensitizing activities. Upon intravenous administration of the perflenapent emulsion, this agent increases the oxygen-carrying capacity of blood, enhances the transport of oxygen to hypoxic and ischemic tissues and increases the oxygen concentration in these tissues. Hypoxic tumors are correlated with increased resistance to radiation treatment; therefore, since perflenapent may increase tumor oxygenation, it may improve the tumor’s sensitivity to radiation therapy.
perflubron: A synthetic radiopaque liquid form of perfluorooctyl bromide. Used as a contrast agent for magnetic resonance imaging (MRI), perflubron is also used as a liquid ventilation agent to improve pulmonary gas exchange and lung compliance and may be used in surgery to reduce or eliminate the need for a donor blood. Ventilation with perfluorocarbon fluid improves lung function in conditions involving surfactant deficiency and dysfunction, including respiratory distress syndrome and adult respiratory distress syndrome.
perflutren: A fluorinated hydrocarbon and gaseous substance used as an imaging contrast agent. After administration in microsphere form, perflutren exhibits lower acoustic impedance than blood and improves ultrasound signaling.
perflutren lipid microspheres: An injectable suspension of liposome-encapsuled microspheres containing the fluorocarbon gas perflutren for contrast enhancement in ultrasound procedures. Because the acoustic impedance of perflutren lipid microspheres is much lower than that of blood, impinging ultrasound waves are scattered and reflected at the microsphere-blood interface and may be visualized with ultrasound imaging.
perflutren protein-type A microspheres: A sterile non-pyrogenic suspension of microspheres of human serum albumin with the stable, high-molecular-weight fluorocarbon gas perflutren, used as a contrast enhancement agent for ultrasound procedures. Because the acoustic impedance of perflutren protein-type A microspheres is much lower than that of blood, impinging ultrasound waves are scattered and reflected at the microsphere-blood interface and may be visualized with ultrasound imaging. At the frequencies used in adult echocardiography (2-5 MHZ), the microspheres resonate which further increases the extent of ultrasound scattering and reflection.
perfosfamide: The active metabolite of the nitrogen mustard cyclophosphamide with potent antineoplastic and immunosuppressive properties. Perfosfamide alkylates DNA, thereby inhibiting DNA replication and RNA and protein synthesis.
Pergamid: (Other name for: perfosfamide)
Periactin: (Other name for: cyproheptadine hydrochloride)
perifosine: An orally active alkyl-phosphocholine compound with potential antineoplastic activity. Targeting cellular membranes, perifosine modulates membrane permeability, membrane lipid composition, phospholipid metabolism, and mitogenic signal transduction, resulting in cell differentiation and inhibition of cell growth. This agent also inhibits the anti-apoptotic mitogen-activated protein kinase (MAPK) pathway and modulates the balance between the MAPK and pro-apoptotic stress-activated protein kinase (SAPK/JNK) pathways, thereby inducing apoptosis. Perifosine has a lower gastrointestinal toxicity profile than the related agent miltefosine.
perillyl alcohol: A naturally occurring monoterpene related to limonene with antineoplastic activity. Perillyl alcohol inhibits farnesyl transferase and geranylgeranyl transferase, thereby preventing post-translational protein farnesylation and isoprenylation and activation of oncoproteins such as p21-ras, and arresting tumor cells in the G1 phase of the cell cycle.
perindopril erbumine: The tert-butylamine salt of perindopril, the ethyl ester of a non-sulfhydryl angiotensin converting enzyme (ACE) inhibitor with antihypertensive activity. Upon hydrolysis, perindopril erbumine is converted to its active form perindoprilat, inhibiting ACE and the conversion of angiotensin I to angiotensin II; consequently, angiotensin II-mediated vasoconstriction and angiotensin II-stimulated aldosterone secretion from the adrenal cortex are inhibited and diuresis and natriuresis ensue.
Perjeta: (Other name for: pertuzumab)
PERK inhibitor HC-5404-FU: The hemifumarate salt form of HC-5404, an orally bioavailable inhibitor of the serine/threonine kinase protein kinase R (PKR)–like endoplasmic reticulum kinase (PERK; eukaryotic translation initiation factor 2-alpha kinase 3; EIF2AK3; PEK) with potential antineoplastic activity. Upon oral administration of PERK inhibitor HC-5404-FU, HC-5404 inhibits the activity of PERK. This prevents the activation of the PERK pathway and inhibits unfolded protein response (UPR) stress adaptation, which may lead to tumor cell apoptosis and the inhibition of tumor growth. PERK, one of the key sensors for the UPR, plays a key role in the response to and resolution of endoplasmic reticulum (ER) stress and also in tumor angiogenesis and survival.
PERK inhibitor NMS-03597812: An orally bioavailable inhibitor of the serine/threonine kinase protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK; eukaryotic translation initiation factor 2-alpha kinase 3; EIF2AK3; PEK), with potential antineoplastic activity. Upon oral administration, PERK inhibitor NMS-03597812 inhibits the activity of PERK. This prevents the activation of the PERK pathway and inhibits unfolded protein response (UPR) stress adaptation, which may lead to tumor cell apoptosis and the inhibition of tumor growth. PERK, one of the key sensors for the UPR, plays a key role in the response to and resolution of endoplasmic reticulum (ER) stress and also in tumor angiogenesis and survival.
Permitil: (Other name for: fluphenazine hydrochloride)
Persantine: (Other name for: dipyridamole)
personalized ALL-specific multi-HLA-binding peptide vaccine: An individualized peptide-based cancer vaccine comprised of three to five human leukocyte antigen (HLA) binding tumor-specific peptides obtained from the autologous mutated proteins from the tumor cells of patients with acute lymphoblastic leukemia (ALL), with potential immunomodulating and antineoplastic activity. Upon intradermal administration of the personalized multi-HLA-binding peptide vaccine, the peptides may induce a tumor-specific cytotoxic T-lymphocyte (CTL) response against the peptides that are expressed by the tumor cells.
personalized and adjusted neoantigen peptide vaccine PANDA-VAC: A peptide-based, personalized cancer therapeutic vaccine consisting of up to 8 patient-specific tumor peptides, which are immunogenic and unique to the patient's tumor and identified through DNA and RNA sequencing of a patient's tumor cells, combined with the immunostimulant polyinosinic-polycytidylic acid stabilized with polylysine and carboxymethylcellulose (poly-ICLC), with potential immunomodulating and antineoplastic activities. Upon administration, personalized and adjusted neoantigen peptide vaccine PANDA-VAC stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the neoantigens, leading to tumor cell lysis. The adjuvant poly-ICLC is a ligand for toll-like receptor-3 (TLR3) and induces the release of cytokines which may help to boost the immune response against the selected neoantigens. The vaccine may be adjusted after initial therapy according to sequencing data.
personalized cancer neoantigen vaccine GAd-PEV: A personalized neoantigen priming vaccine comprised of a great ape (gorilla) adenoviral (GAd) vector encoding numerous patient-specific tumor neoantigens, which are identified based on patient-specific tumor mutations obtained from the individual’s tumor, with potential immunostimulatory and antineoplastic activities. The neoantigens are the same as the ones in the booster vaccine MVA-PEV. Upon administration of the priming vaccine personalized cancer neoantigen vaccine GAd-PEV, the neoantigens are expressed and presented to the immune system. This may induce CD8+ and CD4+ neoantigen-specific T-cell responses against the patient’s tumor cells expressing the neoantigens.
personalized cancer neoantigen vaccine MVA-PEV: A personalized neoantigen booster vaccine comprised of a modified Vaccinia Ankara (MVA) viral vector encoding numerous patient-specific tumor neoantigens, which are identified based on patient-specific tumor mutations obtained from the individual's tumor, with potential immunostimulatory and antineoplastic activities. The neoantigens are the same as the ones in the priming vaccine GAd-PEV. Following administration of the priming vaccine GAd-PEV, the administration of the booster vaccine, personalized cancer neoantigen vaccine MVA-PEV, may further enhance CD8+ and CD4+ neoantigen-specific T-cell responses against the patient’s tumor cells expressing the neoantigens.
personalized genomic vaccine 001: A synthetic peptide-based, personalized cancer vaccine consisting of multiple patient-specific tumor peptides, which are immunogenic and unique to the patient's tumor, combined with the immunostimulant polyinosinic-polycytidylic acid stabilized with polylysine and carboxymethylcellulose (poly-ICLC), with potential immunomodulating and antineoplastic activities. Upon vaccination with the personalized genomic vaccine 001 (PGV001), the peptides stimulate the host immune system to mount a specific and potent cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the neoantigens, which results in tumor cell lysis. The adjuvant Poly-ICLC is added to boost the immune response to the peptides and together will expand immune cells to target cancer. The adjuvant poly-ICLC is a ligand for toll-like receptor-3 (TLR3) and induces the release of cytokines which may help to boost the immune response against the selected neoantigens.
personalized liposomal neoantigen-based peptide vaccine EVX-01: A personalized liposomal peptide vaccine composed of specific cancer neoepitopes, which are highly patient-specific immunogenic tumor associated antigens (TAAs), with potential immunostimulatory and antineoplastic activities. Upon administration of the personalized liposomal neoantigen-based peptide vaccine EVX-01, the neoepitopes induce cytotoxic T-lymphocyte (CTL)-mediated immune responses against tumor cells expressing these specific TAAs.
personalized live-attenuated double-deleted Listeria monocytogenes: A proprietary, personalized live, attenuated, double-deleted (pLADD) strain of the Gram-positive bacterium Listeria monocytogenes encoding multiple, patient-specific neoantigens, with potential immunostimulatory and antineoplastic activities. Upon intravenous administration, the tumor-associated antigens (TAAs) expressed in pLADD are taken up by antigen-presenting cells (APCs), including dendritic cells (DCs), and are processed and presented to the immune system by both major histocompatibility complex (MHC) class I and II molecules. This activates the immune system and leads to both an innate immune response and the recruitment and activation of tumor-specific cytotoxic T lymphocytes (CTLs) against the TAAs specifically expressed by the patient's tumor cells, which eventually results in tumor cell lysis.
personalized neoantigen DNA vaccine GNOS-PV01: A personalized cancer vaccine consisting of patient-specific neoantigen-coding DNA plasmids, which are immunogenic and unique to the patient's tumor, with potential immunomodulating and antineoplastic activities. Upon administration of GNOS-PV01, the patient-specific neoantigens are translated in cells and elicit a specific and potent cytotoxic T-lymphocyte (CTL) response against tumor cells expressing these neoantigens, resulting in tumor cell lysis. Each patient specific formulation may contain multiple DNA plasmids, and each plasmid may contain multiple neoantigen DNA sequences, allowing the delivery of multiple neoantigen DNA sequences simultaneously.
personalized neoantigen DNA vaccine GNOS-PVO2: A personalized cancer vaccine consisting of patient-specific neoantigen-coding DNA plasmids, which are immunogenic and unique to the patient's tumor, with potential immunomodulating and antineoplastic activities. Upon intradermal delivery by electroporation of GNOS-PVO2, the patient-specific neoantigens are translated in cells and elicit a specific and potent cytotoxic T-lymphocyte (CTL) response against tumor cells expressing these neoantigens, resulting in tumor cell lysis. Each patient-specific formulation may contain multiple DNA plasmids, and each plasmid may contain multiple neoantigen DNA sequences, allowing the delivery of multiple neoantigen DNA sequences simultaneously.
personalized neoantigen follicular lymphoma vaccine: A peptide-based, personalized follicular lymphoma therapeutic vaccine consisting of up to 20 neoantigens and peptides derived from patient-specific follicular lymphoma immunogenic epitopes, combined with the immunostimulant poly-ICLC, with potential immunomodulating and antineoplastic activities. Upon administration, the personalized neoantigen follicular lymphoma vaccine stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the neoantigens, which results in tumor cell lysis. The adjuvant poly-ICLC, composed of double-stranded RNA molecules of polyinosinic-polycytidylic acid stabilized with poly L-lysine in carboxymethylcellulose, is a ligand for toll-like receptor-3 (TLR3) and induces the release of cytokines which may help to boost the immune response against the selected neoantigens.
personalized neoantigen ovarian cancer vaccine: A peptide-based, personalized ovarian cancer therapeutic vaccine consisting of up to 20 neoantigens and peptides derived from patient-specific ovarian cancer immunogenic epitopes, combined with the immunostimulant poly-ICLC, with potential immunomodulating and antineoplastic activities. Upon administration, the personalized neoantigen ovarian cancer vaccine stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the neoantigens, which results in tumor cell lysis. The adjuvant poly-ICLC, composed of double-stranded RNA molecules of polyinosinic-polycytidylic acid stabilized with poly L-lysine in carboxymethylcellulose, is a ligand for toll-like receptor-3 (TLR3) and induces the release of cytokines which may help to boost the immune response against the selected neoantigens.
personalized neoantigen peptide vaccine iNeo-Vac-P01: A peptide-based, personalized cancer vaccine consisting of patient-specific mutated long peptides, which are immunogenic and unique to the patient's tumor, with potential immunomodulating and antineoplastic activities. Upon vaccination with the personalized neoantigen peptide vaccine iNeo-Vac-P01, the peptides stimulate the host immune system to mount a specific and potent cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the neoantigens, which results in tumor cell lysis.
personalized neoantigen plasmid DNA melanoma vaccine EVX-02: A plasmid DNA melanoma vaccine composed of DNA plasmid encoding multiple, melanoma patient-specific neoepitopes, which are highly immunogenic tumor associated antigens (TAAs), with potential immunostimulatory and antineoplastic activities. Upon intramuscular (IM) administration of personalized neoantigen plasmid DNA melanoma vaccine EVX-02, the plasmid DNA is taken up by antigen-presenting cells (APCs) and the expressed neoepitopes induce cytotoxic T-lymphocyte (CTL)-mediated immune responses against melanoma cells expressing these specific TAAs.
personalized neoantigen upper gastrointestinal tract cancer vaccine: A personalized upper gastrointestinal (GI) tract cancer vaccine consisting of multiple patient-specific tumor-derived neoantigens, which are identified based on patient-specific tumor mutations obtained from the individual's tumor, with potential immunostimulatory and antineoplastic activities. Upon administration, the personalized neoantigen upper GI tract cancer vaccine stimulates the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the neoantigens, which results in tumor cell lysis.
personalized neoantigen vaccine NECVAX NEO1: A personalized, oral Ty21a-based neoantigen vaccine consisting of eukaryotic expression plasmid encoding patient-specific tumor neoantigens that are immunogenic and unique to the patient's tumor, with potential immunomodulating and antineoplastic activities. Upon oral administration of personalized neoantigen vaccine NECVAX NEO1, the patient-specific neoantigens elicit a specific and potent cytotoxic T-lymphocyte (CTL) response against tumor cells expressing these neoantigens. Ty21a is a live-attenuated Salmonella typhi strain oral typhoid vaccine that is modified and used to deliver the neoantigens-encoding plasmids to the gut-associated lymphoid tissue.
personalized neoantigen-specific T lymphocytes NEO-PTC-01: A preparation of autologous, personalized tumor neoantigen-specific T lymphocytes, with potential immunostimulating and antineoplastic activities. The T cells are derived from the patients’ peripheral blood mononuclear cells (PBMCs) and are primed and activated against tumor-specific neoantigens that are expressed on the patient’s tumor cells or in the tumor microenvironment (TME), and expanded ex vivo. Upon administration, the autologous neoantigen-specific T lymphocytes NEO-PTC-01 recognize and bind to tumor cells expressing the targeted neoantigens, resulting in a cytotoxic T-lymphocyte (CTL)-mediated immune response against the patient's tumor cells.
personalized neoepitope yeast vaccine YE-NEO-001: A cancer vaccine composed of a heat-killed yeast that has been genetically modified to express patient-specific neoantigen epitopes. Upon vaccination, neoepitope yeast vaccine YE-NEO-001 may elicit a targeted CD4+ and CD8+ T-lymphocyte-mediated immune response against tumor cells expressing these specific epitopes.
personalized peptide cancer vaccine mBTCvax: A peptide-based, personalized cancer therapeutic vaccine consisting of patient-specific mutated tumor peptides, which are immunogenic and unique to the patient's tumor, combined with the immunostimulant polyinosinic-polycytidylic acid stabilized with polylysine and carboxymethylcellulose (poly-ICLC), with potential immunomodulating and antineoplastic activities. Upon administration, personalized peptide cancer vaccine mBTCvax stimulates the host immune system to mount a specific and potent cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the neoantigens, which results in tumor cell lysis. The adjuvant poly-ICLC is a ligand for toll-like receptor-3 (TLR3) and induces the release of cytokines which may help to boost the immune response against the selected neoantigens.
personalized peptides-loaded autologous dendritic cell vaccine: A cell-based personalized cancer vaccine composed of autologous dendritic cells (DCs) loaded with the patient’s own tumor-specific peptides, with potential immunostimulatory and antineoplastic activities. Upon administration of the personalized peptides (PEP)-loaded autologous DC vaccine, the DCs activate natural killer cells (NKs) and stimulate a cytotoxic T-lymphocyte (CTL)-mediated immune response against the patient’s tumor cells expressing the PEPs, resulting in tumor cell lysis.
personalized polyepitope plasmid DNA breast cancer vaccine: A polyepitope DNA vaccine composed of a DNA plasmid encoding multiple, highly immunogenic tumor-associated antigens (TAAs) that are specifically selected after genome profiling of the patient's breast cancer cells, with potential immunostimulatory and antineoplastic activities. Upon intramuscular administration and electroporation of the personalized polyepitope plasmid DNA breast cancer vaccine, the expressed TAAs induce cytotoxic T-lymphocyte (CTL) immune responses against tumor cells expressing the TAAs.
personalized synthetic long peptide breast cancer vaccine: A cancer vaccine consisting of one or more long, synthetic peptides derived from patient-specific breast cancer tumor-associated antigens (TAAs), with potential immunomodulating and antineoplastic activities. Upon intramuscular administration of the personalized synthetic long peptide breast cancer vaccine, the peptides stimulate the host immune system to mount a cytotoxic T-lymphocyte (CTL) response against tumor cells expressing the TAAs, which results in tumor cell lysis.
personalized synthetic long peptide vaccine: A personalized peptide vaccine consisting of synthetic long peptides (SLPs), ranging from 20-35 amino acids in size, that are derived from two or more of the patient's tumor-specific mutant antigens (TSMAs), with potential immunostimulatory and antitumor activities. A patient's tumor is isolated, TSMAs are identified, assessed and prioritized, and two or more TSMAs are selected to be further processed into SLPs. Upon administration, personalized SLP vaccine may stimulate the host immune system to mount a cytotoxic T-cell lymphocyte (CTL)-mediated immune response against the TSMAs expressed by the tumor cells.
Pertofrane: (Other name for: desipramine hydrochloride)
pertuzumab: A humanized recombinant monoclonal antibody directed against the extracellular dimerization domain of the HER-2 tyrosine kinase receptor. Binding of the antibody to the dimerization domain of the HER-2 tyrosine kinase receptor protein directly inhibits the ability of the HER-2 tyrosine kinase receptor protein (the most common pairing partner) to dimerize with other HER tyrosine kinase receptor proteins; inhibiting receptor protein dimerization prevents the activation of HER signaling pathways, resulting in tumor cell apoptosis.
pertuzumab zuvotolimod: An immunotherapeutic composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor 2 (EGFR2; HER2; ErbB2) conjugated to a Toll-like receptor 8 (TLR8; CD288) agonist, with potential immunostimulating and antineoplastic activities. Upon intravenous administration pertuzumab zuvotolimod, the anti-HER2 monoclonal antibody targets and binds to HER2 expressed on tumor cells, thereby localizing the TLR8 agonist directly to the tumor site. In turn, the TLR8 agonist moiety binds to TLR8 expressed on myeloid cells within the tumor microenvironment (TME). This activates myeloid cells, including tumor-associated macrophages (TAMs), myeloid cell-derived suppressive cells (MDSCs), and conventional dendritic cells (cDCs). This may lead to the activation of nuclear factor NF-kappa-B, the production of pro-inflammatory cytokines and chemokines, macrophage-induced tumor cell killing, inflammasome activation, activation of cytolytic natural killer (NK) cells and neutrophils, and the induction of a Th1-weighted anti-tumor immune response. It also reverses the suppression of senescent naive and tumor-specific T cells, and enhances the anti-tumor cytotoxic T-lymphocyte (CTL) immune response. TLR8, like other TLRs, recognizes pathogen-associated molecular patterns (PAMPs) and plays a key role in innate and adaptive immunity. HER2, a tyrosine kinase receptor, is overexpressed by many cancer cell types.
pertuzumab, trastuzumab, and hyaluronidase-zzxf: A ready-to-use fixed-dose combination of pertuzumab and trastuzumab, both recombinant humanized monoclonal antibodies directed against the tyrosine kinase receptor (TKR) human epidermal growth factor receptor 2 (HER2; HER-2; receptor tyrosine-protein kinase erbB-2), and hyaluronidase-zzxf, a biosimilar of the recombinant form of the naturally occurring endoglycosidase hyaluronidase, with antineoplastic activity that can be used for the treatment of HER2-overexpressing breast cancers. Upon subcutaneous administration, hyaluronidase-zzxf temporarily breaks down the hyaluronan barrier, which decreases viscosity of, and allows both pertuzumab and trastuzumab to spread rapidly through the interstitial space. This improves access to lymphatic and capillary vessels and facilitates the absorption of both antibodies into the bloodstream. Pertuzumab targets and binds to the extracellular dimerization domain (subdomain II) of HER2 and blocks ligand-dependent heterodimerization of HER2 with other HER family members, including EGFR, HER3 and HER4. This inhibits ligand-initiated intracellular signaling and prevents the activation of the mitogen-activated protein (MAP) kinase and the phosphoinositide 3-kinase (PI3K) signaling pathways, leading to growth arrest and apoptosis in HER2-overexpressing tumor cells, respectively. Trastuzumab targets and binds to subdomain IV of HER2 and inhibits ligand-independent, HER2 mediated cell proliferation and inhibits the PI3K signaling pathway in HER2-overexpressing tumor cells. Both antibodies induce an antibody-dependent cell-mediated cytotoxicity (ADCC) against HER2-expressing tumor cells. HER2 is overexpressed in many adenocarcinomas, particularly breast adenocarcinomas.
petadeferitrin: An orally bioavailable iron-chelating agent and derivative of desferrithiocin, with iron chelating and protective activities in diseases of iron overload. Upon oral administration, petadeferitrin targets, binds to and chelates free iron. This induces the excretion of iron, prevents iron accumulation and prevents cellular and/or tissue damage associated with iron overload.
Petiveria alliacea extract: An herbal extract derived from the plant Petiveria alliacea, with potential antineoplastic activity. Petiveria alliacea contains dibenzyl trisulphide (DTS), flavonoids, flavonoid glycosides and coumarin, and may exert antineoplastic activity through multiple pathways including the induction of G2 cell cycle arrest and apoptosis, and the modulation of cell metabolism.
petrolatum-mineral oil-lanolin-ceresin ointment: A petrolatum-based ointment absorbed by dry and moist skin, petrolatum-mineral oil-lanolin-ceresin ointment is non-comedogenic, non-irritating, and non-sensitizing. It can reduce healing time of cracked, dry skin on hands, elbows, and knees, and helps prevent diaper rash. The original ointment also contained mineral oil, ceresin, lanolin alcohol. Its use is indicated in atopic dermatitis, eczema, and psoriasis when extra protection from a heavier base is needed.
pevonedistat: A small molecule inhibitor of Nedd8 activating enzyme (NAE) with potential antineoplastic activity. Pevonedistat binds to and inhibits NAE, which may result in the inhibition of tumor cell proliferation and survival. NAE activates Nedd8 (Neural precursor cell expressed, developmentally down-regulated 8), an ubiquitin-like (UBL) protein that modifies cellular targets in a pathway that is parallel to but distinct from the ubiquitin-proteasome pathway (UPP). Functioning in diverse regulatory activities, proteins conjugated to UBLs like Nedd8 typically are not targeted for proteasomal degradation.
pexastimogene devacirepvec: An oncolytic thymidine kinase (TK)-deleted vaccinia poxvirus expressing human GM-CSF (hGM-CSF) with antineoplastic activity. Upon intratumoral or intravenous administration, pexastimogene devacirepvec selectively infects and lyses tumor cells. While vaccinia displays a natural tumor cell tropism, deletion of the TK gene increases the tumor selectivity of vaccinia by limiting viral replication to cells expressing high levels of TK, such as certain cancer cells. hGM-CSF expression by this agent helps recruit antigen presenting cells (APCs), such as dendritic cells (DCs) and macrophages, to virally infected tumor cells, thereby initiating an antitumoral immune response.
pexidartinib hydrochloride: The hydrochloride salt form of pexidartinib, a small-molecule receptor tyrosine kinase (RTK) inhibitor of proto-oncogene receptor tyrosine kinase (KIT), colony-stimulating factor-1 receptor (CSF1R) and FMS-like tyrosine kinase 3 (FLT3), with antineoplastic activity. Upon oral administration, pexidartinib targets, binds to and inhibits phosphorylation of KIT, CSF1R and FLT3 harboring an internal tandem duplication (ITD) mutation. This results in the inhibition of tumor cell proliferation. FLT3, CSF1R and FLT3 are overexpressed or mutated in many cancer cell types and play major roles in tumor cell proliferation and metastasis.
pexmetinib: An orally bioavailable small-molecule inhibitor of p38 and Tie2 kinases with potential antineoplastic, anti-inflammatory and antiangiogenic activities. Pexmetinib binds to and inhibits the activities of p38 and Tie2 kinases, which may inhibit the production of proinflammatory cytokines and may decrease tumor angiogenesis and tumor cell growth and survival. p38 is a MAP kinase that is often upregulated in cancer cells, playing a crucial part in the production of a variety of cytokines involved in inflammation and cellular proliferation such as tumor necrosis factor (TNF) and interleukin (IL)-1 and -6. Tie2 is an endothelial cell specific receptor that is activated by angiopoietins, growth factors required for angiogenesis. This agent has also been reported to inhibit other kinases including vascular endothelial growth factor receptor (VEGFR2) and Src tyrosine kinases.
PGLA/PEG copolymer-based paclitaxel: A controlled-release, intratumoral paclitaxel formulation in which paclitaxel is incorporated into a thermosensitive, biodegradable triblock copolymer consisting of poly(lactide-co-glycolide) (PLGA) and polyethylene glycol (PEG). Upon intratumoral injection, paclitaxel is released slowly and continuously into tumor tissues from the gelled thermosensitive triblock copolymer over a period of 4 to 6 weeks; in tumor cells, paclitaxel binds to tubulin and inhibits the disassembly-assembly dynamics of microtubules, resulting in cell cycle arrest and cell death. The thermosensitive triblock copolymer component of this formulation transforms from a water-soluble polymer at room temperature to a water-insoluble, biodegradable gel depot at body temperature; intratumoral controlled-release of paclitaxel from the gel minimizes systemic exposure to paclitaxel and the paclitaxel toxicity profile.
pH low insertion peptide-exatecan conjugate CBX-12: A conjugate composed of a pH low insertion peptide (pHLIP) linked to the camptothecin analog exatecan, with potential antineoplastic activity. Upon administration of pHLIP-exatecan conjugate CBX-12, the pHLIP moiety specifically targets and gets inserted into the cellular membrane of tumor cells in environments with low extracellular pH. Then the exatecan moiety is released intracellularly via glutathione reduction of the linker. Exatecan inhibits DNA topoisomerase I activity, thereby inhibiting DNA replication and resulting in cell cycle arrest and tumor cell apoptosis. Tumor cell environments are more acidic than normal, healthy tissue environments. The pHLIP forms an alpha helix and becomes inserted across the cell membrane specifically at the low extracellular pH found within tumors.
pH-low insertion peptide-indocyanine green: An imaging agent composed of a pH-low insertion peptide (pHLIP) probe coupled with the near-infrared (NIR) fluorescent dye indocyanine green (ICG), that may be used for cancer imaging using NIR imaging. Upon administration of pHLIP-ICG during surgery, the pHLIP moiety specifically targets and gets inserted into the cellular membrane of tumor cells as the tumor cell environments are more acidic than normal, healthy tissue environments. More specifically, the pHLIP forms an alpha helix and becomes inserted across the cell membrane specifically at the low extracellular pH found within tumors whereas they are unfolded and unbound at higher pHs. Upon NIR imaging, tumor cells and the extent of acidity can be visualized and assessed, marking the tumor cells for surgical removal.
PH20 hyaluronidase-expressing adenovirus VCN-01: An oncolytic, replication-competent adenovirus encoding the human glycosylphosphatidylinositol-anchored enzyme PH20 hyaluronidase with potential antitumor activity. After intratumoral administration, PH20 hyaluronidase-expressing adenovirus VCN-01 selectively replicates in tumor cells, which may both cause oncolytic virus-induced cell death and induce the infection of adjacent tumor cells. In addition, the virus expresses hyaluronidase, which hydrolyzes and degrades the hyaluronic acid (HA) that coats tumor cells. The degradation of HA may result in a decrease for both the viscosity of the interstitial space and the tumor's interstitial fluid pressure (IFP). This increases viral spread and may result in the inhibition of tumor cell growth. In addition, HA degradation facilitates the penetration of chemotherapeutic agents into the tumor. HA is a glycosaminoglycan found in the extracellular matrix (ECM) and is frequently overproduced by various tumor cell types. The presence of HA in tumors correlates with increases in tumor cell growth, metastatic potential, tumor progression and resistance to chemotherapeutic agents.
Phaleria macrocarpa Extract DLBS-1425: An extract of the flesh from the fruit of Phaleria macrocarpa, an Indonesian herbal medicine, with potential antineoplastic activity. Although the active ingredients and exact components are unclear, gallic acid and its derivatives in DLBS-1425 appear to inhibit the phosphoinositide-3 kinase (PI3K)/protein kinase B (AKT) signaling pathway by reducing PI3K transcription followed by a reduction in AKT phosphorylation. This extract also appears to induce apoptosis through induction of pro-apoptotic genes such as BAX, BAD and PUMA and inhibition of the apoptosis suppressor Bcl-2.
pharmacological ascorbate: A high dose (HD) of ascorbic acid, a pro-oxidant agent, with potential antineoplastic and radio-chemo-sensitizing activities. Upon intravenous (IV) administration, pharmacological ascorbate is able to generate reactive oxygen species (ROS) by donating an electron to oxygen (O2) and forming hydrogen peroxide (H2O2), thereby causing oxidative stress and overwhelming the cell’s anti-oxidant defense mechanisms. This induces DNA double-stranded breaks (DSBs) and cell death. Tumor cells are highly susceptible to ascorbate-mediated oxidative stress and cytotoxicity while normal, healthy cells are mostly unaffected. This induces the cell death of susceptible tumor cells and decreases tumor cell growth. Higher plasma ascorbate concentrations are achieved upon higher intravenous doses of ascorbate; oral administration of ascorbate is limited and uptake does not increase after a certain amount is administered. Only IV ascorbate produces plasma concentrations high enough to induce ascorbate-mediated cytotoxicity to susceptible tumor cells. In addition, HD parenteral ascorbate enhances radio- and chemo-sensitivity of susceptible cancer cells.
PHC: (Other name for: cholecalciferol/d-alpha tocopherol/L-selenomethionine/green tea extract/saw palmetto berry extract/daidzein/genistein/lycopene prostate health supplement)
Phellodendron amurense bark extract: A proprietary formulation consisting of a Phellodendron amurense (Amur cork tree) bark extract, often used in traditional Chinese medicine, with anti-inflammatory, anti-oxidant and potential chemopreventive and antineoplastic activities. Phellodendron amurense bark extract contains certain isoquinoline alkaloids, flavone glycosides and phenolic compounds. Upon administration of Phellodendron amurense bark extract, the various phytochemicals in this formulation modulate multiple signal transduction pathways. This agent appears to block the activation of the transcription factor cAMP response binding protein (CREB) and inhibits Akt signaling, thereby inhibiting tumor cell growth and inducing apoptosis in Akt- and CREB-overexpressing cancer cells. In addition, this agent inhibits cyclooxygenase type 2 (COX-2), nuclear factor kappa b (NF-kB) and tumor necrosis factor alpha (TNF-a)-mediated signaling; COX-2, NF-kB and TNF-a are upregulated in certain types of cancer and during inflammation.
phenelzine sulfate: A hydrazine derivative and a potent non-selective monoamine oxidase (MAO) inhibitor with anxiolytic and antidepressant properties. Phenelzine sulfate irreversibly binds to MAO, thereby blocking the oxidative deamination of monoamines resulting in an increased concentration of biogenic amines and a concurrent decrease in catabolism of monoamine neurotransmitters, norepinephrine and serotonin, in the brain. In addition, through its primary metabolite phenylethylidenehyrazine (PEH), phenelzine causes elevated GABA levels in the caudate-putamen and nucleus accumbens thereby exerting its anxiolytic effects.
Phenergan: (Other name for: promethazine hydrochloride)
phenethyl isothiocyanate: An isothiocyanate found in cruciferous vegetables with chemopreventive and potential antitumor activities. Although the mechanism of action is unclear, phenethyl Isothiocyanate (PEITC) was shown to induce apoptosis in tumor cells, possibly mediated through its metabolic intermediates, reactive oxygen species (ROS). PEITC also is able to activate ERK and JNK signal transduction, which in turn induces expression of stress-responsive genes. Specifically, this agent has been shown to reactivate gene expression of a detoxification enzyme, glutathione S-transferase that is silenced in prostate carcinoma.
phenethyl isothiocyanate-containing watercress juice: A juice extracted from watercress containing high amounts of phenethyl isothiocyanate (PEITC), with potential chemopreventive and antitumor activities. Although the mechanism(s) of action through which PEITC exerts its effect(s) has yet to be fully elucidated, PEITC is able to induce apoptosis in tumor cells through the induction of reactive oxygen species (ROS). Additionally, PEITC is able to modulate extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinase (JNK) and mitogen-activated protein kinase (MAPK) signal transduction pathways, activating the expression of stress-responsive genes and eventually inducing apoptosis. PEITC also inhibits the expression of genes involved in tumor progression such as HIF, STAT-3, HER2, BCL-XL, and XIAP and induces the expression of genes involved in tumor suppression such as p53, ATF-2, and p57. Furthermore, this agent has been shown to reactivate the gene expression of certain detoxification enzymes.
phenformin hydrochloride: The hydrochloride salt form of phenformin, an agent belonging to the biguanide class of antidiabetics with antihyperglycemic activity. Phenformin is not used clinically due to the high risk of lactic acidosis that is associated with its use.
phenobarbital: A long-acting barbituric acid derivative with antipsychotic property. Phenobarbital binds to and activates the gamma-aminobutyric acid (GABA)-A receptor, thereby mimicking the inhibitory actions of GABA in the brain. The activation effects of the phenobarbital-receptor-ionophore complex include increased frequency of chloride channel openings, membrane hyperpolarization and ultimately synaptic inhibition and decreased neuronal excitability. In addition, this agent inhibits glutamate induced depolarization.
phenoxybenzamine hydrochloride: The hydrochloride salt form of phenoxybenzamine, a synthetic, dibenzamine alpha-adrenergic antagonist with antihypertensive and vasodilatory properties. Phenoxybenzamine non-selectively and irreversibly blocks the postsynaptic alpha-adrenergic receptor in smooth muscle, thereby preventing vasoconstriction, relieving vasospasms, and decreasing peripheral resistance. Reflex tachycardia may occur and may be enhanced by blockade of alpha-2 receptors which enhances norepinephrine release. Phenoxybenzamine is reasonably anticipated to be a human carcinogen.
phenprocoumon: An orally available, long-acting derivative of coumarin with anticoagulant activity. Upon administration, phenprocoumon inhibits the vitamin K epoxide reductase enzyme; inhibition of this enzyme prevents the formation of the reduced, active form of vitamin K (vitamin KH2), which is essential for the carboxylation of glutamate residues of vitamin K-dependent proteins. This prevents the activation of vitamin K-dependent coagulation factors II, VII, IX, and X and the anticoagulant proteins C and S, which abrogates both thrombin production and thrombus formation.
phentolamine mesylate: The mesylate salt of a synthetic imidazoline with alpha-adrenergic antagonist activity. As a competitive alpha-adrenergic antagonist, phentolamine binds to alpha-1 and alpha-2 receptors, resulting in a decrease in peripheral vascular resistance and vasodilatation. This agent also may block 5-hydroxytryptamine (5-HT) receptors and stimulate release of histamine from mast cells.
Phesgo: (Other name for: pertuzumab, trastuzumab, and hyaluronidase-zzxf)
phosphatidylcholine-bound silybin: An oral preparation of the flavonoid silybin with potential antioxidant and chemopreventive activities. Silybin, also known as silibinin, is a mixture of two stereoisomers, denoted silybin A and silybin B, and is the major active constituent of silymarin, a mixture of flavonolignans extracted from blessed milk thistle (Silybum marianum). Silybin modulates P-glycoprotein (P-gp)-mediated cellular efflux; has oxygen radical-scavenging effects; inhibits the arachidonic acid pathway; and inhibits various cytochrome P450 enzymes. This agent may also exhibit anti-angiogenic activity, possibly by inducing endothelial cell apoptosis via modulation of the transcription factor NF-kB, the Bcl-2 family of proteins, and caspases. Complexing silybin with phosphatidylcholine increases its bioavailability.
PhosphoLean: (Other name for: N-oleyl-phosphatidylethanolamine/epigallocatechin gallate supplement)
Phosphoral: (Other name for: sodium phosphate)
phosphorodiamidate morpholino oligomer AVI-4126: A c-Myc antisense phosphorodiamidate morpholino oligomer (PMO) with potential antineoplastic activity. Phosphorodiamidate morpholino oligomer AVI-4126 binds to c-Myc mRNA and blocks its translation, which may result in the death of tumor cells overexpressing c-Myc. Differing from traditional antisense oligodeoxynucleotides (ODNs), neutrally charged PMOs are composed of subunits of nucleic acid bases linked to a synthetic backbone and, so, are less prone to enzymatic degradation. c-Myc, a proto-oncogene overexpressed in a variety of cancers, is involved in cellular proliferation, differentiation, and apoptosis.
phosphorus P32: A radioactive isotope of phosphorus with beta particle-emitting radiocytotoxic activity. Emitted by phosphorus P32, beta particles directly damage cellular DNA and, by ionizing intracellular water to produce several types of cytotoxic free radicals and superoxides, indirectly damage intracellular biological macromolecules, resulting in tumor cell death.
Photobac: (Other name for: methyl bacteriopurpurinimide)
Photochlor: (Other name for: HPPH)
photocyanine: A metal complex compound of phthalocyanide with photosensitizing activity. Upon injection with photocyanide and subsequent introduction to photodynamic therapy (PDT), photocyanide becomes activated and forms reactive oxygen species that induce apoptosis.
photodynamic compound TLD-1433: A non-toxic ruthenium-based coordination-complex and photosensitizer, with potential antineoplastic activity upon photodynamic therapy (PDT). Upon intravesical administration, light-activated photodynamic compound (PDC) TLD-1433 targets and binds to transferrin (Tf) and is subsequently taken up by Tf receptors which are located on tumor cells. Upon exposure to green light (525nm), TLD-1433 becomes activated locally and induces the generation of reactive oxygen species (ROS) and singlet oxygen. The release of free radicals may induce apoptosis and destroy the tumor cells. Cancer cells have many more Tf receptors than normal cells,
Photolon: (Other name for: phytochlorin sodium-polyvinylpyrrolidone complex)
photosensitizer agent REM-001: A second-generation photodynamic therapy (PDT)-based agent, with potential antineoplastic activity upon PDT. Upon administration, photosensitizer agent REM-001 specifically targets, binds to and is taken up by tumor cells. Upon exposure to light, REM-001 becomes activated locally and may induce apoptosis and destroy the tumor cells.
photosensitizer LUZ 11: A bacteriochlorin-based photosensitizer, with antineoplastic activity upon photodynamic therapy (PDT). Following intravenous administration, the photosensitizer LUZ 11 preferentially accumulates in hyperproliferative tissues, such as tumors. Local application of laser light at the tumor site results in the absorption of light by this agent and a photodynamic reaction between LUZ 11 and oxygen. This results in the production of reactive oxygen species (ROS), which includes singlet oxygen molecules, the superoxide ion, and other cytotoxic free radicals. The formation of ROS induces free radical-mediated DNA damage and cell death.
Phyllocontin: (Other name for: aminophylline)
phytochemical: The term 'phyto' originated from a Greek word meaning plant. Phytonutrients are certain organic components of plants, and these components are thought to promote human health. Fruits, vegetables, grains, legumes, nuts and teas are rich sources of phytonutrients. Unlike the traditional nutrients (protein, fat, vitamins, minerals), phytonutrients are not 'essential' for life, so some people prefer the term 'phytochemical'. (USDA Agricultural Research Service)
phytochlorin sodium-polyvinylpyrrolidone complex: A photosensitizer composed of the sodium salt form of chlorin e6 and its derivatives complexed with a low-molecular weight polyvinylpyrrolidone (PVP) polymer component, with diagnostic and antineoplastic activities upon photodynamic therapy (PDT). Upon intravenous administration, the photosensitizer phytochlorin-PVP sodium complex preferentially accumulates in hyperproliferative tissues, such as tumors. Local application of light with a certain wavelength to the tumor site results in the absorption of light by this agent, leading to its photoactivation. This results in a photodynamic reaction between phytochlorin and oxygen, which causes the production of reactive oxygen species (ROS), including singlet oxygen molecules, the superoxide ion, and other cytotoxic free radicals. The formation of ROS induces free radical-mediated oxidative DNA damage followed by apoptosis of tumor cells. Chlorin e6-PVP is able to penetrate deeply into tissues and is therefore able to treat hard-to-reach tumors.
Phytonadione: An analogue of the naphthoquinone vitamin K found in plants. The vitamins K are essential for blood coagulation as it is necessary for the hepatic synthesis of the coagulation factors II, VII, IX, and X; deficiency results in a bleeding diathesis. These vitamins are lipo-soluble; absorption via intestinal lymphatics requires the presence of bile salts.
PI-88: A mixture of highly sulfated, monophosphorylated mannose oligosaccharides, derived from the extracellular phosphomannan of the yeast Pichia (Hansenula) holstii, with potential antiangiogenic activity. Heparanase inhibitor PI-88 inhibits the endo-beta-D-glucuronidase heparanase, which may interfere with the heparanase-mediated degradation of heparan-sulfate proteoglycans in extracellular matrices, an important step in the metastatic process. This agent may also bind with high affinity to the heparan sulfate-binding domains of vascular endothelial growth factor (VEGF) and fibroblast growth factors 1 and 2, thereby reducing their functional activities and inhibiting VEGF and FGF stimulation of tumor angiogenesis. Increased heparanase activity has been implicated in tumor angiogenesis and metastasis.
PI3K alpha/beta inhibitor BAY1082439: An orally bioavailable inhibitor of the class I phosphoinositide 3-kinase (PI3K) alpha and beta isoforms with potential antineoplastic activity. PI3K alpha/beta inhibitor BAY1082439 selectively inhibits both PI3K alpha, including mutated forms of PIK3CA, and PI3K beta in the PI3K/Akt/mTOR pathway, which may result in tumor cell apoptosis and growth inhibition in PI3K-expressing and/or PTEN-driven tumor cells. By specifically targeting class I PI3K alpha and beta, this agent may be more efficacious and less toxic than pan PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and results in increased tumor cell growth, survival, and resistance to chemotherapy and radiotherapy. PIK3CA, one of the most highly mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K. PTEN, a tumor suppressor protein and negative regulator of PI3K activity, is often mutated in a variety of cancer cells.
PI3K alpha/delta inhibitor TQ-B3525: An orally available selective inhibitor of the alpha and delta isoforms of phosphatidylinositol 3-kinase (PI3-kinase subunit alpha/delta; PI3K-alpha/delta; PI3Kalpha/delta), with potential antineoplastic activity. Upon oral administration, PI3K alpha/delta inhibitor TQ-B3525 selectively targets, binds to, and inhibits PI3K alpha and delta and prevents the activation of the PI3K/AKT signaling pathway. This decreases proliferation of and induces cell death in PI3K-alpha/delta over-expressing tumor cells. PI3K-alpha/delta also plays a key role in the B-cell receptor (BCR) signaling pathway and the proliferation of certain hematologic cancer cells. The targeted inhibition of PI3K-alpha/delta is designed to preserve PI3K signaling in normal, non-neoplastic cells, thereby minimizing serious side effects.
PI3K alpha/mTOR inhibitor PWT33597 mesylate: The mesylate salt form of PWT33597, an orally bioavailable dual inhibitor of phosphatidylinositide 3-kinase (PI3K) alpha and mammalian target of rapamycin (mTOR) kinase with potential antineoplastic activity. PI3K alpha/mTOR dual inhibitor PWT33597 selectively inhibits both PI3K alpha kinase and mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in PI3K/mTOR-overexpressing tumor cells. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K.
PI3K delta inhibitor SHC014748M: An orally available selective inhibitor of the delta isoform of phosphatidylinositol 3-kinase (PI3-kinase subunit delta; PI3K-delta; PI3Kdelta), with potential antineoplastic activity. Upon oral administration, PI3K delta inhibitor SHC014748M selectively binds to and inhibits PI3K delta and prevents the activation of the PI3K/AKT signaling pathway. This decreases proliferation of and induces cell death in PI3K delta over-expressing tumor cells. PI3K delta also plays a key role in the B-cell receptor (BCR) signaling pathway and the proliferation of certain hematologic cancer cells. The targeted inhibition of PI3K delta is designed to preserve PI3K signaling in normal, non-neoplastic cells, thereby minimizing serious side effects.
PI3K inhibitor ACP-319: An orally available inhibitor of phosphatidylinositol 3-kinase (PI3K), with potential antineoplastic activity. PI3K inhibitor ACP-319 inhibits PI3K, which prevents the activation of the PI3K/AKT (protein kinase B)-mediated signaling pathway. This results in the inhibition of growth and survival of PI3K-overexpressing tumor cells. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis.
PI3K inhibitor BGT226: A phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor BGT226 specifically inhibits PIK3 in the PI3K/AKT kinase (or protein kinase B) signaling pathway, which may trigger the translocation of cytosolic Bax to the mitochondrial outer membrane, increasing mitochondrial membrane permeability; apoptotic cell death may ensue. Bax is a member of the proapoptotic Bcl2 family of proteins.
PI3K inhibitor GDC-0941 bismesylate: The orally bioavailable bismesylate salt of a potent small-molecule thieno[3,2-d]pyrimidine inhibitor of the class I phosphatidylinositol 3 kinase (PI3K) isoforms p100alpha and p100delta with potential antineoplastic activity. PI3K inhibitor GDC-0941 selectively binds to PI3K isoforms in an ATP-competitive manner, inhibiting the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and activation of the PI3K/Akt signaling pathway; inhibition of tumor cell growth, motility and survival in susceptible tumor cell populations may result. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis; dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.
PI3K inhibitor GSK1059615: A phosphoinositide 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor GSK1059615 inhibits PI3K in the PI3K/AKT kinase signaling pathway, which may trigger the translocation of cytosolic Bax to the mitochondrial outer membrane and an increase in mitochondrial membrane permeability, followed by apoptosis. Bax is a member of the proapoptotic Bcl-2 family of proteins. PIK3, an enzyme often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.
PI3K inhibitor GSK2126458: A small-molecule pyridylsulfonamide inhibitor of phosphatidylinositol 3-kinase (PI3K) with potential antineoplastic activity. PI3K inhibitor GSK2126458 binds to and inhibits PI3K in the PI3K/mTOR signaling pathway, which may trigger the translocation of cytosolic Bax to the mitochondrial outer membrane, increasing mitochondrial membrane permeability and inducing apoptotic cell death. Bax is a member of the proapoptotic Bcl2 family of proteins. PI3K, often overexpressed in cancer cells, plays a crucial role in tumor cell regulation and survival.
PI3K inhibitor PX-866: A small-molecule wortmannin analogue inhibitor of the alpha, gamma, and delta isoforms of phosphoinositide 3-kinase (PI3K) with potential antineoplastic activity. PI3K inhibitor PX-866 inhibits the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and activation of the PI3K/Akt signaling pathway, which may result in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Activation of the PI3K/Akt signaling pathway is frequently associated with tumorigenesis and dysregulated PI3K/Akt signaling may contribute to tumor resistance to a variety of antineoplastic agents.
PI3K inhibitor TL117: An orally bioavailable phosphatidylinositol 3-kinase (PI3K) inhibitor, with potential antineoplastic activity. Upon oral administration, PI3K inhibitor TL117 specifically inhibits the activity of PI3K, and prevents the activation of the PI3K/Akt (protein kinase B)-mediated signaling pathway. This may result in the inhibition of both tumor cell growth and survival in PI3K-overexpressing tumor cells. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.
PI3K inhibitor WX-037: A phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor WX-037 specifically inhibits PI3K, which prevents the activation of the PI3K/protein kinase B-mediated signaling pathway. This may result in the inhibition of both tumor cell growth and survival in PI3K-overexpressing tumor cells. Activation of the PI3K signaling pathway is frequently associated with tumorigenesis. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents.
PI3K inhibitor ZSTK474: An orally available, s-triazine derivative, ATP-competitive phosphatidylinositol 3-kinase (PI3K) inhibitor with potential antineoplastic activity. PI3K inhibitor ZSTK474 inhibits all four PI3K isoforms. Inhibiting the activation of the PI3K/AKT kinase (or protein kinase B) signaling pathway results in inhibition of tumor cell growth and survival in susceptible tumor cell populations. Dysregulated PI3K signaling may contribute to tumor resistance to a variety of antineoplastic agents. This agent does not induce apoptosis but rather induces strong G(0)/G(1) arrest, which might contribute to its favorable efficacy in tumor cells.
PI3K p110beta/delta inhibitor CVL237: A dual selective inhibitor of the beta and delta isoforms of the 110 kDa catalytic subunit of class I phosphoinositide-3 kinase (PI3K-beta/delta), with potential antineoplastic activity. PI3K-beta/delta inhibitor CVL237 selectively inhibits the PI3K-beta and -delta isoforms and prevents their activation, which inhibits PI3K-beta/delta-mediated signal transduction pathways. This decreases proliferation and induces cell death in susceptible tumor cells. Unlike other isoforms of PI3K, PI3K-beta and -delta are overexpressed primarily in solid and hematological tumor cells and play crucial roles in tumor cell survival, and immunoregulation. The targeted inhibition of these PI3Ks allows this agent to potentially be more efficacious and less toxic than pan PI3K inhibitors, which also affect normal, healthy cells.
PI3K-alpha inhibitor HS-10352: An orally bioavailable, small molecule inhibitor of the class I phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) catalytic subunit alpha (PIK3CA; PI3K p110alpha), with potential antineoplastic activity. Upon oral administration, PI3K-alpha inhibitor HS-10352 selectively targets, binds to and inhibits wild-type PIK3CA and its mutated forms, in the PI3K/Akt (protein kinase B)/mammalian target of rapamycin (mTOR) pathway. This results in both apoptosis and growth inhibition in PIK3CA-expressing tumor cells. By specifically targeting PIK3CA, this agent may be more efficacious and less toxic than pan-PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is often found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to chemo- and radio-therapy. PIK3CA, one of the most frequently mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K.
PI3K-alpha inhibitor JS105: An orally bioavailable inhibitor of the class I phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) catalytic subunit alpha (PIK3CA), with potential antineoplastic activity. Upon oral administration, PI3K-alpha inhibitor JS105 selectively targets, binds to and inhibits PIK3CA in the PI3K/Akt (protein kinase B)/mammalian target of rapamycin (mTOR) pathway. This results in apoptosis and growth inhibition in PIK3CA-expressing tumor cells. By specifically targeting PIK3CA, JS105 may be more efficacious and less toxic than pan-PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is often found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to chemo- and radio-therapy. PIK3CA, one of the most frequently mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K.
PI3K-alpha inhibitor TOS-358: An orally bioavailable, covalent inhibitor of class I phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) catalytic subunit alpha (PIK3CA; PI3K p110alpha), with potential antineoplastic activity. Upon oral administration, PI3K-alpha inhibitor TOS-358 selectively targets, binds to and covalently inhibits wild-type PIK3CA and its mutated forms in the PI3K/Akt (protein kinase B)/mammalian target of rapamycin (mTOR) pathway. This results in both apoptosis and growth inhibition in PIK3CA-expressing tumor cells. By specifically targeting PIK3CA, this agent may be more efficacious and less toxic than pan-PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is often found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to chemo- and radio-therapy. PIK3CA, one of the most frequently mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K.
PI3K-beta inhibitor GSK2636771: An orally bioavailable, substituted benzimidazole inhibitor of the class I phosphoinositide 3-kinase (PI3K) beta isoform with potential antineoplastic activity. PI3K beta inhibitor GSK2636771 selectively inhibits PI3K beta kinase activity in the PI3K/Akt/mTOR pathway, which may result in tumor cell apoptosis and growth inhibition in PI3K beta-expressing and/or PTEN-driven tumor cells. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to both chemotherapy and radiotherapy. PI3K beta is the p110-beta catalytic subunit of the class I PI3K. PTEN, a tumor suppressor protein and negative regulator of PI3K activity, is often mutated in a variety of cancer cells.
PI3K-beta Inhibitor SAR260301: An orally bioavailable inhibitor of the class I phosphatidylinositol 3-kinase (PI3K) beta isoform with potential antineoplastic activity. PI3K beta inhibitor SAR260301 selectively inhibits PI3K beta kinase activity in the PI3K/Akt/mTOR pathway, which may result in apoptosis and growth inhibition in PI3K beta-expressing and/or phosphatase and tensin homolog (PTEN)-deficient tumor cells. Dysregulation of the PI3K/Akt/mTOR pathway is frequently found in solid tumors and contributes to increased tumor cell growth, tumor cell survival, and resistance to both chemotherapy and radiotherapy. PI3K beta is the p110-beta catalytic subunit of the class I PI3K. PTEN, a tumor suppressor protein and negative regulator of PI3K activity, is often mutated in a variety of cancer cells. By specifically targeting class I PI3K beta, this agent may be more efficacious and less toxic than pan-PI3K inhibitors.
PI3K-delta inhibitor AMG 319: A highly selective, potent, and orally bioavailable small molecule inhibitor of the delta isoform of the 110 kDa catalytic subunit of class IA phosphoinositide-3 kinases (PI3K) with potential immunomodulating and antineoplastic activities. PI3K-delta inhibitor AMG 319 prevents the activation of the PI3K signaling pathway through inhibition of the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3), thus decreasing proliferation and inducing cell death. Unlike other isoforms of PI3K, PI3K-delta is expressed primarily in hematopoietic lineages. The targeted inhibition of PI3K-delta is designed to preserve PI3K signaling in normal, non-neoplastic cells.
PI3K-delta inhibitor BGB-10188: An orally available selective inhibitor of the delta isoform of phosphatidylinositol 3-kinase (PI3-kinase subunit delta; PI3K-delta; PI3Kdelta), with potential antineoplastic activity. Upon oral administration, PI3K-delta inhibitor BGB-10188 selectively binds to and inhibits PI3K-delta and prevents the activation of the PI3K/AKT signaling pathway. This decreases proliferation of and induces cell death in PI3K-delta over-expressing tumor cells. PI3K-delta also plays a key role in the B-cell receptor (BCR) signaling pathway and the proliferation of certain hematologic cancer cells. The targeted inhibition of PI3K-delta is designed to preserve PI3K signaling in normal, non-neoplastic cells, thereby minimizing serious side effects.
PI3K-gamma inhibitor HS248: An orally bioavailable selective inhibitor of the gamma isoform of phosphoinositide-3 kinase (PI3Kg), with potential immunomodulating and antineoplastic activities. Upon oral administration, PI3Kg inhibitor HS248 targets and inhibits the PI3Kg isoform and prevents the activation of the PI3Kg-AKT-mediated signaling pathway. As PI3Kg plays an important role in immune suppression and promotes immunosuppressive myeloid cell polarization during tumor growth and metastasis, the inhibition PI3Kg may abrogate the immune-suppressive nature in the tumor microenvironment (TME) and impair PI3Kg-AKT-mediated macrophage polarization. This may promote anti-tumor immunity, may increase CD8-positive T-cell activation and M1-like macrophages and may lead to a reduction in cellular proliferation in PI3Kg-expressing tumor cells. By selectively targeting this isoform, PI3K signaling in normal, non-neoplastic cells is minimally impacted or not affected at all, which minimizes the side effect profile for this agent. PI3Kg is highly expressed in leukocytes and plays a critical role in activation of myeloid cells at sites of inflammation and tumorigenesis, T-cell recruitment into the TME, chemokine-mediated chemotaxis and growth factor signaling.
PI3K-gamma inhibitor IPI-549: An orally bioavailable, highly selective small molecule inhibitor of the gamma isoform of phosphoinositide-3 kinase (PI3K-gamma) with potential immunomodulating and antineoplastic activities. Upon administration, IPI-549 prevents the activation of the PI3K-gamma-mediated signaling pathways, which may lead to a reduction in cellular proliferation in PI3K-gamma-expressing tumor cells. In addition, this agent is able to modulate anti-tumor immune responses and inhibit tumor-mediated immunosuppression. Unlike other isoforms of PI3K, the gamma isoform is overexpressed in certain tumor cell types and immune cells; its expression increases tumor cell proliferation and survival. By selectively targeting the gamma isoform, PI3K signaling in normal, non-neoplastic cells is minimally or not affected, which results in a reduced side effect profile.
PI3K-gamma inhibitor ZX-4081: An orally bioavailable selective inhibitor of the gamma isoform of phosphoinositide-3 kinase (PI3Kg), with potential immunomodulating and antineoplastic activities. Upon oral administration of PI3Kg inhibitor ZX-4081, this agent targets and inhibits the PI3Kg isoform and prevents the activation of the PI3Kg-AKT-mediated signaling pathway. As PI3Kg plays an important role in immune suppression and promotes immunosuppressive myeloid cell polarization during tumor growth and metastasis, the inhibition of PI3Kg may abrogate the immune-suppressive nature in the tumor microenvironment (TME) and impair PI3Kg-AKT-mediated macrophage polarization. This may promote anti-tumor immunity, may increase CD8-positive T-cell activation and M1-like macrophages and may lead to a reduction in cellular proliferation in PI3Kg-expressing tumor cells. By selectively targeting this isoform, PI3K signaling in normal, non-neoplastic cells is minimally impacted or not affected at all, which minimizes the side effect profile for this agent. PI3Kg is highly expressed in leukocytes and plays a critical role in activation of myeloid cells at sites of inflammation and tumorigenesis, T-cell recruitment into the TME, chemokine-mediated chemotaxis and growth factor signaling.
PI3K/mTOR dual kinase inhibitor XL765: An orally bioavailable small molecule targeting the phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) kinases in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR dual kinase inhibitor XL765 inhibits both PI3K kinase and mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in susceptible tumor cell populations. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated in a PI3K-independent fashion in response to nutrient and energy deprivation. Accordingly, this agent maybe more potent compared to an agent that inhibits either PI3K kinase or mTOR kinase alone.
PI3K/mTOR inhibitor CLL442: A topical inhibitor of class I phosphoinositide 3-kinase (PI3K) isoforms and mammalian target of rapamycin kinase (mTOR), with potential antineoplastic activity. Upon topical administration, PI3K/mTOR inhibitor CLL442 targets and inhibits class I PI3K isoforms and mTOR kinase. This disrupts phosphorylation of substrates downstream of PI3K and mTOR and may result in apoptosis and growth inhibition in susceptible tumor cells. The PI3K/mTOR pathway is upregulated in a variety of tumor cells and plays a key role in promoting cancer cell proliferation, survival and motility.
PI3K/mTOR inhibitor HEC 68498: An orally bioavailable, small molecule inhibitor of class I phosphoinositide 3-kinase (PI3K) isoforms and mammalian target of rapamycin kinase (mTOR), with potential anti-fibrotic, anti-inflammatory and antineoplastic activities. Upon oral administration, PI3K/mTOR inhibitor HEC 68498 targets and inhibits class I PI3K isoforms and mTOR kinase. This disrupts phosphorylation of substrates downstream of PI3K and mTOR and may result in apoptosis and growth inhibition in susceptible tumor cells and may inhibit inflammation and fibrosis. The PI3K/mTOR pathway is upregulated in a variety of tumor cells and plays a key role in promoting cancer cell proliferation, survival, motility and resistance to chemotherapy and radiotherapy. It also plays a key role in inflammation and fibrosis. mTOR, a serine/threonine kinase downstream of PI3K, may also be activated in a PI3K-independent fashion; therefore, this agent may be more potent than an agent that inhibits either PI3K or mTOR alone.
PI3K/mTOR inhibitor LY3023414: An orally bioavailable, small molecule inhibitor of certain class I phosphoinositide 3-kinase (PI3K) isoforms and mammalian target of rapamycin kinase (mTOR) in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR inhibitor LY3023414 inhibits both certain PI3K isoforms and mTOR in an ATP-competitive manner which may inhibit both the PI3K/mTOR signaling pathway in and proliferation of tumor cells overexpressing PI3K and/or mTOR. The PI3K/mTOR pathway is upregulated in a variety of tumor cells and plays a key role in promoting cancer cell proliferation, and survival, motility and resistance to chemotherapy and radiotherapy. mTOR, a serine/threonine kinase downstream of PI3K, may also be activated in a PI3K-independent fashion; therefore, this agent may be more potent than an agent that inhibits either PI3K or mTOR alone. In addition, LY3023414 may inhibit DNA-dependent protein kinase (DNA-PK), thereby inhibiting the ability of tumor cells to repair damaged DNA. DNA-PK is activated upon DNA damage and plays a key role in repairing double-stranded DNA breaks.
PI3K/mTOR kinase inhibitor DS-7423: An orally bioavailable inhibitor of phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) kinase in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR kinase inhibitor DS-7423 inhibits both PI3K kinase and mTOR kinase, which may result in tumor cell apoptosis and growth inhibition in susceptible tumor cells. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K. Consequently, this agent may potentially be more potent than an agent that inhibits either PI3K kinase or mTOR kinase.
PI3K/mTOR kinase inhibitor PF-04691502: An agent targeting the phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR kinase inhibitor PF-04691502 inhibits both PI3K and mTOR kinases, which may result in apoptosis and growth inhibition of cancer cells overexpressing PI3K/mTOR. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independent of PI3K.
PI3K/mTOR kinase inhibitor VS-5584: A potent and selective inhibitor of both phosphatidylinositol 3 kinase (PI3K) and mammalian target of rapamycin (mTOR) kinase in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. PI3K/mTOR kinase inhibitor VS-5584 inhibits mTOR kinase and all class I PI3K isoforms. Consequently, this disrupts phosphorylation of substrates downstream of PI3K and mTOR and may result in apoptosis and growth inhibition in susceptible tumor cells. Activation of the PI3K/mTOR pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy. mTOR is a serine/threonine kinase downstream of PI3K, which also has PI3K-independent activity. Consequently, this agent may potentially be more potent than an agent that inhibits either PI3K kinase or mTOR kinase.
PI3K/mTOR kinase inhibitor WXFL10030390: An orally bioavailable, small molecule inhibitor of certain phosphoinositide 3-kinase (PI3K) isoforms and mammalian target of rapamycin kinase (mTOR) in the PI3K/mTOR signaling pathway, with potential antineoplastic activity. Upon oral administration, PI3K/mTOR inhibitor WXFL10030390 (WX390) inhibits mTOR kinase and certain PI3K isoforms. Consequently, this disrupts phosphorylation of substrates downstream of PI3K and mTOR and may result in apoptosis and growth inhibition in susceptible tumor cells. The PI3K/mTOR pathway is upregulated in a variety of tumor cells and plays a key role in promoting cancer cell proliferation, and survival, motility and resistance to chemotherapy and radiotherapy. mTOR, a serine/threonine kinase downstream of PI3K, may also be activated in a PI3K-independent fashion; therefore, this agent may be more potent than an agent that inhibits either PI3K or mTOR alone.
PI3K/mTOR/ALK-1/DNA-PK inhibitor P7170: An orally bioavailable inhibitor of phosphoinositide 3-kinase (PI3K), mammalian target of rapamycin (mTOR), activin receptor-like kinase 1 (ALK-1) and DNA-dependent protein kinase (DNA-PK), with potential anti-angiogenic and antineoplastic activities. Upon oral administration, PI3K/mTOR/ALK-1/DNA-PK inhibitor P7170 inhibits the activity of all four kinases. This prevents PI3K/mTOR and ALK-1-mediated signaling pathways and may lead to the inhibition of cancer cell growth in PI3K/mTOR-overexpressing tumor cells and angiogenesis in ALK-1-overexpressing endothelial cells. Also, by inhibiting DNA-PK, this agent inhibits the ability of tumor cells to repair damaged DNA. The PI3K/mTOR pathway is upregulated in a variety of tumors and plays an important role in regulating cancer cell proliferation, growth, and survival. ALK-1, a member of the transforming growth factor beta (TGF-b) type I receptor family, is overexpressed on endothelial cells in a variety of tumor types and increases endothelial cell proliferation and migration. DNA-PK is activated upon DNA damage and plays a key role in repairing double-stranded DNA breaks.
PI3K/mTORC1/mTORC2 inhibitor DCBCI0901: An inhibitor of phosphatidylinositide 3-kinase (PI3K), raptor-mTOR (mTOR complex 1 or mTORC1) and rictor-mTOR (mTOR complex 2 or mTORC2) with potential antineoplastic activity. Upon intravenous infusion, PI3K/mTORC1/mTORC2 inhibitor DCBCI0901 binds to and inhibits PI3K as well as both mTORC1 and mTORC2, which may result in both apoptosis and a decrease in cell proliferation in tumor cells overexpressing PI3K, mTORC1, and mTORC2. Activation of the PI3K/mTOR signaling pathway promotes cell growth, survival, and resistance to chemotherapy and radiotherapy; mTOR, a serine/threonine kinase downstream of PI3K, may also be activated independently of PI3K.
PI3Ka/mTOR inhibitor PKI-179: A second generation, small-molecule mimetic of ATP that targets the mammalian target of rapamycin (mTOR) with potential antineoplastic activity. PKI-179 selectively inhibits mTOR and phosphoinositide-3-kinase (PI3K) alpha. By inhibiting the PI3K/mTOR signaling pathway, this agent may inhibit tumor cell proliferation and survival.
PI3Kalpha inhibitor AZD8835: An orally bioavailable inhibitor of the class I phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) catalytic subunit alpha (PIK3CA), with potential antineoplastic activity. PI3K alpha inhibitor AZD8835 selectively binds to and inhibits PIK3CA and its mutated forms, in the PI3K/Akt (protein kinase B)/mammalian target of rapamycin (mTOR) pathway. This results in both apoptosis and growth inhibition in PIK3CA-expressing tumor cells. By specifically targeting PIK3CA, this agent may be more efficacious and less toxic than pan-PI3K inhibitors. Dysregulation of the PI3K/Akt/mTOR pathway is often found in solid tumors and results in the promotion of tumor cell growth, survival, and resistance to chemo- and radio-therapy. PIK3CA, one of the most frequently mutated oncogenes, encodes the p110-alpha catalytic subunit of the class I PI3K.
PI3Kbeta inhibitor AZD8186: An inhibitor of the beta isoform of phosphoinositide-3 kinase (PI3K), with potential antineoplastic activity. Upon administration, PI3Kbeta inhibitor AZD8186 selectively inhibits the activity of PI3Kbeta in the PI3K/Akt/mTOR signaling pathway, which may result in a decrease of tumor cell proliferation. It also induces cell death in PI3K-expressing cancer cells. By specifically targeting class I PI3K beta, this agent may be more efficacious and less toxic than pan PI3K inhibitors. PI3K-mediated signaling is often dysregulated in cancer cells and contributes to increased tumor cell growth, survival, and tumor resistance to a variety of antineoplastic agents.
PI3Kdelta inhibitor GS-9901: An orally bioavailable, small molecule inhibitor of the delta isoform of phosphoinositide-3 kinase (PI3Kdelta) with potential immunomodulating and antineoplastic activities. Upon oral administration, PI3Kdelta inhibitor GS-9901 selectively binds to the delta isoform of PI3K and inhibits its activity. This inhibits the activation of the PI3Kdelta-mediated signaling pathway and prevents proliferation of PI3Kdelta-overexpressing tumor cells. Unlike other isoforms of PI3K, PI3Kdelta is expressed primarily in certain tumor cell types and plays a key role in tumor cell proliferation, motility and survival. The targeted inhibition of PI3Kdelta is designed to preserve PI3K signaling in normal, non-neoplastic cells and thus reduces toxicity to normal, healthy cells.
PI3Kdelta inhibitor INCB040093: An orally bioavailable, selective inhibitor of the delta isoform of the 110 kDa catalytic subunit of class I phosphoinositide-3 kinases (PI3K) with potential antineoplastic activity. PI3Kdelta inhibitor INCB040093 specifically inhibits PI3Kdelta, which prevents both the production of the second messenger phosphatidylinositol-3,4,5-trisphosphate (PIP3) and the activation of the PI3K/AKT kinase signaling pathway. This decreases proliferation and induces cell death in PI3K-overexpressing tumor cells. Unlike other isoforms of PI3K, PI3Kdelta is often overexpressed in tumor cells, especially those of hematologic origin, and plays a crucial role in tumor cell regulation and survival. The targeted inhibition of PI3Kdelta allows for PI3K signaling in normal, non-neoplastic cells.
PI3Kdelta/gamma inhibitor ZX-101A: An orally bioavailable inhibitor of the delta and gamma isoforms of phosphoinositide-3 kinase (PI3K), with potential antineoplastic activity. Upon administration of PI3Kdelta/gamma inhibitor ZX-101A, this agent targets and inhibits the PI3K delta and gamma isoforms and prevents the activation of the PI3K/AKT-mediated signaling pathway. This may lead to a reduction in cellular proliferation in PI3K delta/gamma-expressing tumor cells. ZX-101A may also promote anti-tumor immunity. Unlike other isoforms of PI3K, the delta and gamma isoforms are overexpressed primarily in hematologic malignancies. By selectively targeting these isoforms, PI3K signaling in normal, non-neoplastic cells is minimally impacted or not affected at all, which minimizes the side effect profile for this agent.
pibenzimol: A fluorescent dye of benzimidazole derivative. Pibenzimol binds to AT-specific sites in the minor groove of duplex DNA and inhibits topoisomerase I, and DNA polymerase, thereby preventing DNA replication. This agent prolongs the G2 phase of the cell cycle and initiates apoptosis in tumor cells.
pibrozelesin: A semisynthetic water-soluble derivative of the antineoplastic antibiotic duocarmycin B2. Activated by carboxyl esterase, pibrozelesin alkylates DNA by binding to adenine-thymine (A-T)-rich sequences in the minor groove of DNA, thereby inhibiting DNA replication and inducing apoptosis.
Picato: (Other name for: ingenol mebutate)
Picato: (Other name for: ingenol mebutate gel)
picibanil: A lyophilized formulation containing cultures of a low-virulent strain of Streptococcus pyogenes, treated and killed with pencillin G, with potential sclerosing, immunostimulating and antineoplastic activities. Besides its activity as a sclerosing agent, picibanil appears to have multiple effects on the immune system as a non-specific immunostimulant. This agent activates the host immune system by stimulating the activity of natural killer (NK) cells, macrophages and lymphocytes, and by enhancing the production of several key immune mediators, including interleukins (ILs) and tumor necrosis factor (TNF).
picoplatin: A new generation organic platinum analog with an extended spectrum of antineoplastic activity. Designed to overcome platinum drug resistance, picoplatin alkylates DNA, forming both inter- and intra-strand cross-linkages, resulting in inhibition of DNA replication and transcription, and the induction of apoptosis.
picropodophyllin: A cyclolignan alkaloid found in the mayapple plant family (Podophyllum peltatum), and a small molecule inhibitor of the insulin-like growth factor 1 receptor (IGF1R) with potential antineoplastic activity. Picropodophyllin specifically inhibits the activity and downregulates the cellular expression of IGF1R without interfering with activities of other growth factor receptors, such as receptors for insulin, epidermal growth factor, platelet-derived growth factor, fibroblast growth factor and mast/stem cell growth factor (KIT). This agent shows potent activity in the suppression o f tumor cell proliferation and the induction of tumor cell apoptosis. IGF1R, a receptor tyrosine kinase overexpressed in a variety of human cancers, plays a critical role in the growth and survival of many types of cancer cells.
pidilizumab: A humanized, immunoglobulin (Ig) G1 monoclonal antibody directed against human inhibitory receptor programmed cell death 1 (PD-1; PDCD1), with potential immune checkpoint inhibitory and antineoplastic activities. Pidilizumab binds to PD-1 and blocks the interaction between PD-1 and its ligands, PD-1 ligand 1 (PD-L1) and PD-1 ligand 2 (PD-L2). This prevents the activation of PD-1 and its downstream signaling pathways. This may restore immune function through the activation of natural killer (NK) cells and cytotoxic T-lymphocytes (CTLs) against tumor cells. PD-1, an inhibitory receptor belonging to the B7-receptor family expressed on activated T-lymphocytes, B-cells and NK cells, negatively regulates T-cell activation and effector function when activated by its ligands; it plays an important role in tumor evasion from host immunity.
pidnarulex: An orally bioavailable inhibitor of RNA polymerase I (Pol I), with potential antineoplastic activity. Upon oral administration, pidnarulex selectively binds to and inhibits Pol I, prevents Pol I-mediated ribosomal RNA (rRNA) synthesis, induces apoptosis, and inhibits tumor cell growth. Pol I, the multiprotein complex that synthesizes rRNA, is upregulated in cancer cells and plays a key role in cell proliferation and survival. Hyperactivated rRNA transcription is associated with uncontrolled cancer cell proliferation.
Pifeltro: (Other name for: doravirine)
pilocarpine hydrochloride: The hydrochloride salt of a natural alkaloid extracted from plants of the genus Pilocarpus with cholinergic agonist activity. As a cholinergic parasympathomimetic agent, pilocarpine predominantly binds to muscarinic receptors, thereby inducing exocrine gland secretion and stimulating smooth muscle in the bronchi, urinary tract, biliary tract, and intestinal tract. When applied topically to the eye, this agent stimulates the sphincter pupillae to contract, resulting in miosis; stimulates the ciliary muscle to contract, resulting in spasm of accomodation; and may cause a transitory rise in intraocular pressure followed by a more persistent fall due to opening of the trabecular meshwork and an increase in the outflow of aqueous humor.
PIM kinase inhibitor LGH447: An orally available pan-PIM protein kinase inhibitor with potential antineoplastic activity. PIM kinase inhibitor LGH447 binds to and inhibits the activities of PIM-1, -2 and -3 serine/threonine kinases, which may result in the interruption of the G1/S phase cell cycle transition, the expression of the pro-apoptotic Bcl2 protein, and tumor cell apoptosis in cells that overexpress PIMs. PIM kinases, downstream effectors of many cytokine and growth factor signaling pathways, play key roles in cell cycle progression and apoptosis inhibition and may be overexpressed in various malignancies.
Pim kinase inhibitor SGI-1776: A small-molecule pan-Pim protein kinase inhibitor with potential antineoplastic activity. Pim kinase inhibitor SGI-1776 binds to and inhibits the activities of Pim-1, -2 and -3, serine-threonine kinases, which may result in the interruption of the G1/S phase cell cycle transition, the expression of pro-apoptotic Bcl2 proteins and tumor cell apoptosis. PIM kinases play key roles in cell cycle progression and apoptosis inhibition and may be overexpressed in various malignancies.
PIM kinase inhibitor TP-3654: An orally available, second-generation and selective ATP-competitive inhibitor of proviral integration site for Moloney murine leukemia virus (PIM) kinases, with potential antineoplastic activity. Upon oral administration, PIM kinase inhibitor TP-3654 selectively binds to and prevents the activation of the PIM kinases. This prevents the activation of PIM-mediated signaling pathways and inhibits proliferation in cells that overexpress PIM. PIMs, constitutively active proto-oncogenic serine/threonine kinases, are upregulated in various types of cancers and play key roles in tumor cell proliferation and survival.
pimasertib: An orally bioavailable small-molecule inhibitor of MEK1 and MEK2 (MEK1/2) with potential antineoplastic activity. Pimasertib selectively binds to and inhibits the activity of MEK1/2, preventing the activation of MEK1/2-dependent effector proteins and transcription factors, which may result in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 (MAP2K1/K2) are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.
pimasertib hydrochloride: The hydrochloride salt form of pimasertib, an orally bioavailable small-molecule inhibitor of mitogen activated protein kinase kinases 1 (MEK1) and 2 (MEK2), with potential antineoplastic activity. Upon oral administration, pimasertib selectively binds to and inhibits the activity of MEK1 and 2, thereby preventing the activation of MEK1/2-dependent effector proteins and transcription factors. This results in the inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK1/2 (MAP2K1/K2) are dual-specificity threonine/tyrosine kinases that play key roles in the activation of the RAS/RAF/MEK/ERK pathway and are often upregulated in a variety of tumor cell types.
pimecrolimus cream: A 33-epi-chloro-derivative of the ascomycin macrolactam with immunosuppressant properties. Pimecrolimus binds to the receptor macrophilin-12 (FKBP-12) forming a complex that blocks the calcium-dependent signal transduction cascade mediated by calcineurin. Via dephosphorylation, calcineurin is the enzyme responsible for activating nuclear factor of activated T-cells (NF-AT), a T cell transcriptional regulatory factor. As a consequence, the synthesis and release of Th1- (T helper 1) and Th2- (T helper 2) type cytokines, and other inflammatory mediators from T-cells and mast cells are blocked and the expression of signals essential for the activation of inflammatory T-lymphocytes is inhibited. However, pimecrolimus mode of action is cell-selective and does not affect Langerhans' cells/dendritic cells and primary fibroblasts.
pimicotinib: An orally bioavailable inhibitor of colony stimulating factor 1 receptor (CSF1R; CSF-1R; CD115; M-CSFR), with potential immunomodulatory and antineoplastic activities. Upon oral administration, pimicotinib targets and binds to CSF1R, thereby blocking CSF1R activation and CSF1R-mediated signaling. This inhibits the activities of tumor-associated macrophages (TAMs) and myeloid-derived suppressor cells (MDSCs), and prevents immune suppression in the tumor microenvironment (TME). This enhances antitumor T-cell immune responses and inhibits the proliferation of tumor cells. CSF1R, also known as macrophage colony-stimulating factor receptor (M-CSFR) and CD115 (cluster of differentiation 115), is a cell-surface receptor that plays major roles in tumor cell proliferation and metastasis.
pimitespib: A specific inhibitor of heat shock protein 90 (Hsp90) subtypes alpha and beta, with potential antineoplastic and chemo/radiosensitizing activities. Upon oral administration, pimitespib specifically binds to and inhibits the activity of Hsp90 alpha and beta; this results in the proteasomal degradation of oncogenic client proteins, which inhibits client protein dependent-signaling, induces apoptosis, and inhibits the proliferation of cells overexpressing HSP90alpha/beta. Hsp90, a family of molecular chaperone proteins that are upregulated in a variety of tumor cells, plays a key role in the conformational maturation, stability, and function of "client" proteins within the cell,; many of which are involved in signal transduction, cell cycle regulation and apoptosis, including kinases, cell-cycle regulators, transcription factors and hormone receptors. As TAS-116 selectively inhibits cytosolic HSP90alpha and beta only and does not inhibit HSP90 paralogs, such as endoplasmic reticulum GRP94 or mitochondrial TRAP1, this agent may have less off-target toxicity as compared to non-selective HSP90 inhibitors.
pimodivir: An orally bioavailable non-nucleoside inhibitor of the polymerase basic protein 2 (PB2) subunit of the influenza A virus polymerase complex with potential antiviral activity. Upon administration, pimodivir occupies the 7-methyl GTP (m7GTP) binding site of PB2, thereby blocking the cap-snatching activity of the influenza polymerase complex and inhibiting the synthesis of viral mRNA. PB2 is one of three subunits that make up the influenza A viral polymerase complex, which is responsible for replication and transcription of the viral RNA (vRNA) genome in the nuclei of infected cells.
pimonidazole: A nitroimidazole with hypoxic selectivity and radiosensitizing property. Pimonidazole is reduced in hypoxic environments as in tumor cells, thereby it can be used as an hypoxia marker. In hypoxic cells, reduced pimonidazole binds to -SH-containing molecules such as glutathione and proteins, and the resulting complexes accumulated in tissues, thereby sensitizing cells to be more susceptible for radiation treatment.
pimonidazole hydrochloride: A substituted nitroimidazole salt. Hypoxic cells bioreductively activate and bind pimonidazole. This agent may be used as a hypoxia marker for detecting oxygen gradients in living tissues. Pimonidazole also exhibits radiosensitizing properties.
pimurutamab: A glycoengineered humanized version of the monoclonal antibody of cetuximab, with potential antineoplastic activity. Upon intravenous administration, pimurutamab selectively targets and binds to the extracellular domain of the epidermal growth factor receptor (EGFR), thereby preventing the activation and subsequent dimerization of the receptor. This may prevent EGFR-mediated signaling and inhibit EGFR-dependent tumor cell proliferation. In addition, the glyco-optimization promotes antibody-dependent cell-mediated cytotoxicity (ADCC). EGFR, a member of the epidermal growth factor family of extracellular protein ligands, may be overexpressed on the cell surfaces of certain tumor types.
pinaverium bromide: An orally available bromide salt form of pinaverium, a calcium channel blocker (CCB) with antispasmodic activity. Upon oral administration, pinaverium blocks the voltage-dependent calcium channels and inhibits calcium ion influx into the smooth muscle cells located in the gastrointestinal (GI) tract. This prevents smooth muscle contraction and relaxes the GI tract. In addition, pinaverium may both reduce bowel uptake of and facilitate the function of locally active, co-administered drugs.
pinometostat: AA small molecule inhibitor of histone methyltransferase with potential antineoplastic activity. Upon intravenous administration, pinometostat specifically blocks the activity of the histone lysine-methyltransferase DOT1L, thereby inhibiting the methylation of nucleosomal histone H3 on lysine 79 (H3K79) that is bound to the mixed lineage leukemia (MLL) fusion protein which targets genes and blocks the expression of leukemogenic genes. This eventually leads to an induction of apoptosis in the leukemic cells bearing the MLL gene translocations. DOT1L, a non-SET domain-containing histone methyltransferase, specifically methylates H3K79 and plays a key role in normal cell differentiation and in the development of leukemia with MLL gene rearrangement on chromosome 11 and promotes the expression of leukemia-causing genes.
pioglitazone hydrochloride: The hydrochloride salt of an orally-active thiazolidinedione with antidiabetic properties and potential antineoplastic activity. Pioglitazone activates peroxisome proliferator-activated receptor gamma (PPAR-gamma), a ligand-activated transcription factor, thereby inducing cell differentiation and inhibiting cell growth and angiogenesis. This agent also modulates the transcription of insulin-responsive genes, inhibits macrophage and monocyte activation, and stimulates adipocyte differentiation.
pipendoxifene: A nonsteroidal 2-phenyl indole and a selective estrogen receptor modulator (SERM) with potential antineoplastic activity. Pipendoxifene antagonizes binding of estradiol to estrogen receptor alpha (ER alpha), thereby inhibiting ER alpha-mediated gene expression, interfering with estrogen activity and inhibiting estrogen-stimulated growth in estrogen-dependent breast cancer. In addition, this agent also exerts intrinsic estrogenic activity depending on the tissue types.
piperacillin sodium: The sodium salt of piperacillin, a broad-spectrum semisynthetic, ampicillin-derived ureidopenicillin antibiotic with bactericidal activity. Piperacillin binds to and inactivates penicillin-binding proteins (PBPs), enzymes located on the inner membrane of the bacterial cell wall, resulting in the weakening of the bacterial cell wall and cell lysis. PBPs participate in the terminal stages of assembling the bacterial cell wall, and in reshaping the cell wall during cell division. Inactivation of PBPs interferes with the cross-linkage of peptidoglycan chains necessary for bacterial cell wall strength and rigidity.
piperazinedione: A crystalline antibiotic fermentation product isolated from the bacterium Streptomyces griseoluteus with antineoplastic activity. Piperazinedione alkylates DNA at the N-7 position of guanine, inhibiting DNA replication and inducing cell cycle arrest.
piperine extract (standardized): A standardized extract containing the active alkaloid piperine, derived from the fruit of the plant Piper nigrum (black pepper) and/or the plant Piper longum L. (long pepper), with thermogenic properties. Co-ingestion of piperidine enhances the bioavailability of various nutrients, including beta-carotene, curcumin, selenium, pyridoxine and coenzyme Q10. In addition, this agent may exert anti-inflammatory and anti-tumor activities and may enhance the production of serotonin.
Pipracil: (Other name for: piperacillin sodium)
Piqray: (Other name for: alpelisib)
pirarubicin: An analogue of the anthracycline antineoplastic antibiotic doxorubicin. Pirarubicin intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. This agent is less cardiotoxic than doxorubicin and exhibits activity against some doxorubicin-resistant cell lines.
pirfenidone: An orally active synthetic antifibrotic agent structurally similar to pyridine 2,4-dicarboxylate. Pirfenidone inhibits fibroblast, epidermal, platelet-derived, and transforming beta-1 growth factors, thereby slowing tumor cell proliferation. This agent also inhibits DNA synthesis and the production of mRNA for collagen types I and III, resulting in a reduction in radiation-induced fibrosis.
piritramide: A diphenylpropylamine and opioid receptor agonist, with analgesic activity. Upon administration, piritramide binds to and activates mu-opioid receptors in the central nervous system (CNS), thereby mimicking the effects of endogenous opioids and producing analgesic relief.
piritrexim: A synthetic antifolate agent with antiparasitic, antipsoriatic and antitumor properties. Piritrexim inhibits the enzyme dihydrofolate reductase enzyme, thereby disrupting folate metabolism and DNA synthesis and cell division.
pirotinib: An orally bioavailable inhibitor of the receptor tyrosine kinase (RTK) epidermal growth factor receptor (ErbB; EGFR) family, with potential antineoplastic activity. Upon administration, pirotinib selectively and irreversibly binds to and inhibits the epidermal growth factor receptors 1 (ErbB1; EGFR), 2 (ErbB2; HER2), and 4 (ErbB4; HER4). This may result in the inhibition of cell growth and angiogenesis in tumors overexpressing these RTKs. EGFRs play major roles in both tumor cell proliferation and tumor vascularization, and are overexpressed in many cancer cell types.
piroxantrone: An anthrapyrazole antineoplastic antibiotic. Piroxantrone intercalates into DNA and interacts with topoisomerase II, thereby inhibiting DNA replication and repair and RNA and protein synthesis. Although less cardiotoxic than doxorubicin, this agent exhibits a narrow spectrum of antineoplastic activity.
piroxicam: A nonsteroidal oxicam derivative with anti-inflammatory, antipyretic and analgesic properties. As a non-selective, nonsteroidal anti-inflammatory drug (NSAID), piroxicam binds and chelates both isoforms of cyclooxygenases (COX1 and COX2), thereby stalling phospholipase A2 activity and conversion of arachidonic acid into prostaglandin precursors at the rate limiting cyclooxygenase enzyme step. This results in inhibition of prostaglandin biosynthesis. As a second, independent effect, piroxicam inhibits the activation of neutrophils thereby contributing to its overall anti-inflammatory effects.
pIRS2 phosphopeptide-tetanus peptide vaccine: A vaccine composed of a phosphorylated peptide from the tumor associated antigen insulin receptor substrate-2 (IRS2) and a tetanus-derived peptide, with potential immunomodulating and antineoplastic activities. Upon administration of pIRS2 phosphopeptide-tetanus peptide vaccine, the pIRS2 phosphopeptide may stimulate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against phosphopeptide-containing tumor cells. The tetanus peptide serves as an immunoadjuvant and induces a helper T-cell response which may help stimulate an immune response against the pIRS2-expressing melanoma tumor cells. IRS2 is upregulated in a variety of cancer cells.
pirtobrutinib: An orally available, selective, non-covalent Bruton's tyrosine kinase (BTK) inhibitor with potential antineoplastic activity. Upon oral administration, pirtobrutinib selectively and reversibly binds to BTK. This prevents both the activation of the B-cell antigen receptor (BCR) signaling pathway and BTK-mediated activation of downstream survival pathways, thereby inhibiting the growth of malignant B-cells that overexpress BTK. Reversible binding of LOXO-305 may preserve antitumor activity in the presence of certain acquired resistance mutations, including C481 mutated BTK, and limit toxicity associated with inhibition of other non-BTK kinases. BTK, a member of the Src-related BTK/Tec family of cytoplasmic tyrosine kinases, is overexpressed or mutated in B-cell malignancies; it plays an important role in the development, activation, signaling, proliferation and survival of B lymphocytes.
pitavastatin calcium: A calcium salt formulation of pitavastatin, a novel statin that induces plaque regression and elevates HDL-cholesterol levels.
Pitocin: (Other name for: recombinant oxytocin)
pixantrone dimaleate: The dimaleate salt of a synthetic, noncardiotoxic aza-anthracenedione analogue with potential antineoplastic activity. Pixantrone intercalates into DNA and induces topoisomerase II-mediated DNA strand crosslinks, resulting in inhibition of DNA replication and tumor cell cytotoxicity.
pixatimod: A synthetic sugar modified heparan sulfate mimetic and agonist of toll-like receptor 9 (TLR9), with potential immunostimulating, antineoplastic and anti-viral activities. Upon administration, pixatimod binds to and activates TLR9 expressed by dendritic cells (DCs) and B cells. This initiates cytokine release from DCs and activates innate immune signaling pathways, and leads to the activation of natural killer (NK) cells to destroy tumor cells. The combination of pixatimod with certain checkpoint inhibitors may enhance the activation of cytotoxic T lymphocytes to further kill tumor cells. In addition, pixatimod inhibits the cleavage of heparan sulfate from cell surface proteoglycan by heparanase (HPSE) and inhibits the infiltration of tumor-associated macrophages (TAMs). TLR9, a member of the TLR family, plays a fundamental role in pathogen recognition and activation of innate immunity.
PK-R allosteric activator AG-348: An orally available, small-molecule, allosteric activator of the red cell isoform of pyruvate kinase (PK-R), with potential to improve hemolytic anemia in patients with pyruvate kinase deficiency (PKD). Upon oral administration, AG-348 binds to and activates PK-R, thereby enhancing glycolytic pathway activity, improving adenosine triphosphate (ATP) levels and reducing 2,3-diphosphoglycerate (2,3-DPG) levels. Mutations in PK-R cause deficiency in PK-R which prevents adequate red blood cell (RBC) glycolysis, leading to a buildup of the upstream glycolytic intermediate 2,3-DPG and deficiency in the PK-R product ATP.
PKC-beta inhibitor MS-553: An orally available inhibitor of the beta-isoform of protein kinase C (PKC), with potential immunosuppressive and antineoplastic activities. Upon oral administration, PKC-beta inhibitor MS-553 selectively binds to and inhibits PKC-beta, which prevents the activation of PKC-beta-mediated signaling pathways. This may lead to the induction of cell cycle arrest and apoptosis in susceptible tumor cells. PKC-beta, a serine/threonine protein kinase overexpressed in certain types of cancer cells, is involved in tumor cell differentiation, proliferation, invasion and survival.
PKMYT1 inhibitor XL495: An orally bioavailable small molecule inhibitor of the human membrane-associated tyrosine- and threonine-specific cdc2-inhibitory kinase (PKMYT1), with potential antineoplastic activity. Upon oral administration, PKMYT1 inhibitor XL495 targets, binds to and inhibits the activity of PKMYT1. This results in the inhibition of CDK1 phosphorylation, which may promote both premature mitosis and a prolonged mitotic arrest, and lead to the accumulation of unrepaired DNA damage and apoptosis in susceptible tumor cells, such as CCNE1-overexpressing tumor cells. PKMYT1 phosphorylates CDK1 specifically when CDK1 is complexed to cyclins, which blocks progression from G2 into mitosis.
placebo: An inactive substance, treatment or procedure that is intended to provide baseline measurements for the experimental protocol of a clinical trial.
pladienolide derivative E7107: A synthetic urethane derivative of pladienolide D with potential antineoplastic activity. Pladienolide derivative E7107 is generated from the 12-membered macrolide pladienolide D, one of several macrolides derived from the bacterium Streptomyces platensis Mer-11107. This agent appears to bind to the 130-kDa subunit 3 (spliceosome-associated protein 130; SAP130) of the splicing factor 3b (SF3b), resulting in inhibition of pre-messenger RNA splicing and the arrest of cell-cycle progression. The splicing factor SF3b is a multiprotein complex integral to the accurate excision of introns from pre-messenger RNA; the subunit SAP130 associates with U2 snRNP and is recruited to prespliceosomal complexes.
plamotamab: A bispecific, Fc domain-containing, monoclonal antibody with potential antineoplastic activity. Plamotamab contains two antigen-recognition sites: one for human CD3, a T cell surface antigen, and one for human CD20, a tumor-associated antigen (TAA) that is exclusively expressed on B cells during most stages of B-cell development and is often overexpressed in B-cell malignancies. Upon administration, plamotamab binds to both T cells and CD20-expressing B-lineage tumor cells. The resulting cross-linkage may trigger a potent cytotoxic T-lymphocyte (CTL) response against the CD20-expressing tumor B cells. Inclusion of an Fc domain on the antibody prolongs the half-life of the bispecific antibody and enhances T-cell-mediated tumor cell killing because the agent is able to bind to Fc receptors.
Plan B: (Other name for: levonorgestrel)
plant-derived hematopoiesis enhancer PG2: A proprietary botanical formulation derived from a traditional Chinese medicinal (TCM) plant with hematopoietic activity. Although the mechanism of action has yet to be fully elucidated, plant-derived hematopoiesis enhancer PG2 appears to stimulate multi-lineage progenitor cells that may be closely related to the hematopoietic stem cell. In both chemotherapy- and radiation therapy-induced animal models of myelosuppression, this agent has been shown to restore granulocyte, erythrocyte, and platelet counts to normal levels. Plant-derived hematopoiesis enhancer PG2 stimulates the production of numerous cytokines such as granulocyte-colony stimulating factor (G-CSF) and may stimulate the production of neuroendocrine hormones.
Plaquenil: (Other name for: hydroxychloroquine sulfate)
Plasma-Lyte A: (Other name for: balanced crystalloid solution)
plasmacytoid dendritic cell vaccine: A whole cell vaccine derived from a distinct subset of dendritic cells (DCs) with a plasma cell-like morphology that exhibits immunomodulating activity. Plasmacytoid dendritic cells (pDCs) express a characteristic set of surface markers, such as CD123 (interleukin-3 receptor alpha chain), BDCA-2 (blood dendritic cell antigen 2; CD303) and BDCA-4 (CD304), as well as intracellular toll-like receptors 7 and 9. Upon stimulation, the activated pDCs produce substantial amounts of interferon (IFN) alpha, and to a lesser degree IFN-beta, as well as other cytokines and chemokines, such as tumor necrosis factor alpha and interleukins 1, 6 and 8. In addition, these pDCs, directly or indirectly stimulate T-cells, B-cells and natural killer cells. This may potentially lead to increased immunity against tumor cells.
PlasmaLyte-A: (Other name for: balanced crystalloid solution)
plasmid DNA vaccine pING-hHER3FL: A plasmid DNA cancer vaccine encoding the tumor-associated antigen (TAA) human epidermal growth factor receptor type-3 (HER-3; HER3), with potential antineoplastic and immunomodulating activities. Upon intramuscular administration of the plasmid DNA vaccine pING-hHER3FL and after cellular uptake by muscle cells, the plasmid DNA expresses HER-3 which, may elicit both antigen-specific cytotoxic T-lymphocyte (CTL) and humoral immune responses against tumor cells expressing HER-3. HER-3 plays a key role in tumor cell proliferation and its overexpression is associated with poor prognosis. HER-3 is associated with tumor cell resistance to anti-HER-2 therapeutics.
plasmid encoding antiangiogenic metargidin peptide: A plasmid encoding the protein antiangiogenic metargidin plasmid (AMEP), the disintegrin domain of ADAM-15 (metargidin), with potential antiangiogenic and antimetastatic activities. Upon intratumoral electrotransfer of plasmid encoding AMEP, AMEP binds to cellular integrin receptors alpha-v-beta-3 (avb3) and alpha-5-beta-1 (a5b1), which are upregulated on activated endothelial cells and a variety of tumor cells. Binding to the integrin receptors may inhibit angiogenesis and may inhibit tumor cell proliferation.
Plasmodium vivax: A protozoan parasite in the family Plasmodiidae. P. vivax is the most frequent and widely distributed causative agent of tertian malaria.
Plasmodium vivax–infected red blood cells: A preparation of red blood cells (RBCs) that have been infected with the malaria parasite Plasmodium vivax (P. vivax), with potential immunomodulating and antineoplastic activities. Upon administration of the P. vivax-infected RBCs, the P. vivax infection stimulates host immune responses against the P. vivax-infected RBCs. This also stimulates both innate and adaptive anti-tumor immune responses. This leads to the production of cytokines, including interferon-gamma (IFN-g) and tumor-necrosis factor alpha (TNF-a), the proliferation and activation of natural killer (NK) cells, dendritic cells (DCs), CD4-positive T lymphocytes, and cytotoxic T lymphocytes (CTLs). This results in the inhibition of tumor cell proliferation, induction of tumor cell apoptosis, and prevents angiogenesis.
platelet-rich plasma: An autologous preparation of platelet-rich plasma (PRP) that may potentially be used to treat fecal incontinence in patients who underwent low anterior resection for rectal cancer. Upon injection of the therapeutic autologous PRP into the anal canal, the plasma may improve and treat fecal incontinence.
platinum acetylacetonate-titanium dioxide nanoparticles: A preparation of platinum acetylacetonate supported by sol-gel technology functionalized titania, with potential antineoplastic activity. Upon intravenous administration, the platinum moiety forms complexes with nucleophilic groups such as GC-rich sites in DNA, inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links, resulting in apoptosis and cell growth inhibition. Compared to platinum alone, the nanoparticle formulation allows increased delivery of platinum to the tumor site, thereby increasing efficacy while reducing systemic toxicity.
Plavix: (Other name for: clopidogrel bisulfate)
plecanatide: An agonist of intestinal guanylate cyclase type C (GC-C) which is almost structurally identical to human uroguanylin, with laxative and anti-nociceptive activities. Upon oral administration, plecanatide binds to and activates GC-C receptors located on endothelial cells on the luminal surface of the intestinal epithelium. This increases the concentration of intracellular cyclic guanosine monophosphate (cGMP). cGMP activates the cystic fibrosis transmembrane conductance regulator (CFTR) ion channel and stimulates the secretion of chloride and bicarbonate into the intestinal lumen. This also promotes sodium excretion into the lumen and osmosis. The increased intestinal fluid secretion accelerates gastrointestinal transit of intestinal contents, improves bowel movement, softens stool, and relieves constipation. In addition, plecanatide exerts its anti-nociceptive effects by increasing the concentration of extracellular cGMP which inhibits the activity of pain-sensitive nerves, decreases muscle contractions and may relieve intestinal pain.
Plectin-1 Targeting Agent PTP-01: An imaging agent containing a plectin-1 (Plec1; plectin) targeting peptide (PTP), with potential use for the detection of Plec1-expressing tumor cells using single-photon emission computed tomography (SPECT). Upon administration, the Plec1 targeting agent PTP-01 specifically targets and binds to Plec1 on Plec1-expressing cancer cells. Upon SPECT imaging, the Plec1-expressing cancer cells can be visualized. Plec1, a pro-tumorigenic protein, is normally found inside the cytoplasm of healthy cells but is only selectively expressed on the cell surface of various cancer cells and plays an important role in cancer cell proliferation, migration and invasion.
PLED-based MnSOD mimetic: A derivative of pyridoxyl ethyldiamine (PLED) and mimetic of the human mitochondrial manganese superoxide dismutase (MnSOD), with antioxidant, metal chelating and potential chemoprotective activities. Upon administration, PLED-based MnSOD mimetic mimics MnSOD and scavenges oxygen free radicals such as superoxide anion, hydrogen peroxide, and hydroxyl radical, thereby preventing oxygen free radical damage to macromolecules such as DNA and minimizing oxygen free radical-related chemotoxicity in normal tissues. In addition, this agent is able to strongly bind to iron.
Plenvu: (Other name for: PEG-3350/sodium sulfate/sodium chloride/potassium chloride/sodium ascorbate/ascorbic acid-based laxative)
plerixafor: A bicyclam with hematopoietic stem cell-mobilizing activity. Plerixafor blocks the binding of stromal cell-derived factor (SDF-1alpha) to the cellular receptor CXCR4, resulting in hematopoietic stem cell (HSC) release from bone marrow and HSC movement into the peripheral circulation.
Pletal: (Other name for: cilostazol)
plevitrexed: An orally bioavailable, small molecule, non-polyglutamatable, antifolate quinazoline derivative thymidine synthetase inhibitor with potential antineoplastic activity. Plevitrexed is transported into the cell via the physiological reduced folate carrier (RFC) system. Intracellularly, this agent selectively binds to the folate binding site of thymidylate synthase and inhibits thymidine synthesis, which may result in DNA synthesis inhibition and apoptosis.
plicamycin: An antibiotic isolated from the bacterium Streptomyces plicatus with antineoplastic activity. Plicamycin, also known as mithramycin, binds to the minor groove of DNA at GC-rich sites, resulting in inhibition of RNA synthesis; this agent also inhibits mRNA expression, resulting in a reduction in protein synthesis. In addition, plicamycin may inhibit bone resorption by down regulating transcription of c-src, an oncogene involved in bone metabolism and resorption.
plinabulin: An orally active diketopiperazine derivative with potential antineoplastic activity. Plinabulin selectively targets and binds to the colchicine-binding site of tubulin, thereby interrupting equilibrium of microtubule dynamics. This disrupts mitotic spindle assembly leading to cell cycle arrest at M phase and blockage of cell division. In addition, plinabulin may also inhibit growth of proliferating vascular endothelial cells, thereby disrupting the function of tumor vasculature that further contributes to a decrease in tumor cell proliferation.
plitidepsin: A cyclic depsipeptide isolated from the marine tunicate Aplidium albicans. Plitidepsin displays a broad spectrum of antitumor activities, inducing apoptosis by triggering mitochondrial cytochrome c release, initiating the Fas/DC95, JNK pathway and activating caspase 3 activation. This agent also inhibits elongation factor 1-a, thereby interfering with protein synthesis, and induces G1 arrest and G2 blockade, thereby inhibiting tumor cell growth.
plixorafenib: An orally bioavailable inhibitor and specific dimer breaker of the serine/threonine-protein kinase B-raf (BRAF) protein, with potential antineoplastic activity. Upon oral administration, plixorafenib selectively binds to and inhibits the activity of dimeric BRAF mutants, including BRAF fusions and splice variants, and BRAFV600 monomers, while sparing RAF function in normal cells. This inhibits the proliferation of tumor cells which express these mutated forms of BRAF. BRAF, a member of the raf family of serine/threonine protein kinases, plays a role in the regulation of mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) signaling pathways, which may be constitutively activated due to BRAF gene mutations. Mutated forms and fusions of BRAF are associated with a number of neoplastic diseases.
PLK1 inhibitor CYC140: A competitive inhibitor for adenosine triphosphate (ATP) binding to polo-like kinase 1 (PLK1; PLK-1; STPK13), with potential antineoplastic activity. Upon administration, PLK1 inhibitor CYC140 selectively targets, binds to and inhibits PLK1, which disrupts mitosis and induces selective G2/M cell-cycle arrest followed by apoptosis in PLK1-overexpressing tumor cells. PLK1, named after the polo gene of Drosophila melanogaster, is a serine/threonine kinase that is crucial for the regulation of mitosis, and plays a key role in tumor cell proliferation, transformation, and invasion. PLK1 expression is upregulated in a variety of tumor cell types and high expression is associated with increased aggressiveness and poor prognosis.
PLK1 inhibitor TAK-960: An orally available, Polo-like kinase 1 (PLK1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor TAK-960 selectively inhibits PLK1, inducing selective G2/M cell-cycle arrest followed by apoptosis in a variety of tumor cells while causing reversible cell-cycle arrest at the G1 and G2 stages without apoptosis in normal cells. PLK1 inhibition may result in the inhibition of proliferation in PLK1-overexpressed tumor cells. PLK1, named after the polo gene of Drosophila melanogaster, is a serine/threonine kinase crucial in the regulation of mitosis.
PLK4 inhibitor RP-1664: An orally bioavailable inhibitor of polo-like kinase 4 (PLK4), with potential antineoplastic activity. Upon oral administration, PLK4 inhibitor RP-1664 selectively inhibits PLK4, which results in the disruption of mitosis and the induction of apoptosis. This inhibits the proliferation of tumor cells that overexpress PLK4 and/or tripartite motif-containing protein 37 (TRIM37). PLK4, a member of the polo family of serine/threonine kinases overexpressed in a variety of cancer cell types, plays a crucial role in the regulation of centriole duplication during the cell cycle. Tumors with a high level of the E3 ubiquitin-protein ligase TRIM37 rely on PLK4 for survival.
plozalizumab: A humanized monoclonal antibody directed against the human chemokine receptor 2 (CCR2), with potential antiangiogenic, immunomodulating, antimetastatic, and antineoplastic activities. Plozalizumab binds to CCR2 and prevents binding of the endothelium-derived CLL2 (monocyte chemoattractant protein-1 or MCP1) to its receptor CCR2, which may result in inhibition of CCR2 activation and so inhibition of angiogenesis, tumor cell migration, and tumor cell proliferation. In addition, this agent may reduce levels of C-reactive protein (CRP). The G-protein coupled receptor CCR2 is expressed on the surface of monocytes and macrophages, stimulates the migration and infiltration of these cell types, and plays an important role in inflammation, angiogenesis, and tumor cell migration and proliferation.
Pluvicto: (Other name for: lutetium Lu 177 vipivotide tetraxetan)
PLZ4-coated paclitaxel-loaded micelle formulation: A nanoparticle-based formulation consisting of polymeric micelles encapsulating the taxane paclitaxel that are coated with the bladder cancer-targeting ligand PLZ4, a cyclic peptide with amino acid sequence of QDGRMGF, with potential antineoplastic activity. Upon administration of the PLZ4-coated paclitaxel-loaded micelle formulation, the PLZ4 moiety specifically targets and binds to bladder cancer cells while avoiding normal, healthy cells. This specifically delivers paclitaxel to bladder cancer cells and, due to the acidic conditions in the tumor and the pH-responsive nature of the micelles, paclitaxel is released in the tumor environment. Paclitaxel binds to microtubules, promotes microtubule assembly, and prevents depolymerization, thus interfering with normal mitosis. Compared to the administration of paclitaxel alone, this formulation increases the solubility of paclitaxel, enhances its specific retention in cancer tissue, and increases its therapeutic effect, while decreasing its toxicity. In addition, the micelle formulation and the addition of PLZ4 may allow for the delivery of higher doses of paclitaxel to bladder cancer cells while minimizing systemic toxicity.
PM00104: A synthetic tetrahydroisoquinoline alkaloid related to the marine natural compounds Jorumycin and the family of Renieramycins, obtained from molluscs and sponges, respectively, with potential antineoplastic activity. PM00104 reversibly binds to DNA and interferes with DNA replication, transcription, and translation. DNA binding by this agent does not trigger DNA damage checkpoint responses, hence PM00104 exhibits a reversible cytotoxicity.
pneumococcal 13-valent conjugate vaccine: A pneumococcal conjugate vaccine containing 13 different strains of the bacterium Streptococcus pneumoniae, used in children and studied in immunocompromised patients for the prevention of pneumococcal disease. The pneumococcal 13-valent conjugate vaccine contains capsular antigen polysaccharides derived from the S. pneumoniae serotypes 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F and 23F that are individually conjugated to a nontoxic diphtheria cross-reactive material (CRM) carrier protein (CRM197). Upon vaccination, pneumococcal 13-valent conjugate vaccine induces active immunization against 13 different serotypes of S. pneumoniae and protects against pneumococcal disease.
pneumococcal 20-valent conjugate vaccine: A pneumococcal conjugate vaccine containing 20 different strains of the bacterium Streptococcus pneumoniae, that is used for the prevention of pneumococcal disease. The pneumococcal 20-valent conjugate vaccine contains capsular antigen polysaccharides derived from the S. pneumoniae serotypes 1, 3, 4, 5, 6A, 6B, 7F, 8, 9V, 10A, 11A, 12F, 14, 15B, 18C, 19A, 19F, 22F, 23F, and 33F that are individually conjugated to a nontoxic diphtheria cross-reactive material 197 (CRM197) carrier protein. Upon intramuscular vaccination, pneumococcal 20-valent conjugate vaccine induces active immunization against 20 different serotypes of S. pneumoniae and protects against pneumococcal disease.
pneumococcal 7-valent conjugate vaccine: An active immunizing agent used to prevent infection by the bacterium Streptococcus pneumoniae. Pneumococcal 7-valent conjugate vaccine consists of a solution of saccharides of the capsular antigens of Streptococcus serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F individually conjugated to diphtheria CRM 197 protein.
pneumococcal polyvalent vaccine: An polyvalent vaccine used to prevent infection by the bacterium Streptococcus pneumoniae. Pneumococcal polyvalent vaccine contains higly purified capsular antigens from the 23 most prevalent or invasive pneumococcal types of Streptococcus pneumoniae to ensure cross-protection. Following vaccination, protective capsular type-specific antibody levels typically develop by the third week; serotype-specific antibody levels generally decline after 5-10 years.
Pneumovax 23: (Other name for: pneumococcal polyvalent vaccine)
pNGVL3-hICD vaccine: A plasmid DNA cancer vaccine encoding the intracellular domain (ICD) of the HER-2/neu proto-oncogene. Upon administration and after cellular uptake by skin or muscle cells, the pNGVL3-hICD vaccine plasmid expresses the HER-2/neu protein, which, after intracellular processing, may elicit both antigen-specific cytotoxic T-lymphocyte (CTL) and humoral immune responses against tumor cells expressing HER-2. The HER-2/neu ICD protein is highly immunogenic and, as a subdominant epitope, may be associated with decreased immune tolerance.
pNGVL3-hICD vaccine AST-301: A plasmid DNA therapeutic cancer vaccine encoding the intracellular domain (ICD) of the HER-2/neu proto-oncogene, with potential immunomodulating and antineoplastic activities. Upon administration, the pNGVL3-hICD vaccine AST-301 expresses the HER-2/neu protein and elicits a HER-2-specific cytotoxic T-lymphocyte (CTL) immune response against tumor cells expressing HER-2. The HER-2/neu ICD protein is highly immunogenic and, as a subdominant epitope, may be associated with decreased immune tolerance.
pNGVL4a-CRT-E6E7L2 DNA vaccine: A therapeutic DNA vaccine encoding human calreticulin (CRT) linked to human papillomavirus (HPV) type 16 E6, E7, and L2 proteins, with potential immunomodulating and antineoplastic activities. Upon administration via intramuscular injection with electroporation, the pNGVL4a-CRT-E6E7L2 DNA vaccine expresses HPV16 E6, E7 and L2 proteins, which may elicit a cytotoxic T-lymphocyte (CTL) response and humoral immune responses against tumor cells expressing these proteins, resulting in tumor cell lysis and tumor cell death. In addition, HPV16 L2-specific neutralizing antibody may prevent a broad spectrum of HPV infections and HPV-associated cancers. The heat shock protein CRT may potentiate MHC class I presentation to antigen-specific CD8-positive T cells, enhancing the induction of cellular immunity and the potency of the vaccine.
pNGVL4a-CRT/E7(detox) DNA vaccine: A cancer vaccine consisting of the DNA plasmid pNGVL4a-A encoding calreticulin (CRT) linked to a detox form of human papillomavirus (HPV) type 16 E7 antigen, with potential immunomodulating and antineoplastic activities. Upon administration, this vaccine may generate a potent cytotoxic T-lymphocyte (CTL) response against E7-expressing tumor cells, resulting in tumor cell death. For E7(detox), the amino acids in E7 at positions 24 (cysteine to glycine) and 26 (glutamic acid to glycine) were substituted. CRT, a 46 kDa protein located in the lumen of the cell's endoplasmic reticulum (ER), may potentiate MHC class I presentation of HPV-16 E7 to E7-specific CD8-positive T cells. In addition, pNGVL4a-A contains two short immunostimulatory DNA sequences (ISS) in the noncoding region, which may elicit the production of IFN- and IL-12 in transfected keratinocytes and dermal antigen presenting cells (APCs), resulting in a potent T helper cell type 1 response.
pNGVL4a-Sig/E7(detox)/HSP70 DNA and HPV16 L2/E6/E7 fusion protein TA-CIN vaccine PVX-2: A cancer vaccine consisting of a combination of two vaccines, a prime pNGVL4a-Sig/E7(detox)/HSP70 DNA vaccine and a boost HPV16 L2/E6/E7 fusion protein TA-CIN vaccine, with potential immunostimulating and antineoplastic activities. pNGVL4a-Sig/E7(detox)/HSP70 DNA vaccine is an antigen-specific DNA cancer vaccine consisting of the coding sequences of a signal peptide (pNGVL4a-Sig), a detox form of the human papillomavirus type 16 (HPV-16) antigen E7, and the heat shock protein 70 (HSP70). Upon administration, this prime vaccine may generate potent cytotoxic CD8(+) T-cell responses against E7-expressing tumor cells, resulting in tumor cell death. HPV16 L2/E6/E7 fusion protein TA-CIN vaccine is a recombinant human papillomavirus (HPV), genetically engineered fusion protein vaccine in which the three HPV16 viral proteins L2, E6 and E7 are fused together in a single tandem fusion protein (TA-CIN; HPV16 L2\E6\E7). Upon administration, this boost vaccine may stimulate the immune system to generate HPV16 E6\E7-specific CD4+ and CD8+ T-cell responses as well as the induction of L2-specific antibodies. In addition, this vaccine may prevent infection and the development of other HPV16-associated diseases. L2, a minor viral capsid protein, is able to induce a strong antibody response against certain HPV types.
pNGVL4a-Sig/E7(detox)/HSP70 DNA vaccine: An antigen-specific DNA cancer vaccine consisting of the coding sequences of a signal peptide (pNGVL4a-Sig), a detox form of the human papillomavirus type 16 (HPV-16) antigen E7, and the heat shock protein 70 (HSP70). Upon administration, this vaccine may generate potent cytotoxic CD8(+) T-cell responses against E7-expressing tumor cells, resulting in tumor cell death.
PNP-expressing ovine atadenovirus FP253: An ovine atadenovirus encoding E. coli purine nucleoside phosphorylase (PNP) with prodrug activating activity. Under the control of a prostate-directed promoter, PNP-expressing atadenovirus vaccine FP253 expresses PNP in prostate tissue only after intraprostatic administration; this enzyme catalyzes systemically administered fludarabine prodrug into the active agent, 2-fluoroadenine. Localized prodrug activation provides prostate-targeted chemotherapy, potentially reducing systemic side effects.
Pnu-Imune 23: (Other name for: pneumococcal polyvalent vaccine)
Pol theta inhibitor ART4215: An orally bioavailable and selective inhibitor of DNA polymerase (pol) theta, with potential chemosensitizing and antineoplastic activities. Upon oral administration, Pol theta inhibitor ART4215 targets, binds to and inhibits the activity of pol theta. This prevents pol theta-mediated repair of damaged DNA and may have a synergistic effect if administered in combination with agents that cause DNA damage. Pol theta plays a key role in DNA synthesis and repair.
polaprezinc: An orally bioavailable chelate composed of zinc and L-carnosine, with potential gastroprotective, anti-oxidant, anti-ulcer and anti-inflammatory activities. Upon administration, polaprezinc increases the expression of various anti-oxidant enzymes, such as superoxide dismutase 1 (SOD-1), SOD-2, heme oxygenase-1 (HO-1), glutathione S-transferase (GST), glutathione peroxidase (GSH-px), peroxidredoxin-1 (PRDX1; PRXI) and PRXD5 (PRXV) in the gastric mucosa, which protect cells against reactive oxygen species (ROS). In addition, this agent inhibits the activity of the transcription factor nuclear factor-kappaB (NF-kB) and reduces the expression of several pro-inflammatory cytokines, such as interleukin (IL) 1beta, IL-6, IL-8, and tumor necrosis factor alpha (TNF-a). Polaprezinc also increases the expression of various growth factors, such as platelet-derived growth factor-B (PDGF-B), vascular endothelial growth factor (VEGF), and nerve growth factor (NGF), and various heat shock proteins (HSPs), including HSP90, HSP70, HSP60, HSP47, HSP27, and HSP10. This protects against damages to, and accelerates healing of the gastric mucosa.
polatuzumab vedotin-piiq: An antibody-drug conjugate (ADC) composed of a monoclonal antibody directed against B-cell antigen receptor complex-associated protein beta chain (CD79B) conjugated, via a protease-cleavable peptide linker, to monomethyl auristatin E (MMAE), an auristatin derivative and a potent microtubule inhibitor, with potential antineoplastic activity. Upon administration, the monoclonal antibody moiety of polatuzumab vedotin-piiq selectively binds to CD79B, a protein which is abundantly expressed on the surface of B-cells. Upon internalization and proteolytic cleavage, MMAE binds to tubulin and inhibits its polymerization, resulting in G2/M phase arrest and tumor cell apoptosis. CD79B, a component of the B-cell receptor (BCR), plays a key role in B-cell receptor signaling and is expressed on the surface of almost all types of malignant B-cells.
polfermetinib: An orally bioavailable, brain penetrating inhibitor of mitogen-activated protein kinase kinase (MAP2K; MAPKK; MEK), with potential antineoplastic activity. Upon oral administration, polfermetinib specifically targets, binds to and inhibits the catalytic activity of MEK, thereby inhibiting the activation of MEK-dependent effector proteins, including extracellular signal-regulated kinase (ERK), and inhibits the proliferation of tumor cells in which the RAS/RAF/MEK/ERK signaling pathway is overactivated. The threonine/tyrosine protein kinase MEK plays a key role in the RAS/RAF/MEK/ERK signaling pathway, which is frequently upregulated in a variety of tumor cell types and regulates key cellular activities including cell growth, proliferation, survival, differentiation and apoptosis.
polidocanol: An alkyl polyglycol ether of lauryl alcohol with sclerosing and potential antineoplastic activities. Upon intralesional administration, polidocanol induces endothelial cell injury by disrupting calcium signaling and nitric oxide pathways. Following endothelial damage, platelets aggregate at the site of injury and attach to the venous wall, resulting in a dense network of platelets, cellular debris, and fibrin that occludes the vessel. Inducing endothelial cell damage within melanoma metastases may incite an antitumor response in untreated bystander lesions and inhibit the growth of in transit metastases and other cutaneous lesions.
poliglusam: A naturally occurring polysaccharide composed of beta-1,4-linked glucosamine residues with potential antineoplastic activity. Upon administration, poliglusam may, through a not yet fully elucidated mechanism, reduce advanced glycation end product (AGE) levels. This may reduce the interaction between AGEs and the receptor for advanced glycation end products (RAGE, AGER), which is overexpressed in some tumor types and is associated with poor patient outcomes. AGE-RAGE interaction may induce the phosphorylation and subsequent degradation of retinoblastoma protein (Rb), a key cell cycle inhibitor and tumor suppressor, through the phosphoinositide 3-kinase (PI3K)/protein kinase B (PKB, Akt) signaling pathway. Hyperphosphorylation of Rb leads to the dissociation of the Rb-E2F complex, which triggers the activation of genes required for G1/S transition and tumorigenesis. Reducing AGE levels may limit AGE-RAGE interaction and normalize the G1 to S-phase transition, potentially reducing the development and progression of certain cancers. AGEs are non-enzymatic protein modifications produced during the normal aging process that have been shown to play a role in the development and progression of some cancers.
polihexanide solution: A solution containing the polymer polihexanide, with potential antimicrobial, disinfectant and wound healing activities. Upon application to a wound, polihexanide strongly binds to the wound surface and exerts an antiseptic effect through the binding of the positively charged guanidine groups of polihexanide with the negatively charged phospholipids of the bacterial cell membrane. This compromises the stability of the bacterial cell membrane, which results in the leakage of cytoplasmic components and leads to bacterial cell death. In addition, polihexanide accelerates wound healing by promoting epithelial cell migration and proliferation.
Polivy: (Other name for: polatuzumab vedotin-piiq)
pollen extract PCC-100: A pollen extract with potential use in the management of certain vasomotor symptoms of menopause. Upon administration, pollen extract PCC-100 may, through a non-estrogenic but not fully elucidated mechanism of action, reduce the incidence and severity of vasomotor symptoms and may be a safe alternative for some individuals.
Polo-like kinase 1 inhibitor GSK-461364: A small molecule Polo-like kinase 1 (PLK1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor GSK461364 selectively inhibits Plk1, inducing selective G2/M arrest followed by apoptosis in a variety of tumor cells while causing reversible cell arrest at the G1 and G2 stage without apoptosis in normal cells. Plk1, named after the polo gene of Drosophila melanogaster, is a serine/threonine protein kinase involved in regulating mitotic spindle function in a non-ATP competitive manner.
Polo-like kinase 1 inhibitor MK1496: An orally bioavailable Polo-like kinase 1 (Plk1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor MK1496 selectively inhibits Plk1, inducing selective G2/M arrest followed by apoptosis in a variety of tumor cells while causing reversible cell arrest at the G1 and G2 stage without apoptosis in normal cells. Plk1, named after the polo gene of Drosophila melanogaster, is a serine/threonine protein kinase involved in regulating mitotic spindle function in a non-ATP competitive manner.
Polo-like kinase 1 inhibitor NMS-1286937: An orally bioavailable, small-molecule Polo-like kinase 1 (PLK1) inhibitor with potential antineoplastic activity. Polo-like kinase 1 inhibitor NMS-1286937 selectively inhibits PLK1, inducing selective G2/M cell-cycle arrest followed by apoptosis in a variety of tumor cells while causing reversible cell-cycle arrest at the G1 and G2 stages without apoptosis in normal cells. PLK1 inhibition may result in the inhibition of proliferation in PLK1-overexpressing tumor cells. PLK1 is a serine/threonine protein kinase crucial in the regulation of mitosis.
Polocaine: (Other name for: mepivacaine hydrochloride)
poly AU: A synthetic polyadenylic-polyuridylic acid double-stranded RNA. Poly AU may stimulate the release of cytotoxic cytokines and, by inducing the production of interferon, may increase the number and tumoricidal activities of various immunohematopoietic cells.
poly IC: A synthetic polyinosinic-polycytidylic acid double-stranded RNA. Poly IC may stimulate the release of cytotoxic cytokines and, by inducing interferon-gamma production, may increase the number and tumoricidal activities of various immunohematopoietic cells.
poly ICLC: A synthetic complex of carboxymethylcellulose, polyinosinic-polycytidylic acid, and poly-L-lysine double-stranded RNA. Poly ICLC may stimulate the release of cytotoxic cytokines and, by inducing interferon-gamma production, may increase the tumoricidal activities of various immunohematopoietic cells.
poly-alendronate dextran-guanidine conjugate: A polybisphosphonate dextran-guanidine conjugate with potential anti-resorptive and antineoplastic activities. Alendronic acid and aminoguanidine were conjugated sequentially to oxidized dextran resulting in an average of 8 alendronate and 50 guanidine groups coupled to the dextran backbone. Upon administration, the poly-alendronate dextran-guanidine conjugate inhibits the mevalonate pathway by inhibiting farnesyl diphosphate synthase (FDPS) which leads to a reduction in protein prenylation and to the loss of downstream metabolites essential for osteoclast function. This eventually leads to the induction of apoptosis in osteoclasts. Also, by preventing osteoclast-mediated bone resorption, this agent decreases bone turnover and stabilizes the bone matrix. The guanidine moiety increases the nitrogen content and possibly the activity of the bisphosphonate and its ability to inhibit FDPS. In addition, the guanidine moiety facilitates cell internalization and may contribute to this agent’s cytotoxicity.
poly-gamma glutamic acid: A water-soluble and biodegradable polymer naturally synthesized by various strains of Bacillus and composed of D- and L-glutamic acid polymerized via gamma-amide linkages, with potential antineoplastic activity. Upon administration, poly-gamma glutamic acid may augment the immune response by increasing the production of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) and inducing the activation of macrophage and natural killer (NK) cells. In addition to its tumor control properties, IFN-gamma is a major mediator of innate and adaptive immunity against viral and intracellular bacterial infections. TNF-alpha is a cytokine involved in systemic inflammation, which is capable of inducing apoptotic cell death and exhibits anti-tumoral effects.
poly-TLR agonist polyantigenic vaccine CADI-05: A poly-Toll-like receptor (TLR) agonist polyantigenic vaccine containing heat killed Mycobacterium indicus pranii (Mycobacterium w or Mw) with potential immunostimulating and antineoplastic activities. Upon administration, poly-TLR agonist polyantigenic vaccine activates a number of TLRs, which may result in macrophage and plasmacytoid dendritic cell (pDC) stimulation; secretion of interferon alpha; production of pro-inflammatory cytokines; upregulation of co-stimulatory molecules, enhanced T and B-cell stimulatory responses; T cell proliferation, and a Th1 immune response. TLRs are transmembrane receptors that recognize structurally conserved microbial molecules such as bacterial cell-surface lipopolysaccharides (LPS), lipoproteins, lipopeptides, lipoarabinomannan and flagellin, among others; immune responses stimulated by TLR activation may result in antineoplastic effects.
polyacrylamide hydrogel: A transparent, biocompatible, non-resorbable, homogenous hydrogel containing 97.5% apyrogenic water and 2.5% of the cross-linked, synthetic polyacrylamide. Upon injection into the urethral submucosal tissue, the polyacrylamide hydrogel serves as a bulk forming agent and may possibly increase the strength of the urethral sphincter and thereby prevent or decrease stress-induced urinary incontinence.
polyamine analogue PG11047: A second generation polyamine analogue, synthesized through the restriction of molecular conformations of parent polyamine compounds, with potential antineoplastic activity. Polyamine analogue PG11047 may displace endogenous polyamines from DNA binding sites, thereby interfering with cell cycle processes dependent upon polyamine binding and function, and resulting in cell-cycle arrest, induction of apoptosis, depletion of polyamines, and interference with gene and ligand-receptor activities involved with cell growth. This agent may exhibit decreased toxicity and enhanced cytotoxicity profiles compared to first-generation polyamine compounds. In tumor cells, there is an increase dependence on polyamines as well as a dysregulated polyamine metabolic pathway resulting in abnormal or sustained tumor growth.
polyamine analogue SBP-101: An analogue of naturally occurring polyamine (PA), with potential antineoplastic activity. Upon subcutaneous administration, SBP-101 displaces endogenous PAs from PA-binding sites on the cell surface, which prevents internalization of PA. This inhibits PA-dependent cell cycle processes and results in cell cycle arrest, the induction of apoptosis, and inhibition of tumor cell proliferation. PA uptake is upregulated in various tumor types and increased levels of PA leads to enhanced tumor cell growth.
polyamine transport inhibitor AMXT-1501 dicaprate: The dicaprate salt form of AMXT-1501, an orally bioavailable polyamine transport inhibitor, with immunostimulating and antineoplastic activities. Upon administration, AMXT-1501 targets, binds to and blocks polyamine transport from the bloodstream into the tumor microenvironment (TME), thereby preventing cancer cell uptake. This decreases polyamine concentrations inside the TME and tumor cell, inhibits tumor cell proliferation and induces apoptosis. In addition, AMXT-1501 may abrogate polyamine-mediated immune suppression in the TME. Polyamines, naturally found in normal, heathy cells, are required for normal cell growth and division. In cancer cells, polyamines play key roles in tumor cell proliferation and tumor-induced suppression of the patient's immune system.
polycarbophil/carbomer/glycerin/palm oil glyceride/mineral oil-containing vaginal moisturizer: A commercial combination preparation that contains an adhesive polycarbophil polymer, which is used for vaginal lubrication. Polycarbophil is an insoluble compound that absorbs water and, after topical administration, adheres to vaginal epithelial cells. As a result, it helps both moisturize vaginal tissue and relieve the discomfort that is associated with vaginal dryness.
polyethylene glycol 1000 cetyl ether cream: A cream containing a non-ionic surfactant belonging to the polyethylene glycol (PEG) family. Polyethylene glycol 1000 cetyl ether is used as an ointment base, but can also be used as an emulsifier and solubilizer.
polyethylene glycol 3350-containing enema NER1008: An enema containing the osmotic agent polyethylene glycol (PEG) 3350, also called macrogol 3350, with laxative activity. Upon rectal administration of the PEG3350-containing enema NER1008, PEG creates an osmotic gradient, which promotes the retention of water in the bowel. This increases the water content of stool, which results in increased gastrointestinal (GI) motility, decreased stool transit time and evacuation of colonic contents.
polyethylene glycol hydrogel: A 2- or 3-dimensional hydrophilic, cross-linked polymer of polyethylene glycol (PEG). These hydrogels can be used as scaffolds for tissue engineering or as drug delivery carriers.
polyethylene glycol recombinant endostatin: A formulation containing recombinant endostatin attached to polyethylene glycol (PEG), with potential anti-angiogenic and antineoplastic activities. Endostatin, a 20 kDa C-terminal proteolytic fragment of collagen XVIII, induces microvascular endothelial cell apoptosis and inhibits endothelial proliferation and angiogenesis, which may result in a reduction of tumor cell growth. Modification with PEG extends the circulation half-life of endostatin, improves stability and increases solubility in organic solvents.
polyethyleneglycol-7-ethyl-10-hydroxycamptothecin: A polyethylene glycol (PEG) conjugate of 7-ethyl-10-hydroxycamptothecin with potential antineoplastic activity. After hydrolysis in vivo, 7-ethyl-10-hydroxycamptothecin (SN38), an active metabolite of irinotecan, is released from polyethyleneglycol-7-ethyl-10-hydroxycamptothecin (PEG-SN38); 7-ethyl-10-hydroxycamptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, resulting in single-stranded and double-stranded DNA breaks, the inhibition of DNA replication, and the induction of apoptosis. This agent is designed to deliver the active metabolite to tumor cells without the need for conversion as is the case with irinotecan. Compared to unPEGylated 7-ethyl-10-hydroxycamptothecin, PEGylation improves solubility and allows for parental delivery, and may result in a longer half-life and higher exposure for tumor cells.
polyethyleneglycol-7-ethyl-10-hydroxycamptothecin DFP-13318: A long-acting formulation composed of 7-ethyl-10-hydroxycamptothecin (SN38), a camptothecin derivative and active metabolite of irinotecan conjugated to polyethylene glycol (PEG), via a proprietary, cleavable linker, with potential antineoplastic activity. Upon administration, the proprietary linkage system allows for very slow release of SN38 from the formulation. Upon release, SN38 selectively stabilizes covalent topoisomerase I-DNA complexes, and results in single-stranded and double-stranded DNA breaks, the inhibition of DNA replication, and the induction of apoptosis. This agent is designed to deliver the active metabolite to tumor cells without the need for conversion as is the case with irinotecan. Compared to other PEG-SN38-based formulations, the linker system in DFP-13318 increases its half-life and the exposure time for tumor cells, while decreasing both blood plasma concentrations and exposure to off-target organs; this results in increased efficacy.
Polygam S/D: (Other name for: therapeutic immune globulin)
polyglutamate camptothecin: A therapeutic formulation consisting of camptothecin, an alkaloid isolated from the Chinese tree Camptotheca acuminata, conjugated with polyglutamate. During the S phase of the cell cycle, camptothecin selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. Conjugation with polyglutamate renders this agent more water soluble and less toxic than the parent molecule.
polyinosinic-polycytidylic acid/inactivated rabies virus vaccine YS-ON-001: A cancer vaccine composed of inactivated rabies vaccine (RV-V) and polyinosinic-polycytidylic acid (poly IC; poly I-C), an immunostimulant and Toll-like receptor 3 (TLR3) agonist, with potential immunostimulating and antineoplastic activities. Upon administration of the poly IC/inactivated RV-V YS-ON-001, the RV-V stimulates the immune system in various ways, such as promoting the activation and proliferation of T helper type 1 (Th1) cells, dendritic cells (DCs), B cells and natural killer cells (NKs), promoting macrophage M1 polarization, downregulating regulatory T cells (Tregs), and inducing the production of anti-tumor cytokines. This re-activates immune responses in the suppressed tumor microenvironment (TME), leading to an induction of cytotoxic T-lymphocyte (CTL)-mediated immune response against the tumor cells, which cause tumor cell apoptosis and a reduction of tumor cell proliferation. Poly IC, a synthetic double-stranded RNA with one strand composed of a inosinic acid polymer and the other strand a cytidylic acid polymer, binds to TLR3 and stimulates the release of cytotoxic cytokines, such as interferon-gamma (IFNg). This may boost the immune response against the tumor cells.
polymer-conjugated IL-15 receptor agonist NKTR-255: A long-acting formulation composed of the human cytokine interleukin-15 (IL-15) that is conjugated by polymers, with potential immunomodulating and anti-tumor activities. Upon administration of polymer-conjugated IL-15 receptor agonist NKTR-255, the IL-15 moiety targets and binds to the alpha subunit of the IL-15 receptor on natural killer (NK) and T cells, thereby activating the IL-15-mediated pathway. This leads to the expansion and activation of natural killer (NK) cells and memory CD8+ T cells, thereby enhancing the anti-tumor activity of NKs and long-term memory T-lymphocyte immune responses. This may increase tumor cell killing and decrease tumor cell proliferation. In addition, NKTR-255 may, when combined with a tumor-directed antibody, enhance the antibody-dependent cell-mediated cytotoxicity (ADCC) mechanism. IL-15 is a pro-inflammatory cytokine that plays a key role in the regulation of T- and NK cell activation, proliferation and promotion of their anti-tumor effects. Compared to IL-15 alone, the polymer formulation allows for increased retention at the tumor site and reduced clearance, thereby increasing the effect of IL-15.
polymer-encapsulated luteolin nanoparticle: A nanoparticle formulation containing the poorly water-soluble naturally-occurring flavonoid luteolin encapsulated within a water-soluble polymer, with potential anti-oxidant, anti-inflammatory, apoptosis-inducing and chemopreventive activities. Upon administration of the polymer-encapsulated luteolin nanoparticle, luteolin scavenges free radicals, protects cells from reactive oxygen species (ROS)-induced damage and induces direct tumor cell cycle arrest and apoptosis in tumor cells. This inhibits tumor cell proliferation and suppresses metastasis. Compared to luteolin alone, encapsulation increases the delivery of luteolin to the tumor cells by protecting the drug against clearance and degradation, increases blood circulation time and enhances delivery into the tumor through the leaky vasculature.
polymeric camptothecin prodrug XMT-1001: A polymeric prodrug of camptothecin (CPT) with potential antineoplastic activity. Polymeric camptothecin prodrug XMT-1001 consists of CPT conjugated to the 60-70 kDa, inert, bio-degradable, hydrophilic copolymer poly[1-hydroxymethylene hydroxymethyl formal] (PHF). Through a dual-phase, non-enzymatic release mechanism, CPT is first released in plasma from XMT-1001 as the lipophilic prodrugs CPT-SI (a succinimidoglycinate derivative) and CPT-SA (a succinamidoyl glycinate derivative), which are then hydrolyzed within tissues to release the lactone form of CPT. CPT inhibits the catalytic activity of DNA topoisomerase I, thereby inhibiting DNA replication and inducing apoptosis. This agent may exhibit a more favorable pharmacokinetic profile than other agents in the same class.
polymeric nanoparticle-conjugated camptothecin DAN-222: A polymeric nanoparticle formulation of the topoisomerase I inhibitor camptothecin (CPT), an alkaloid isolated from the Chinese tree Camptotheca acuminata, covalently conjugated, via a linker, to a biocompatible polymer scaffold, with potential antineoplastic activity. Upon intravenous administration of polymeric nanoparticle-conjugated CPT DAN-222, the nanoparticles accumulate in tumor tissue and CPT is released from the formulation at the tumor site and taken up by tumor cells. During the S phase of the cell cycle, CPT selectively stabilizes topoisomerase I-DNA covalent complexes, thereby inhibiting religation of topoisomerase I-mediated single-strand DNA breaks and producing potentially lethal double-strand DNA breaks when encountered by the DNA replication machinery. Compared to CPT alone, the nanoparticle formulation has a prolonged half-life and greatly improves the biodistribution of CPT resulting in an accumulation of CPT at the tumor site, which enhances tumor exposure while greatly reducing toxic side effects.
Polymox: (Other name for: amoxicillin)
PolyMVA: (Other name for: alpha-lipoic acid-palladium/vitamin/mineral supplement)
polymyxin B: A mixture of the polypeptides polymyxins B1 and B2, both obtained from Bacillus polymyxa strains, with antimicrobial activity. Polymyxin B exerts its antimicrobial effect through its cationic detergent action on cell membranes. Specifically, this antibiotic binds to the negatively charged site in the lipopolysaccharide layer of the bacterial cell membrane via electrostatic affinity with the positively charged amino groups in the cyclic peptide portion. Subsequently, the fatty acid portion of polymyxin B dissolves in the hydrophobic region of the bacterial cell membrane. This results in an alteration in cell membrane structure, disruption of cell wall integrity and an increase in permeability for water and molecules. This will eventually lead to bacterial cell death.
polymyxin-B immobilized fiber PMX-20R: A cartridge containing a polystyrene-based composite woven fiber that is covalently attached to the anti-microbial cyclic cationic polypeptide antibiotic polymyxin-B (PMX) and can potentially be used for hemoperfusion purposes. Upon extracorporeal treatment, a patient's blood flows through the fibers in the polymyxin-B immobilized fiber PMX-20R cartridge and the circulating endotoxins from the blood are selectively adsorbed by PMX, which has positively charged amino groups that bind to the negatively charged site in the lipid A portion of the lipopolysaccharide (LPS) layer of the bacterial cell membrane. This removes endotoxins from the blood and, upon administration of the blood back into the patient, helps treat or reduce the incidence of endotoxemia and sepsis.
Polyphenon E Ointment: (Other name for: kunecatechins ointment)
polypodium leucotomos extract: A nutritional supplement composed of an aqueous extract derived from the leaves of the tropical fern belonging to the Polypodiaceae family, Polypodium leucotomos (PL; Phlebodium aureum), with potential photoprotective, skin protective, anti-inflammatory, immunomodulating and antioxidant activities. This extract contains many phenolic compounds, such as ferulic, caffeic, coumaric and vanillic acid, which are mainly responsible for this extract's effects. Upon administration, Polypodium leucotomos extract (PLE) exerts antioxidant activity by scavenging free radicals and inhibiting the generation and release of reactive oxygen species (ROS), thereby preventing ultraviolet (UV)-induced as well as ROS-induced DNA damage. In addition, the chemicals in this extract protect antioxidant enzymes and modulate expression of cancer and inflammation-related genes, including the induction of the expression of tumor suppressor genes and the inhibition of the expression of pro-inflammatory cytokines and inflammatory enzymes, thereby inhibiting the activation of signal transduction pathways involved in carcinogenesis and inflammation, respectively. PLE also stimulates tissue inhibitors of metalloproteinases (TIMPs) and inhibits matrix metalloproteinases (MMPs).
polysaccharide-K: A protein-bound polysaccharide derived from the mushroom Trametes versicolor (Turkey Tail) with immunoadjuvant and potential antitumor activities. Although its mechanism of action has yet to be fully elucidated, in vitro and in vivo studies indicate that polysaccharide-K induces peripheral blood monocyte secretion of IL-8 and TNF-alpha, induces T cell proliferation, and prevents cyclophosphamide-induced immunosuppression. This agent has also been reported to stimulate macrophages to produce reactive nitrogen intermediates and superoxide anions and to promote apoptosis in the promyelocytic leukemia cell line HL-60.
polysialic acid: A highly negative-charged carbohydrate composed of a linear polymer of alpha 2,8-linked sialic acid residue with potential immunotherapeutic activity. Polysialic acid (PSA) is mainly attached to the neural cell adhesion molecule (NCAM), a membrane-bound glycoprotein overexpressed in certain types of cancers. In embryonic tissue PSA-NCAM is abundantly expressed and PSA plays an important role in formation and remodeling of the neural system through modulation of the adhesive properties of NCAM, thereby reducing cell-cell interactions and promoting cellular mobility. In adult tissue however, the expression of PSA-NCAM is associated with a variety of malignant tumors, signifying its potential role in tumor metastasis. When administered in a vaccine formulation, PSA may stimulate a cytotoxic T cell response against tumors expressing PSA, thereby resulting in a reduction in tumor size.
polysiloxane/gadolinium chelates-based nanoparticles: A nanoparticle formulation composed of a polysiloxane-based inorganic matrix bound to cyclic chelates composed of the chelating agent DOTA (1,4,7,10-tetra-azacyclododecane-1-glutaric anhydride-4,7,10-triacetic acid) covalently bound to the paramagnetic contrast enhancer gadolinium (Gd), a high-Z material, with potential use in enhancing diagnostic images upon magnetic resonance imaging (MRI) and potential radiosensitizing activity. Upon intravenous administration of polysiloxane matrix-gadolinium chelates-based nanoparticles, the nanoparticles extravasate to tumor sites due to the unique, hyperpermeable environment of the tumor vasculature. In addition, the small nanoparticles allow for deep penetration into the tumor, where they subsequently accumulate. Upon placement in a magnetic field, this agent produces a large magnetic moment and creates a large local magnetic field, which can enhance the relaxation rate of nearby protons. This change in proton relaxation dynamics increases the MRI signal intensity of tissues in which this agent has accumulated; therefore, contrast and visualization of those tissues are enhanced compared to unenhanced MRI. The ultra-small nanoparticles, less than 5 nm in diameter, allow for rapid renal clearance and reduced toxicity. Due to their magnetic properties, these nanoparticles make tumor cells more sensitive to radiation therapy.
polyunsaturated fatty acid: A fatty acid containing more than one double bond (C=C). The essential fatty acids omega-3 and omega-6 are polyunsaturated fatty acids (PUFAs) that contain 2 or more cis double bonds. Dietary intake of some PUFAs may have beneficial effects on blood pressure, serum lipds, and inflammation. Some PUFAs, such as omega-3 PUFAs, may have antineoplastic or chemopreventive activities.
polyvalent antigen-KLH conjugate vaccine: A multivalent cancer vaccine comprised of the five tumor-associated antigens (TAAs) globo H, GM2 ganglioside, Tn-MUC1, TF, and sTn conjugated with the immunoadjuvant keyhole limpet hemocyanin (KLH), with potential antineoplastic activity. Upon administration, polyvalent antigen-KLH conjugate vaccine may induce production of IgG and IgM antibodies and antibody-dependent cell-mediated cytotoxicity (ADCC) against tumor cells expressing these TAAs, resulting in tumor cell death and tumor growth inhibition. Globo H (globo H hexasaccharide 1); GM2 ganglioside; Tn-MUC1 (human tumor-associated epithelial mucin 1 carrying the tumor-specific glycan Tn); TF (Thompson-Friedreich); and sTn (sialyl-Tn) are overexpressed in a variety of cancer cells. KLH is a hapten carrier and serves as an immunostimulant to improve immune recognition of antigens.
polyvalent melanoma vaccine: A cancer vaccine consisting of whole irradiated heterologous melanoma cells which express multiple melanoma-related antigens. Polyvalent melanoma vaccine may stimulate an antitumoral cytotoxic T-cell immune response in the host, resulting in inhibition of tumor cell proliferation and tumor cell death.
polyvinylpyrrolidone-sodium hyaluronate gel: An oral bioadherent gel containing polyvinylpyrrolidone (PVP) and sodium hyaluronate with muco-protective activity. Upon oral application, this gel adheres to the mucosal surface of the mouth and throat, forming a thin layer that acts as a barrier to protect exposed and sensitized nerve endings from the painful stimuli associated with eating, drinking, and talking.
pomalidomide: An orally bioavailable derivative of thalidomide with potential immunomodulating, antiangiogenic and antineoplastic activities. Although its exact mechanism of action has yet to be fully elucidated, pomalidomide appears to inhibit TNF-alpha production, enhance the activity of T cells and natural killer (NK) cells and enhance antibody-dependent cellular cytotoxicity (ADCC). In addition, pomalidomide may inhibit tumor angiogenesis, promote cell cycle arrest in susceptible tumor cell populations, and stimulate erythropoeisis.
Pomalyst: (Other name for: pomalidomide)
pomegranate juice: A natural juice isolated from the fruit of the plant Punica granatum with antioxidant, potential antineoplastic, and chemopreventive activities. Pomegranate juice contains flavonoids which promote differentiation and apoptosis in tumor cells by down-regulating vascular endothelial growth factor (VEGF) and stimulating migration inhibitory factor (MIF), thereby inhibiting angiogenesis. The flavanoids in pomegranate juice also scavenge reactive oxygen species (ROS) and, in some cell types, may prevent ROS-mediated cell injury and death.
pomegranate liquid extract: A liquid extract preparation derived from pomegranate (Punica granatum) seeds with antioxidant, and potential antineoplastic and chemopreventive activities. Pomegranate liquid extract contains flavonoids which may promote differentiation and apoptosis in tumor cells by down-regulating vascular endothelial growth factor (VEGF) and stimulating migration inhibitory factor (MIF), thus inhibiting angiogenesis.Pomegranate liquid extract flavanoids also scavenge reactive oxygen species (ROS) and, in some cell types, may prevent ROS-mediated cell injury and death.
pomegranate-extract pill: A pill formulation of polyphenol extracts derived from the fruit of the deciduous shrub Punica granatum with antioxidant and potential chemopreventive activities. By binding and neutralizing free-radical compounds, the polyphenol extracts contained in pomegranate-extract pill may prevent their genotoxic and carcinogenic effects.
POMx: (Other name for: pomegranate-extract pill)
ponatinib hydrochloride: The hydrochloride salt form of an orally bioavailable multitargeted receptor tyrosine kinase (RTK) inhibitor with potential antiangiogenic and antineoplastic activities. Ponatinib inhibits unmutated and all mutated forms of Bcr-Abl, including T315I, the highly drug therapy-resistant missense mutation of Bcr-Abl. This agent also inhibits other tyrosine kinases including those associated with vascular endothelial growth factor receptors (VEGFRs) and fibroblast growth factor receptors (FGFRs); in addition, it inhibits the tyrosine kinase receptor TIE2 and FMS-related tyrosine kinase receptor-3 (Flt3). RTK inhibition by ponatinib may result in the inhibition of cellular proliferation and angiogenesis and may induce cell death. Bcr-Abl is a fusion tyrosine kinase encoded by the Philadelphia chromosome.
ponesimod: An orally available sphingosine-1-phosphate receptor 1 (S1PR1, S1P1) agonist that acts as a functional antagonist, with potential immunomodulating activity. Upon oral administration, ponesimod selectively binds to S1PR1 on lymphocytes and causes transient receptor activation followed by S1PR1 internalization and degradation. This results in the sequestration of lymphocytes in lymph nodes. By preventing egress of lymphocytes, ponesimod reduces both the number of circulating peripheral lymphocytes and the infiltration of lymphocytes into target tissues. This prevents a lymphocyte-mediated immune response. S1PR1, a G-protein coupled receptor, plays a key role in lymphocyte migration from lymphoid tissues.
ponsegromab: A monoclonal antibody directed against the human growth differentiation factor 15 (GDF15; MIC-1), with potential anti-cachexia activity. Upon administration, ponsegromab targets and binds to GDF15, thereby preventing the binding of GDF15 to its receptor glial-cell-derived neurotrophic factor (GDNF) family receptor alpha-like (GFRAL) and blocking GDF15/GFRAL-mediated signaling. This may abrogate loss of appetite and uncontrolled weight loss associated with high serum levels of GDF15. GDF15, a stress response cytokine and divergent member of the transforming growth factor beta (TGF-beta) superfamily, plays a key role in the regulation of body weight through central mechanisms. High GDF15 plasma levels, as seen in individuals with advanced cancers, are associated with loss of body mass.
pooled mutant KRAS-targeted long peptide vaccine: A peptide vaccine containing a mixture of long peptides that are derived from tumor-specific mutant forms of the KRAS (K-ras) antigen, with potential immunostimulatory and antitumor activities Upon administration of the pooled mutant KRAS-targeted long peptide vaccine, the KRAS peptides may stimulate the host immune system to mount a cytotoxic T-cell lymphocyte (CTL)-mediated immune response against KRAS-expressing tumor cells. KRAS, a tumor-associated antigen (TAA) that plays a key role in the RAS/mitogen-activated protein kinase (MAPK) signaling pathway, is overexpressed on a variety of tumor cell types.
porcupine inhibitor CGX1321: An orally bioavailable inhibitor of the membrane-bound O-acyltransferase (MBOAT) porcupine (PORCN), with potential antineoplastic, protective and regenerative activities. Upon oral administration, PORCN inhibitor CGX1321 specifically targets and binds to PORCN in the endoplasmic reticulum (ER), thereby inhibiting the post-translational palmitoylation and secretion of Wnt ligands, thus preventing the activation of Wnt-mediated signaling, and inhibiting cell growth in Wnt-driven tumors. In addition, by inhibiting the secretion of Wnt ligands and preventing Wnt-mediated signaling, CGX1321 may also limit fibrosis and promote regeneration of certain tissues upon cell injury. PORCN catalyzes the palmitoylation of Wnt ligands, and plays a key role in Wnt ligand secretion. Wnt signaling is dysregulated in a variety of cancers and plays a key role in tumor cell proliferation. It also plays a key role in tissue regeneration.
porcupine inhibitor ETC-1922159: An orally bioavailable inhibitor of the membrane-bound O-acyltransferase (MBOAT) porcupine (PORCN), with potential antineoplastic activity. Upon oral administration, ETC-1922159 binds to and inhibits PORCN in the endoplasmic reticulum (ER), which blocks post-translational palmitoylation of Wnt ligands and inhibits their secretion. This prevents the activation of Wnt ligands, interferes with Wnt-mediated signaling, and inhibits cell growth in Wnt-driven tumors. Porcupine catalyzes the palmitoylation of Wnt ligands, and plays a key role in Wnt ligand secretion. Wnt signaling is dysregulated in a variety of cancers.
porcupine inhibitor RXC004: An orally available inhibitor of porcupine (PORCN), with potential antineoplastic activity. Upon oral administration, RXC004 binds to and inhibits PORCN in the endoplasmic reticulum (ER), which blocks post-translational acylation of Wnt ligands and inhibits their secretion. This prevents the activation of Wnt ligands, interferes with Wnt-mediated signaling, and inhibits cell growth in Wnt-driven tumors. Porcupine, a membrane-bound O-acyltransferase (MBOAT), is required for the palmitoylation of Wnt ligands, and plays a key role in Wnt ligand secretion and activity. Wnt signaling is dysregulated in a variety of cancers.
porcupine inhibitor WNT974: An orally available inhibitor of porcupine (PORCN), with potential antineoplastic activity. Upon oral administration, WNT974 binds to and inhibits PORCN in the endoplasmic reticulum (ER), which blocks post-translational acylation of Wnt ligands and inhibits their secretion. This prevents the activation of Wnt ligands, interferes with Wnt-mediated signaling, and inhibits cell growth in Wnt-driven tumors. Porcupine, a membrane-bound O-acyltransferase (MBOAT), is required for the palmitoylation of Wnt ligands, and plays a key role in Wnt ligand secretion and activity. Wnt signaling is dysregulated in a variety of cancers.
porcupine inhibitor XNW7201: An orally available inhibitor of porcupine (PORCN), with potential antineoplastic activity. Upon oral administration, PORCN inhibitor XNW7201 targets, binds to and inhibits PORCN in the endoplasmic reticulum (ER), which blocks post-translational acylation of Wnt ligands and inhibits their secretion. This prevents the activation of Wnt ligands, interferes with Wnt-mediated signaling, and inhibits cell growth in Wnt-driven tumors. PORCN, a membrane-bound O-acyltransferase (MBOAT), is required for the palmitoylation of Wnt ligands, and plays a key role in Wnt ligand secretion and activity. Wnt signaling is dysregulated in a variety of cancers and plays a key role in cancer cell survival.
porfimer sodium: The sodium salt of a mixture of oligomers formed by ether and ester linkages of up to eight porphyrin units with photodynamic activity. Absorbed selectively by tumor cells, porfimer produces oxygen radicals after activation by 630 nm wavelength laser light, resulting in tumor cell cytotoxicity. In addition, tumor cell death may occur due to ischemic necrosis secondary to vascular occlusion that appears to be partly mediated by the release of thromboxane A2.
porfiromycin: An N-methyl derivative of the antineoplastic antibiotic mitomycin C isolated from the bacterium Streptomyces ardus and other Streptomyces bacterial species. Bioreduced porfiromycin generates oxygen radicals and alkylates DNA, producing interstrand cross-links and single-strand breaks, thereby inhibiting DNA synthesis. Porfiromycin is preferentially toxic to hypoxic cells.
Portia: (Other name for: ethinyl estradiol/levonorgestrel)
Portrazza: (Other name for: necitumumab)
posaconazole: A broad-spectrum, second generation, triazole compound with antifungal activity. Posaconazole strongly inhibits 14-alpha demethylase, a cytochrome P450-dependent enzyme. Inhibition of 14-alpha-demethylase prevents the conversion of lanosterol to ergosterol, an important component of the fungal cell wall. Inhibition of ergosterol synthesis changes the fungal cell membrane composition and integrity, alters membrane permeability and eventually leads to fungal cell lysis. Compared to other azole antifungals, posaconazole is a significantly more potent inhibitor of sterol 14-alpha demethylase.
poseltinib: An inhibitor of Bruton's tyrosine kinase (BTK) with potential anti-inflammatory activity. Upon administration, poseltinib inhibits the activity of BTK and prevents the activation of the B-cell antigen receptor (BCR) signaling pathway. This prevents the activation of BTK-mediated inflammatory pathways.
Posidur: (Other name for: extended release bupivacaine hydrochloride resorbable matrix formulation)
posoleucel: A population of closely human leukocyte antigen (HLA)-matched, off-the-shelf (OTS), donor-derived cytotoxic T lymphocytes (CTLs) that are specifically reactive towards six viruses, Epstein-Barr virus (EBV), cytomegalovirus (CMV), adenovirus (AdV), human herpesvirus 6 (HHV6; HHV-6), human polyomavirus type I (BKV) and human polyomavirus type II (JC virus; JCV), with potential antiviral activity. Upon infusion into allogeneic hematopoietic stem cell transplant (HSCT) recipients and immunocompromised patients, posoleucel provides virus-specific cellular immunity and causes specific anti-viral effects against active viral infections. This may prevent EBV, CMV, AdV, HHV6, BKV and JCV reactivation and infection, and inhibits viral-associated diseases.
Poteligeo: (Other name for: mogamulizumab-kpkc)
povetacicept: An affinity-optimized Fc fusion protein composed of an engineered variant domain of human tumor necrosis factor receptor superfamily member 13B (TNFRSF13B; TNF receptor superfamily 13B; transmembrane activator and CAML interactor; transmembrane activator and calcium modulator and cyclophilin ligand interactor; TACI) fused to a human immunoglobulin (Ig) fragment crystallizable (Fc) domain, with potential immunomodulating activity. Upon administration, povetacicept targets, binds to and inhibits both a proliferation-inducing ligand (tumor necrosis factor ligand superfamily member 13; TNFSF13; APRIL; TNF superfamily 13) and B-cell activating factor (tumor necrosis factor ligand superfamily member 13B; TNFSF13B; BAFF; BlyS; TNF superfamily 13B). This inhibits their interaction with their cell membrane receptors, including TACI, B-cell maturation antigen (tumor necrosis factor receptor superfamily member 17; TNF receptor superfamily 17; TNFRSF17; BCMA) and B cell-expressed BAFF receptor (tumor necrosis factor receptor superfamily member 13C; TNFRSF13C; BAFF-R). This inhibits B-cell proliferation and maturation, immunoglobulin (Ig) secretion, and survival. By inhibiting the production of autoantibodies, povetacicept inhibits B-cell mediated autoimmune responses. Dysregulated APRIL/ and BAFF signaling is implicated in the pathogenesis of multiple autoimmune diseases.
povidone-iodine solution: An iodophor solution containing a water-soluble complex of iodine and polyvinylpyrrolidone (PVP) with broad microbicidal activity. Free iodine, slowly liberated from the povoiodine-iodine (PVPI) complex in solution, kills eukaryotic or prokaryotic cells through iodination of lipids and oxidation of cytosplasmic and membrane compounds. This agent exhbits a broad range of microbicidal activity against bacteria, fungi, protozoa, and viruses. Slow release of iodine from the PVPI complex in solution minimizes iodine toxicity towards mammalian cells.
powdered mixed berry extract supplement: A dietary powder supplement consisting of a mixture of various, as of yet not fully elucidated, berries, with potential antineoplastic and anti-angiogenic activities. As berries are rich in phytonutrients, such as anthocyanins, flavonols, ellagitannins, galltannins, proanthocyanidins, and phenolic acids, the antineoplastic effects of the powdered mixed berry extract supplement on cancer cells may be attributable to the phytonutrients’ antioxidant and pro-apoptotic activities. Upon administration of the powdered mixed berry extract supplement, the phytochemicals in the berries may work together to reduce angiogenesis, tumor growth and tumor development. Specifically, various phytochemicals may inhibit the multidrug resistance protein-1 (MRP-1), which results in the accumulation of cellular oxidized glutathione (GSSG). Elevated intracellular levels of GSSG causes an increase in oxidative stress. This triggers the induction of oxidative stress-mediated apoptosis and may inhibit tumor and endothelial cell proliferation. MRP-1, overexpressed in many different types of cancer, plays a key role in the efflux of GSSG and thus the maintenance of oxidative homeostasis and survival in tumor cells.
pozelimab: A human immunoglobulin G4 (IgG4) monoclonal antibody directed against terminal complement protein C5, with potential anti-inflammatory activity. Upon administration, pozelimab targets and binds to terminal complement protein C5, thereby blocking C5 cleavage into pro-inflammatory components and preventing the complement-mediated destruction of red blood cells (RBCs) as seen in paroxysmal nocturnal hemoglobinuria (PNH). C5, a complement pathway protein, is expressed at high levels by the liver.
poziotinib: An orally bioavailable, quinazoline-based, mall-molecular and irreversible pan-epidermal growth factor receptor (EGFR or HER) inhibitor with potential antineoplastic activity. Poziotinib inhibits EGFR (HER1 or ErbB1), HER2, HER4 and EGFR mutants, thereby inhibiting the proliferation of tumor cells that overexpress these receptors. EGFRs, cell surface receptor tyrosine kinases, are often upregulated in a variety of cancer cell types and play key roles in cellular proliferation and survival.
poziotinib hydrochloride: The hydrochloride salt form of poziotinib, an orally bioavailable, quinazoline-based, irreversible pan-epidermal growth factor receptor (EGFR or HER) inhibitor, with potential antineoplastic activity. Upon oral administration, poziotinib inhibits EGFR (HER1 or ErbB1), HER2 and HER4, thereby inhibiting proliferation of tumor cells in which these receptors are overexpressed and/or mutated. EGFRs, cell surface receptor tyrosine kinases upregulated or mutated in a variety of cancer cell types, play key roles in cellular proliferation and survival.
PP14 derivative-treated HLA-matched donor mononuclear cell-enriched leukocytes: A preparation of allogeneic HLA-matched leukocytes treated with a derivative of placental protein 14 (PP14) with potential immunomodulating activity. PP14 derivative-treated HLA-matched donor mononuclear cell-enriched leukocytes contain at least fifty-five percent early-apoptotic T cells; after infusion and when processed by recipient dendritic cells, early-apoptotic T cells may help induce a decrease in the donor effector T-cell responses against the recipient of an allogeneic hematopoietic stem cell (HSC) transplant, thereby minimizing allogeneic HSC transplant-related graft-versus-host disease (GVHD). PP14, a 162 amino acid glycosylated protein secreted by the late secretory phase endometrium, binds to T cells in a carbohydrate fashion and has been shown to induce T-cell apoptosis; maternal immune tolerance to the fetus and pregnancy-related remissions of autoimmune disease may involve PP14-induced T cell apoptosis.
PPAR gamma inhibitor FX-909: An orally available inverse agonist and inhibitor of the transcription factor (TF) peroxisome proliferator-activated receptor gamma (PPAR gamma; PPARG), with potential antineoplastic activity. Upon oral administration, PPARG inhibitor FX-909 selectively targets and covalently binds to a region of PPARG that is sequestered from the mutation site. The binding promotes a repressive conformation of PPARG and inhibits the activity of PPARG. This inhibits both basal- and ligand-activated transcription by PPARG and prevents PPARG-mediated transcription of target genes, such as FABP4/Fabp4, AGT/Agt, IVT/Ivd and ARG1/Arg1. This may inhibit proliferation in PPARG-overactivated tumor cells. PPARG, a nuclear receptor, is genetically altered, including amplification, missense mutations, and fusions, in certain tumor cells commonly associated with the luminal lineage subtype.
PPE-expressing replication-defective HSV-1 vector NP2: A replication-defective (ICP4-deleted) herpes simplex virus type 1 (HSV-1) viral vector expressing the human preproenkephalin A (PPE) gene with potential antinociceptive activity. Upon intradermal administration, PPE-expressing replication-defective HSV-1 vector NP2 is transported by retrograde axonal transport to the dorsal root ganglion (DRG) and becomes dormant. In the DRG, the vector transduces sensory neurons with high efficiency, delivering the engineered PPE gene; transduced neurons then express the protein proenkephalin A, the precursor for Met- and Leu-enkephalin. After proteolytic cleavage from proenkephalin A in the DRG neuronal cytosol, transgene-mediated Met- and Leu-enkephalin bind to mu and gamma- opioid receptors, which may result in the inhibition of nociceptive neurotransmission.
PPI-2458: A synthetic derivative of fumagillin with antineoplastic and cytotoxic properties. PPI-2458 irreversibly inhibits the enzyme methionine aminopeptidase type 2 (MetAP2), thereby preventing abnormal cell growth and angiogenesis. PPI-2458 is reported to have a better toxicity profile compared to other agents of its class.
PR-104: A non-toxic, small-molecule, hypoxia-activated, 3,5-dinitrobenzamide nitrogen mustard pre-prodrug with potential antitumor activity. Upon intravenous administration, PR-104 is converted by systemic phosphatases to the alcohol intermediate PR-104A, which is reduced to form the active DNA-crosslinking mustard species hydroxylamine PR-104H intracellularly under hypoxic conditions. PR-104H specifically crosslinks hypoxic tumor cell DNA, resulting in the inhibition of DNA repair and synthesis, cell-cycle arrest, and apoptosis in susceptible hypoxic tumor cell populations while sparing normoxic tissues.
PR1 leukemia peptide vaccine: A cancer vaccine containing PR1, a 9 amino-acid human leukocyte antigen (HLA)-A2 restricted peptide derived from proteinase 3, with potential immunotherapeutic activity. Vaccination with PR1 leukemia peptide vaccine may stimulate the host immune system to mount a cytotoxic T lymphocyte (CTL) response against tumor cells expressing proteinase 3, resulting in tumor cell lysis. Often overexpressed in leukemic cells, proteinase 3 is a serine proteinase that activates progelatinase A and is involved in angiogenesis and metastasis.
pracinostat: An orally bioavailable, small-molecule histone deacetylase (HDAC) inhibitor with potential antineoplastic activity. Pracinostat inhibits HDACs, which may result in the accumulation of highly acetylated histones, followed by the induction of chromatin remodeling; the selective transcription of tumor suppressor genes; the tumor suppressor protein-mediated inhibition of tumor cell division; and, finally, the induction of tumor cell apoptosis. This agent may possess improved metabolic, pharmacokinetic and pharmacological properties compared to other HDAC inhibitors.
Pradaxa: (Other name for: dabigatran etexilate mesylate)
pralatrexate: A folate analogue inhibitor of dihydrofolate reductase (DHFR) exhibiting high affinity for reduced folate carrier-1 (RFC-1) with antineoplastic and immunosuppressive activities. Pralatrexate selectively enters cells expressing RFC-1; intracellularly, this agent is highly polyglutamylated and competes for the folate binding site of DHFR, blocking tetrahydrofolate synthesis, which may result in depletion of nucleotide precursors; inhibition of DNA, RNA and protein synthesis; and apoptotic tumor cell death. Efficient intracellular polyglutamylation of pralatrexate results in higher intracellular concentrations compared to non-polyglutamylated pralatrexate, which is more readily effuxed by the MRP (multidrug resistance protein) drug efflux pump. RFC-1, an oncofetal protein expressed at highest levels during embryonic development, may be over-expressed on the cell surfaces of various cancer cell types.
pralsetinib: An orally bioavailable selective inhibitor of mutant forms of and fusion products involving the proto-oncogene receptor tyrosine kinase RET, with potential antineoplastic activity. Upon administration, pralsetinib binds to and targets various RET mutants and RET-containing fusion product. RET gene mutations and translocations result in the upregulation and/or activation of RET tyrosine kinase activity in various cancer cell types; dysregulation of RET activity plays a key role in the development and regression of these cancers.
Praluent: (Other name for: alirocumab)
PRAME-targeting T-cell receptor/I\inducible caspase 9 BPX-701: Human allogeneic T lymphocytes transduced with a retroviral vector encoding a high-affinity T-cell receptor (TCR) specific for human leukocyte antigen (HLA)-A2-01-restricted, preferentially-expressed antigen in melanoma (PRAME) and containing the chemical induction of dimerization (CID) suicide/safety switch, composed of a drug binding domain coupled to the signaling domain of the suicide enzyme caspase-9, with potential antineoplastic activity. Peripheral blood mononuclear cells (PBMCs) are isolated from a patient, transduced with an anti-PRAME-HLA-A2 restricted TCR, expanded ex vivo, and reintroduced into the HLA-A2-positive patient. Upon reintroduction, PRAME-targeting T-cell receptor-based therapy BPX-701 binds to tumor cells expressing PRAME, which may induce cell death in and halt the growth of PRAME-expressing cancer cells. The tumor-associated antigen PRAME is overexpressed by a variety of cancer cell types. If potential T-cell toxicity due to graft-versus-host disease (GvHD) occurs, the chemical dimerizer rimiducid (AP1903) can be adminstered. Rimiducid binds to the drug binding domain expressed by the BPX-701 T cells, and triggers activation of the caspase-9 domain, which leads to caspase 9-mediated signaling, the induction of apoptosis and to selective and complete elimination of BPX-701 cells.
PRAME-targeting TCR-engineered NK cells: A preparation of natural killer (NK) cells that are engineered to express a T-cell receptor (TCR) specific for the tumor-associated antigen (TAA) preferentially expressed antigen in melanoma (PRAME), with potential antineoplastic activity. Upon administration, the PRAME-targeting TCR-engineered NK cells specifically recognize and bind to PRAME expressed on cancer cells, thereby lysing the PRAME-expressing cancer cells. PRAME is overexpressed by a variety of cancer cell types.
pramipexole dihydrochloride: The hydrochloride salt of pramipexole, a benzothiazole derivative. As a nonergot dopamine agonist, pramipexole binds to D2 and D3 dopamine receptors in the striatum and substantia nigra of the brain. Compared to other dopamine agonists, the use of this agent may be associated with fewer dyskinetic side effects in treated subjects.
pramlintide: A peptide analogue of human amylin with 3 proline substitutions at positions 25, 28 and 29, with antihyperglycemic activity. By mimicking amylin, pramlintide slows gastric emptying, inhibits digestive secretions (gastric acid, pancreatic enzymes, and bile), reduces glucagon secretion, and increases satiety; all of these actions are mediated mostly by glucose-sensitive areas in the brain stem. The overall result is a decrease in blood glucose levels. The use of pramlintide may cause an increased risk of insulin-induced hypoglycemia.
Prandin: (Other name for: repaglinide)
prasterone: A synthetic form of dehydroepiandrosterone with potential chemopreventive activity. Produced endogenously, dehydroepiandrosterone (DHEA) is an intermediate in the conversion of cholesterol to androgens and estrogens. Although the mechanisms of action of exogenously administered DHEA have not been fully illuminated, they may result in both direct and indirect physiologic effects. Direct effects include GABA-a receptor complex and NMDA receptor modulation, and enhanced pancreatic beta cell insulin secretion and antiglucocorticoid activities.
Pravachol: (Other name for: pravastatin sodium)
pravastatin sodium: The sodium salt of pravastatin with cholesterol-lowering and potential antineoplastic activities. Pravastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent lowers plasma cholesterol and lipoprotein levels, and modulates immune responses by suppressing MHC II (major histocompatibility complex II) on interferon gamma-stimulated, antigen-presenting cells such as human vascular endothelial cells. In addition, pravastatin, like other statins, exhibits pro-apoptotic, growth inhibitory, and pro-differentiation activities in a variety of tumor cells; these antineoplastic activities may be due, in part, to inhibition of the isoprenylation of Ras and Rho GTPases and related signaling cascades.
PRC2 inhibitor ORIC-944: An orally bioavailable allosteric inhibitor of polycomb repressive complex 2 (PRC2), with potential antineoplastic activity. Upon oral administration, PRC2 inhibitor ORIC-944 targets and binds to the regulatory embryonic ectoderm development (EED) subunit of PRC2. This prevents the methyltransferase activity of PRC2, spefifically the methylation of histone 3 at lysine27 (H3K27). This depletes H3K27 trimethylation (H3K27me3) and modulates the expression of target genes. This may inhibit tumor cell proliferation. PRC2 is dysregulated in a variety of cancer cell types and is associated with poor prognosis. It is responsible for the methylation of H3K27 leading to transcriptional silencing. EED is essential for the histone methyltransferase activity of PRC2.
PreBioGyn: (Other name for: prebiotic-based vaginal gel)
prebiotic-based vaginal gel: A vaginal gel preparation containing as of yet undisclosed prebiotic microorganisms or prebiotic ingredients, with potential moisturizing and protective activities. Upon intravaginal administration, the prebiotic-based vaginal gel may moisturize the vagina. The prebiotic ingredients may help restore and maintain the beneficial microorganisms in the vagina and maintain a healthy acidic pH. Altogether, this protects the vagina against the actions of harmful bacteria.
Precedex: (Other name for: dexmedetomidine hydrochloride)
Precose: (Other name for: acarbose)
prednisolone: A synthetic glucocorticoid with anti-inflammatory and immunomodulating properties. After cell surface receptor attachment and cell entry, prednisolone enters the nucleus where it binds to and activates specific nuclear receptors, resulting in an altered gene expression and inhibition of proinflammatory cytokine production. This agent also decreases the number of circulating lymphocytes, induces cell differentiation, and stimulates apoptosis in sensitive tumor cells populations.
prednisone: A synthetic glucocorticoid with anti-inflammatory and immunomodulating properties. After cell surface receptor attachment and cell entry, prednisone enters the nucleus where it binds to and activates specific nuclear receptors, resulting in an altered gene expression and inhibition of proinflammatory cytokine production. This agent also decreases the number of circulating lymphocytes, induces cell differentiation, and stimulates apoptosis in sensitive tumor cell populations.
pregabalin: A 3-isobutyl derivative of gamma-amino butyric acid (GABA) with anti-convulsant, anti-epileptic, anxiolytic, and analgesic activities. Although the exact mechanism of action is unknown, pregabalin selectively binds to alpha2delta (A2D) subunits of presynaptic voltage-dependent calcium channels (VDCCs) located in the central nervous system (CNS). Binding of pregabalin to VDCC A2D subunits prevents calcium influx and the subsequent calcium-dependent release of various neurotransmitters, including glutamate, norepinephrine, serotonin, dopamine, and substance P, from the presynaptic nerve terminals of hyperexcited neurons; synaptic transmission is inhibited and neuronal excitability is diminished. Pregabalin does not bind directly to GABA-A or GABA-B receptors and does not alter GABA uptake or degradation.
pregnenolone: An endogenous steroid hormone synthesized from cholesterol, which can act either as a neuroactive steroid or as a prohormone for progestogens, mineralocorticoids, glucocorticoids, androgens, estrogens, and the neuroactive steroids.
Pregnyl: (Other name for: recombinant human chorionic gonadotropin)
preimplantation factor PIF-1: A synthetic version, known as PIF-1, of the peptide preimplantation factor (PIF), an embryo-secreted peptide, with potential activity against graft-versus-host disease (GVHD). PIF-1 is believed to have wide-ranging activity on the immunologic system, including a whole host of immunologic changes that resemble pregnancy, in which there is neither graft-versus-host or host-versus-graft disease between the mother and the embryo. Replication of the immunologic profile of pregnancy through the administration of PIF-1 may thus benefit patients undergoing bone marrow transplant (BMT) who experience graft-versus-host disease (GVHD). Native embryonic PIF has been found to have a multi-targeted effect on various aspects of the immune system, coordinated so that there is a successful embryonic implantation and a successful pregnancy.
preladenant: An orally bioavailable antagonist of the adenosine A2A receptor (A2AR; ADORA2A), with potential immunomodulating and antineoplastic activities. Upon administration, preladenant selectively binds to and inhibits A2AR expressed on T lymphocytes. This blocks tumor-released adenosine from interacting with A2AR and prevents the adenosine/A2AR-mediated inhibition of T lymphocytes. This results in the proliferation and activation of T lymphocytes, and stimulates a T-cell-mediated immune response against tumor cells. A2AR, a G protein-coupled receptor, is highly expressed on the cell surfaces of T cells and, upon activation by adenosine, inhibits T-cell proliferation and activation. Adenosine is often overproduced by cancer cells and plays a key role in immunosuppression.
Prelay: (Other name for: troglitazone)
Prelone: (Other name for: prednisolone)
Premarin: (Other name for: conjugated estrogens)
Prepidil: (Other name for: dinoprostone)
Prevagen: (Other name for: apoaequorin/vitamin D supplement)
Prevnar: (Other name for: pneumococcal 7-valent conjugate vaccine)
Prevnar 13: (Other name for: pneumococcal 13-valent conjugate vaccine)
Prevnar 20: (Other name for: pneumococcal 20-valent conjugate vaccine)
Prevymis: (Other name for: letermovir)
prexasertib: An inhibitor of checkpoint kinase 1 (chk1) with potential antineoplastic activity. Upon administration, prexasertib selectively binds to chk1, thereby preventing activity of chk1 and abrogating the repair of damaged DNA. This may lead to an accumulation of damaged DNA and may promote genomic instability and apoptosis. Prexasertib may potentiate the cytotoxicity of DNA-damaging agents and reverse tumor cell resistance to chemotherapeutic agents. Chk1, a serine/threonine kinase, mediates cell cycle checkpoint control and is essential for DNA repair and plays a key role in resistance to chemotherapeutic agents.
Prialt: (Other name for: ziconotide)
prilocaine hydrochloride: The hydrochloride salt form of prilocaine, an intermediate-acting local anesthetic of the amide type chemically related to lidocaine. Prilocaine hydrochloride binds to voltage-gated sodium ion channels in the neuronal membrane, thereby preventing the permeability of sodium ions. This leads to a stabilization of the neuronal membrane and inhibits depolarization and results in a reversible blockage of nerve impulse generation and propagation along nerve fibres and subsequent reversible loss of sensation.
Prilosec: (Other name for: omeprazole)
primaquine: A synthetic, 8-aminoquinoline derivative with antimalarial properties. Although its mechanism of action is unclear, primaquine bind to and alter the properties of protozoal DNA. This agent eliminates tissue (exo-erythrocytic) malarial infection, preventing the development of the erythrocytic forms of the parasite which are responsible for relapses in Plasmodium vivax and ovale malaria. Primaquine is active against late hepatic stages (hypnozoites, schizonts).
primary prostate cancer tissue/hTERT/survivin mRNA-loaded autologous dendritic cell vaccine: An autologous dendritic cell (DCs) vaccine targeting prostate cancer with immunostimulating activity. The autologous DC vaccine is prepared via transfecting DCs with mRNAs extracted from primary prostate cancer tissue, and mRNAs of human telomerase reverse transcriptase (hTERT) and survivin. Upon administration, this DC vaccine may elicit a potent cytotoxic T-cell (CTL) response against prostate cancer cells, resulting in tumor cell death. Both hTERT and survivin are essential in neoplastic growth, and are considered to be universal tumor antigens.
prime cancer vaccine MVA-BN-CV301: A cancer priming vaccine consisting of a proprietary version of the recombinant vaccinia viral vector, modified vaccinia Ankara-Bavarian Nordic (MVA-BN), encoding both the two human tumor-associated antigens (TAAs) carcinoembryonic antigen (CEA) and mucin-1 (MUC-1), and TRICOM, which is comprised of the three human immune-enhancing co-stimulatory molecules B7-1, ICAM-1 and LFA-3, with potential immunostimulatory and antineoplastic activities. Upon subcutaneous administration of MVA-BN-CV301, followed by multiple boosting doses of the fowlpox virus (FPV) vaccine CV301, a cytotoxic T-lymphocyte (CTL) response against CEA- and MUC-1-expressing tumor cells is activated. In addition, the CV301-dependent anti-tumor CTL response upregulates the expression of programmed cell death ligand 1 (PD-L1); therefore, when CV301 is combined with a programmed cell death 1 (PD-1) immune checkpoint inhibitor, the antitumor effect may be increased. CEA and MUC-1 are overexpressed in a variety of cancers.
priming cancer vaccine GRT-C901: (Other name for: adenoviral tumor-specific neoantigen priming vaccine GRT-C901)
Primosteston: (Other name for: testosterone enanthate)
Prinivil: (Other name for: lisinopril)
prinomastat: A synthetic hydroxamic acid derivative with potential antineoplastic activity. Prinomastat inhibits matrix metalloproteinases (MMPs) (specifically, MMP-2, 9, 13, and 14), thereby inducing extracellular matrix degradation, and inhibiting angiogenesis, tumor growth and invasion, and metastasis. As a lipophilic agent, prinomastat crosses the blood-brain barrier.
Pristiq: (Other name for: desvenlafaxine succinate)
pritelivir: A thiazolylamide and helicase-primase enzyme inhibitor that is active against herpes simplex virus types 1 and 2 (HSV-1 and HSV-2). Pritelivir inhibits the helicase-primase complex and prevents helicase or primase catalytic cycling of viral DNA, which interferes with DNA replication and growth. This agent does not require activation by HSV thymidine kinase and has a longer plasma half-life than nucleoside analogues.
pritumumab: A naturally-produced human immunoglobulin G1 (IgG1) kappa antibody derived from a tumor-specific B-lymphocyte isolated from the regional draining lymph node of a patient with cervical carcinoma and targeted against the cell surface expressed vimentin, ecto-domain vimentin (EDV), with potential immunomodulating and antineoplastic activities. Upon administration, pritumumab targets and binds to EDV, which is expressed on a variety of tumor cell types but is not expressed by normal tissues and cells. This induces tumor cell death by antibody-dependent cell-mediated cytotoxicity (ADCC), and inhibits growth of EDV-expressing tumor cells. Pritumumab is able to penetrate the blood-brain barrier (BBB). Vimentin, an intracellular cytoskeletal protein, is overexpressed during epithelial-to-mesenchymal transition (EMT).
Privigen: (Other name for: human immunoglobulin G)
prizloncabtagene autoleucel: A preparation of autologous T lymphocytes engineered to express a second-generation chimeric antigen receptor (CAR) specific for the two tumor-associated antigens (TAAs) cluster of differentiation 19 (CD19) and CD20, with potential immunostimulating and antineoplastic activities. Upon administration, prizloncabtagene autoleucel targets and binds to CD19- and CD20-expressing tumor B cells. This induces selective toxicity in tumor B-cells expressing these TAAs. Both CD19 and CD20 are B-cell-specific cell surface antigens overexpressed in B-cell lineage malignancies. Targeting both CD19 and CD20 may prevent tumor cell antigen escape and relapse.
PRMT1 inhibitor: Any agent that inhibits protein arginine N-methyltransferase 1 (PRMT1; histone-arginine N-methyltransferase PRMT1; interferon receptor 1-bound protein 4).
PRMT1 inhibitor GSK3368715: An orally available inhibitor of protein arginine N-methyltransferase 1 (PRMT1; Histone-arginine N-methyltransferase PRMT1; Interferon receptor 1-bound protein 4) with potential antineoplastic activity. Upon administration, GSK3368715 inhibits monomethylation and asymmetric dimethylation of arginine-bearing substrates, including histones, estrogen receptors, RNA-binding proteins, and numerous non-histone substrates catalyzed by PRMT1. This may inhibit tumor cell proliferation, migration, and invasion that is potentially driven by PRMT1 overexpression or dysregulation. PRMT1-mediated methylation plays a key role in the modulation of protein function, gene expression and cellular signaling. Dysregulation and overexpression of PRMT1 has been associated with a number of solid and hematopoietic cancers.
PRMT5 inhibitor AUR-105: An orally available inhibitor of protein arginine methyltransferase 5 (PRMT5), with potential antiproliferative and antineoplastic activities. Upon oral administration, PRMT5 inhibitor AUR-105 selectively binds to PRMT5 and inhibits its function. By inhibiting its methyltransferase activity, levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 are decreased. This modulates the expression of genes involved in several cellular processes, including cellular proliferation. This may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, which may lead to decreased growth of rapidly proliferating cells, including cancer cells. PRMT5, a type II methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates involved in signal transduction and cellular transcription, is overexpressed in several neoplasms. Elevated levels are associated with decreased patient survival. Methylthioadenosine phosphorylase (MTAP) is deleted in certain cancer cells leading to an accumulation of methylthioadenosine (MTA). As MTA inhibits PRMT5, MTAP-null cancer cells are specifically sensitive to PRMT5 inhibitors.
PRMT5 inhibitor AZD3470: An orally bioavailable second generation methylthioadenosine (MTA)-selective small molecule inhibitor of the protein arginine methyltransferase 5 (PRMT5), with potential antineoplastic activity. Upon oral administration, PRMT5 inhibitor AZD3470 inhibits PRMT5 in the presence of MTA, thereby specifically inhibiting the function of PRMT5 solely within methylthioadenosine phosphoylase (MTAP)-deleted cancer cells and not in normal, healthy cells. By inhibiting the methyltransferase activity of PRMT5, levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 are decreased. This modulates the expression of genes involved in several cellular processes, including cellular proliferation. This may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, which may lead to decreased growth of rapidly proliferating cancer cells. PRMT5, a type II methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates involved in signal transduction and cellular transcription, is essential for the viability of cancer and normal cells. It is overexpressed in several neoplasms. Elevated levels are associated with decreased patient survival. MTAP is deleted in certain cancer cells leading to an accumulation of the metabolite MTA; MTA binds to and partially inhibits the activity of PRMT5.
PRMT5 inhibitor BGB-58067: A methylthioadenosine (MTA)-selective inhibitor of the protein arginine methyltransferase 5 (PRMT5), with potential antineoplastic activity. Upon administration, PRMT5 inhibitor BGB-58067 targets, binds to and inhibits PRMT5 in the presence of MTA, thereby specifically inhibiting the function of PRMT5 solely within methylthioadenosine phosphorylase (MTAP)-deleted cancer cells and not in normal, healthy cells. By inhibiting the methyltransferase activity of PRMT5, levels of both monomethylated and dimethylated arginine residues in certain histones and non-histone proteins are decreased. This modulates the expression of genes involved in several cellular processes and may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, which may lead to decreased growth of rapidly proliferating cancer cells. PRMT5, a type II methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates involved in signal transduction and cellular transcription, is essential for the viability of cancer and normal cells. It is overexpressed in several neoplasms. Elevated levels are associated with decreased patient survival. MTAP is deleted in certain cancer cells leading to an accumulation of the metabolite MTA. As MTA binds to and partially inhibits the activity of PRMT5, MTAP-deficient cancer cells are specifically sensitive to PRMT5 inhibitors.
PRMT5 inhibitor JNJ-64619178: An orally available small molecule inhibitor of protein arginine methyltransferase 5 (PRMT5), with potential antiproliferative and antineoplastic activities. Upon oral administration, PRMT5 inhibitor JNJ-64619178 selectively targets and irreversibly binds to the S-adenosylmethionine (SAM)- and substrate-binding pockets of the PRMT5/methylosome protein 50 (MEP50) complex, and inhibits its function. By inhibiting its methyltransferase activity, levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 are decreased. This modulates the expression of genes involved in several cellular processes, including cellular proliferation. This may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, which may lead to decreased growth of rapidly proliferating cells, including cancer cells. PRMT5, a type II methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates involved in signal transduction and cellular transcription, is overexpressed in several neoplasms. Elevated levels are associated with decreased patient survival.
PRMT5 inhibitor PRT811: An orally available small molecule inhibitor of protein arginine methyltransferase 5 (PRMT5), with potential antiproliferative and antineoplastic activities. Upon oral administration, PRMT5 inhibitor PRT811 selectively binds to PRMT5 and inhibits its function. By inhibiting its methyltransferase activity, levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 are decreased. This modulates the expression of genes involved in several cellular processes, including cellular proliferation. This may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, which may lead to decreased growth of rapidly proliferating cells, including cancer cells. PRMT5, a type II methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates involved in signal transduction and cellular transcription, is overexpressed in several neoplasms. Elevated levels are associated with decreased patient survival.
PRMT5 inhibitor SH3765: An orally bioavailable inhibitor of protein arginine methyltransferase 5 (PRMT5), with potential antiproliferative and antineoplastic activities. Upon oral administration, PRMT5 inhibitor SH3765 selectively binds to PRMT5 and inhibits its function. By inhibiting its methyltransferase activity, levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 are decreased. This modulates the expression of genes involved in several cellular processes, including cellular proliferation. This may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, which may lead to decreased growth of rapidly proliferating cells, including cancer cells. PRMT5, a type II methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates involved in signal transduction and cellular transcription, is overexpressed in several neoplasms. Elevated levels are associated with decreased patient survival.
PRMT5 inhibitor SKL27969: A central nervous system (CNS)-penetrant, orally bioavailable small molecule inhibitor of protein arginine methyltransferase 5 (PRMT5), with potential antiproliferative and antineoplastic activities. Upon oral administration, PRMT5 inhibitor SKL27969 selectively binds to PRMT5 and inhibits its function. By inhibiting its methyltransferase activity, levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 are decreased. This modulates the expression of genes involved in several cellular processes, including cellular proliferation. This may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, which may lead to decreased growth of rapidly proliferating cells, including cancer cells. PRMT5, a type II methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates involved in signal transduction and cellular transcription, is overexpressed in several neoplasms. Elevated levels are associated with decreased patient survival. Methylthioadenosine phosphorylase (MTAP) is deleted in certain cancer cells leading to an accumulation of methylthioadenosine (MTA). As MTA inhibits PRMT5, MTAP-null cancer cells are specifically sensitive to PRMT5 inhibitors.
PRMT5 inhibitor SYHX2001: An orally bioavailable inhibitor of protein arginine methyltransferase 5 (PRMT5), with potential antiproliferative and antineoplastic activities. Upon oral administration, PRMT5 inhibitor SYHX2001 selectively binds to PRMT5 and inhibits its function. By inhibiting its methyltransferase activity, levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 are decreased. This modulates the expression of genes involved in several cellular processes, including cellular proliferation. This may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, which may lead to decreased growth of rapidly proliferating cells, including cancer cells. PRMT5, a type II methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates involved in signal transduction and cellular transcription, is overexpressed in several neoplasms and is essential for the viability of cancer and normal cells. Elevated levels are associated with decreased patient survival. Methylthioadenosine phosphorylase (MTAP) is deleted in certain cancer cells leading to an accumulation of methylthioadenosine (MTA). As MTA binds to and partially inhibits PRMT5, MTAP-null cancer cells are specifically sensitive to PRMT5 inhibitors. This may spare normal, healthy cells that are without MTAP-deletions and lower systemic toxicity.
PRMT5 inhibitor TNG456: An orally bioavailable, blood-brain-barrier (BBB) penetrant and methylthioadenosine (MTA)-selective inhibitor of the protein arginine methyltransferase 5 (PRMT5), with potential antineoplastic activity. Upon oral administration, PRMT5 inhibitor TNG456 targets, binds to and inhibits PRMT5 that is bound to MTA, thereby specifically inhibiting the function of PRMT5 solely within methylthioadenosine phosphorylase (MTAP)-deleted cancer cells and not in normal, healthy cells. By inhibiting the methyltransferase activity of PRMT5, levels of both monomethylated and dimethylated arginine residues in certain histones and non-histone proteins are decreased. This modulates the expression of genes involved in several cellular processes and may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation. This may lead to decreased growth of rapidly proliferating cancer cells. PRMT5, a type II methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates involved in signal transduction and cellular transcription, is essential for the viability of cancer and normal cells. It is overexpressed in several neoplasms and elevated levels are associated with decreased patient survival. MTAP is deleted in certain cancer cells leading to an accumulation of the metabolite MTA. As MTA binds to and inhibits the activity of PRMT5, MTAP-deficient cancer cells are specifically sensitive to PRMT5 inhibitors.
PRMT5-MTA inhibitor MRTX1719: An orally bioavailable inhibitor of the protein arginine methyltransferase 5 (PRMT5)-methylthioadenosine (MTA) complex, with potential antineoplastic activity. Upon oral administration, PRMT5-MTA inhibitor MRTX1719 selectively binds to the PRMT5-MTA complex that is elevated in methylthioadenosine phosphoylase (MTAP)-deleted cancer cells, thereby specifically inhibiting the function of PRMT5 solely within MTAP-deleted cancer cells and not in normal, healthy cells. By inhibiting the methyltransferase activity of PRMT5, levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 are decreased. This modulates the expression of genes involved in several cellular processes, including cellular proliferation. This may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, which may lead to decreased growth of rapidly proliferating cancer cells. MRTX1719 also causes dysregulated RNA splicing and decreased pRb. Together, this decreases proliferation and increases apoptosis specifically in MTAP-deleted cancer cells. PRMT5, a type II methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates involved in signal transduction and cellular transcription, is essential for the viability of cancer and normal cells. It is overexpressed in several neoplasms. Elevated levels are associated with decreased patient survival. MTAP is deleted in certain cancer cells leading to an accumulation of the metabolite MTA; MTA binds to and partially inhibits the activity of PRMT5.
Pro-Stat 101: (Other name for: concentrated fortified collagen protein hydrolysate liquid supplement)
proapoptotic sulindac analog CP-461: An orally bioavailable second-generation selective apoptotic antineoplastic drug (SAAND) and analog of the nonsteroidal anti-inflammatory drug (NSAID) sulindac, with potential pro-apoptotic and antineoplastic activities. Upon administration, CP-461 specifically binds to and blocks the activity of cyclic guanosine monophosphate-phosphodiesterase (cGMP-PDE), an enzyme that inhibits the normal apoptosis signal pathway. Inhibition of cGMP-PDE permits the apoptotic signal pathway to proceed unopposed, resulting in apoptotic cell death. cGMP-PDE is overexpressed in a variety of cancer cell types; therefore, CP-461 selectively induces apoptosis in cancer cells, with minimal or no effect in healthy cells.
probenecid: A benzoic acid derivative with antihyperuricemic property. Probenecid competitively inhibits the active reabsorption of urate at the proximal tubule in the kidney thereby increasing urinary excretion of uric acid and lowering serum urate concentrations. This prevents urate deposition and promotes resolution of existing urate deposits. In addition, probenecid modulates the transport of organic acids and acidic drugs at the proximal and distal renal tubule, thereby increasing the drug serum concentration.
probiotic acidophilus: A probiotic containing the bacterium Lactobacillus acidophilus with potential antimicrobial and immunomodulatory activities. As a dietary supplement, Lactobacillus acidophilus (L. acidophilus), a naturally-occurring bacteria, may improve digestion and help maintain adequate colonization of the gastrointestinal (GI) tract by modulating the composition of the normal microflora. Because it produces lactic acid and hydrogen peroxide and other substances during fermentation, this bacterium creates an acidic environment unfavorable to pathogens such as Candida albicans. In addition, during colonization of the GI tract, L. acidophilus may form a protective barrier, preventing attachment of pathogens. Dietary supplementation with this bacterium has been shown to enhance natural and acquired immunity in mice.
probiotic supplement WeiLeShu: A probiotic containing as of yet unelucidated bacterial strains, with potential anti-inflammatory and immunomodulating activities. Upon oral administration, the probiotic supplement WeiLeShu modulates the composition of the normal gastrointestinal (GI) microflora, by increasing the beneficial bacteria and decreasing the harmful bacteria, and helps maintain adequate colonization of the GI tract. This improves digestion and prevents GI disturbances. These bacteria create an environment unfavorable to pathogens by adhering to human epithelial cells and forming a protective mucosal barrier. This prevents attachment of pathogens and reduces the risk of infection. By restoring gut microbiota, these bacteria may restore or enhance intestinal immune responses.
procarbazine hydrochloride: The hydrochloride salt of a methylhydrazine derivative with antineoplastic and mutagenic activities. Although the exact mode of cytotoxicity has not been elucidated, procarbazine, after metabolic activation, appears to inhibit the trans-methylation of methionine into transfer RNA (t-RNA), thereby preventing protein synthesis and consequently DNA and RNA synthesis. This agent may also undergo auto-oxidation, resulting in the formation of cytotoxic free radicals which damage DNA through an alkylation reaction.
procaspase activating compound-1 VO-100: An orally bioavailable procaspase activating compound-1 (PAC-1), with potential proapoptotic and antineoplastic activities. Upon administration, VO-100 binds to and forms a chelating complex with zinc (Zn) ions inside cells, which prevents the binding of Zn ions to procaspase-3 (PC3) and abrogates the Zn-mediated inhibition of PC3. This allows for the proteolytic autoactivation of PC3 into the active form caspase-3. This results in the selective caspase-3-mediated induction of apoptosis and cell death in cancer cells. In addition, VO-100 is able to cross the blood-brain-barrier (BBB). PC3, a Zn-inhibited proenzyme, is upregulated in a variety of cancer cell types, while its expression is minimal in normal healthy cells.
prochlorperazine: The maleate salt form of prochlorperazine, a synthetic, piperazine phenothiazine derivative with antiemetic, antipsychotic, antihistaminic, and anticholinergic activities. Prochlorperazine binds to and blocks the postsynaptic dopamine D2-receptor in the chemoreceptor trigger zone (CTZ) of the brain and may prevent chemotherapy-induced emesis. Prochlorperazine maleate also blocks anticholinergic and alpha-adrenergic receptors. Its antagonistic actions on the alpha-1 adrenergic receptors results in sedation, muscle relaxation, and hypotension.
Prochymal: (Other name for: remestemcel-L)
Procrit: (Other name for: epoetin alfa)
Procto-glyvenol: (Other name for: lidocaine mixture with tribenoside)
Proctocort: (Other name for: therapeutic hydrocortisone)
prodencel: An autologous dendritic cell (DC) vaccine targeting prostate cancer (PC)-specific antigen(s), with potential immunostimulatory and antineoplastic activities. Upon administration of prodencel, the DCs stimulate a specific cytotoxic T-lymphocyte (CTL)-mediated immune response against PC cells expressing the antigen(s), resulting in tumor cell lysis.
Prodentis: (Other name for: Lactobacillus reuteri probiotic lozenge)
Prodiaben: (Other name for: chlorpropamide)
prodrug PARP inhibitor TSL-1502: An orally bioavailable glucuronide prodrug of TSL-1502M, an inhibitor of the nuclear enzyme poly(ADP-ribose) polymerase (PARP), with potential chemo/radiosensitizing and antineoplastic activities. Upon oral administration, prodrug PARP inhibitor TSL-1502 is selectively converted by the enzyme beta-glucuronidase in the tumor microenvironment (TME) to its active form TSL-1502M. TSL-1502M selectively targets and binds to PARP and prevents PARP-mediated DNA repair of DNA breaks via the base-excision repair pathway. This enhances the accumulation of DNA strand breaks and promotes genomic instability and eventually leads to G2/M arrest and apoptosis. This may enhance the cytotoxicity of DNA-damaging agents. PARP catalyzes post-translational ADP-ribosylation of nuclear proteins that signal and recruit other proteins to repair damaged DNA and is activated by DNA breaks. The PARP-mediated repair pathway is dysregulated in a variety of cancer cell types. Beta-glucuronidase accumulates in the TME upon release from necrotic tumor cells and certain inflammatory cells.
Proellex: (Other name for: telapristone acetate)
Profasi: (Other name for: recombinant human chorionic gonadotropin)
proflavine hemisulfate: The hemisulfate salt form of proflavine, an acridine-derived fluorescent contrast and disinfectant agent that can potentially be used for cellular imaging and antiseptic purposes. Upon topical application of proflavine hemisulfate, proflavine diffuses into cells and intercalates into DNA, thereby accumulating in and staining the nucleus. During fluorescence imaging, the cell nuclei can be visualized. This allows nuclear morphometry and the identification of cancer cells. In addition, proflavine exerts its antibacterial effect by binding to bacterial DNA, thereby disrupting DNA synthesis and halting bacterial cell growth.
progenipoietin: A recombinant, chimeric, dual-receptor agonist fusion protein with immunohematopoietic activity. Progenipoietin (ProGP) consists of portions of the ligands for granulocyte colony-stimulating factor (G-CSF) and human fetal liver tyrosine kinase-3 (FLT3); variants progenipoietin-1, 2 and 3 differ in the orientation of the two receptor agonists. ProGP binds simultaneously to G-CSF and FLT3 receptors with receptor affinities approximately two- to three-fold higher than the respective native ligands. When administered in vivo, this agent may augment the number of circulating granulocytes and dendritic cells (DCs). ProGP may promote the proliferation of and prevent apoptosis in several human hematopoietic cell lineages, exhibiting the additive activities of a combination of C-GSF and FLT3.
Progenta: (Other name for: telapristone acetate)
progesterone vaginal insert: A tablet preparation formulated for vaginal administration containing a micronized synthetic form of the endogenous steroid hormone progesterone with progesterone activity. Upon vaginal insertion, progesterone binds to the progesterone receptor, resulting in dissociation of heat shock proteins, receptor phosphorylation, and transcription activation through direct or indirect interaction with transcription factors. This agent exerts inhibitory effects on estrogen by decreasing the number of estrogen receptors and increasing its metabolism to inactive metabolites. Progesterone induces secretory changes in the endometrium, decreases uterine contractility during pregnancy, and maintains pregnancy.
Progestin: (Other name for: therapeutic progesterone)
proglumide: An orally bioavailable cholecystokinin (CCK) receptor antagonist, with gastric acid reducing and potential antineoplastic activities. Upon oral administration, proglumide binds to and blocks both cholecystokinin receptor type A (CCK-AR; CCK1-R) and gastrin/cholecystokinin type B receptor (CCK-BR; CCK2-R). This prevents the binding of cholecystokinin and gastrin to the CCK receptors, and inhibits both gastrointestinal (GI) motility and gastric secretions. This may also decrease fibrosis in the tumor microenvironment (TME), increase both the infiltration of T-cells and the penetration of chemotherapeutic agents, and inhibit tumor growth and metastasis. CCK receptors, normally expressed in the GI tract and the nervous system, are overexpressed on fibroblasts and certain cancers.
Proglycem: (Other name for: diazoxide)
Prograf: (Other name for: tacrolimus)
prohibitin-targeting peptide 1: A chimeric, 25-mer peptide that targets prohibitin, with potential antineoplastic activity. Prohibitin-targeting peptide 1 (prohibitin-TP01) consists of a fat-targeting motif (CKGGRAKDC), two repeats of a proapoptotic peptide motif (KLAKLAK) and a GG linker. This peptide binds specifically to prohibitin in the white adipose vasculature; upon receptor-mediated cell internalization, the ligand/receptor complex triggers apoptosis and results in ablation of white fat. Destruction of white fat may potentially have positive consequences for men with prostate cancer since a high level of white fat has been implicated as a critical contributing factor in poor prostate cancer outcome. Prohibitin, a multifunctional membrane-associated protein that is thought to regulate cell survival and growth, has been shown by immunohistochemical analysis to be expressed in the membrane of endothelial cells in white adipose tissue.
Prokine: (Other name for: sargramostim)
Prolarix: (Other name for: caricotamide/tretazicar)
Prolastin-C: (Other name for: alpha-1-proteinase inhibitor human)
Proleukin: (Other name for: aldesleukin)
prolgolimab: A monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, prolgolimab binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.
Prolia: (Other name for: denosumab)
Prolixin: (Other name for: fluphenazine hydrochloride)
Prolutin: (Other name for: therapeutic progesterone)
Proluton: (Other name for: therapeutic progesterone)
Promacta: (Other name for: eltrombopag olamine)
promestriene: A 3-propyl and 17b-methyl ether of estradiol that may be used vaginally to relieve vaginal atrophy and its associated symptoms. Upon intravaginal administration, promestriene acts on the vaginal mucosa and may decrease vaginal atrophy and its associated symptoms, such as vaginal dryness and itching.
promethazine hydrochloride: The hydrochloride salt form of promethazine, a phenothiazine derivative with antihistaminic, sedative and antiemetic properties. Promethazine hydrochloride selectively blocks peripheral H1 receptors thereby diminishing the effects of histamine on effector cells. Promethazine hydrochloride also blocks the central histaminergic receptors, thereby depressing the reticular system causing sedative and hypnotic effects. In addition, promethazine hydrochloride also has centrally acting anticholinergic properties and probably mediates nausea and vomiting by acting on the medullary chemoreceptive trigger zone.
Promycin: (Other name for: porfiromycin)
pronase oral solution: An oral solution containing a mixture of proteinases, which are produced by Streptomyces griseus, with mucolytic activity and potential diagnostic applications. Upon oral administration, pronase is able to cleave peptide chains of polypeptides into individual amino acids, thereby dissolving mucus. The removal of mucus may improve the visibility of parts of the digestive tract, such as the esophagus and the stomach, during endoscopy. Pre-treatment with pronase before endoscopic examination may help in the detection of certain cancers, such as esophageal and gastric cancer.
propacetamol: A water-soluble para-aminophenol derivative and ester prodrug of acetaminophen in which acetaminophen is bound to the carboxylic acid diethylglycine, with analgesic and antipyretic activities. Upon intravenous administration, propacetamol is hydrolyzed by plasma esterases into its active form acetaminophen. Although the exact mechanism of action has yet to be fully elucidated despite its widespread use, acetaminophen enters the central nervous system and acts centrally. This agent binds to cyclooxygenase (COX) and prevents the metabolism of arachidonic acid to prostaglandin. A reduction in prostaglandin formation relieves pain and reduces fever. Acetaminophen may also act centrally on cannabinoid receptors and on N-methyl-D-aspartate (NMDA) receptors.
propofol: A hypnotic alkylphenol derivative. Formulated for intravenous induction of sedation and hypnosis during anesthesia, propofol facilitates inhibitory neurotransmission mediated by gamma-aminobutyric acid (GABA). This agent is associated with minimal respiratory depression and has a short half-life with a duration of action of 2 to 10 minutes.
propranolol hydrochloride: The hydrochloride form of propranolol, a synthetic beta-adrenergic receptor blocker with antianginal, antiarrhythmic, and antihypertensive properties. Propranolol competitively antagonizes beta-adrenergic receptors, thereby inhibiting beta-adrenergic reactions, such as vasodilation, and negative chronotropic and inotropic effects.
Propulsid: (Other name for: cisapride)
propylthiouracil: A thiourea derivative with antithyroid property. Propylthiouracil (PTU) interferes with the oxidation of iodine possibly by interaction with peroxidase or a peroxidase-mediated complex reaction, thereby inhibiting synthesis of thyroid hormones tri-iodothyronine (T3) and thyroxine (T4). In addition, this agent inhibits the Type I 5'-deiodinase (D1), an enzyme involved in the peripheral conversion of thyroxine to tri-iodothyronine. This results in decreased plasma triodothyronine concentrations and decreased entrance of thyroxine into cells thereby reducing thyroid hormone activity.
Prorex: (Other name for: promethazine hydrochloride)
Proscar: (Other name for: finasteride)
Prosta-Q: (Other name for: quercetin/saw palmetto/cranberry/bromelain/papain/zinc supplement)
prostaglandin E2 EP4 receptor inhibitor AN0025: An orally bioavailable antagonist of the prostaglandin E2 (PGE2) receptor type 4 (EP4; EP-4), with potential immunomodulating and antineoplastic activities. Upon oral administration, AN0025 selectively targets, binds to and blocks the activity of immunosuppressive tumor-associated myeloid cells (TAMCs) in the microenvironment. This abolishes TAMC-dependent immunosuppression and reduces tumor cell proliferation. The presence of immunosuppressive myeloid cells in certain tumors is associated with a poor prognosis.
ProstAtak: (Other name for: aglatimagene besadenovec)
prostate cancer vaccine ONY-P1: A cell-based vaccine derived from prostate cancer with potential immunopotentiating and antineoplastic activities. Prostate cancer vaccine ONY-P1 is derived from three irradiated allogeneic prostate cancer cell lines that represent different stages of prostate cancer and express a broad range of prostate and prostate cancer antigens. Upon administration, this vaccine may stimulate a host immune response against prostate cancer cells; in the vaccination schedule, the first two vaccinations are co-administered with bacillus Calmette-Guerin (BCG) as an adjuvant.
Prostate Health Cocktail: (Other name for: cholecalciferol/d-alpha tocopherol/L-selenomethionine/green tea extract/saw palmetto berry extract/daidzein/genistein/lycopene prostate health supplement)
prostate tumor antigen-activated autologous dendritic cell vaccine: A dendritic cell (DC)-based cancer vaccine composed of autologous dendritic cells (DCs) activated with a prostate tumor cell lysate containing tumor-associated antigens (TAAs) with potential immunostimulatory and antineoplastic activities. Upon administration, the prostate tumor antigen-activated autologous DC vaccine may stimulate an anti-tumoral cytotoxic T-lymphocyte (CTL) response against prostate cancer cells expressing prostate tumor cell-specific antigens, which may result in prostate tumor cell lysis.
prostatic acid phosphatase-sargramostim fusion protein PA2024: A genetically-engineered protein formed by the fusion of prostatic acid phosphatase (PAP) and sargramostim (GM-CSF). Vaccination with antigen-presenting cells (APC) loaded with prostatic acid phosphatase-sargramostim fusion protein may elicit a cytotoxic T-cell response against tumor cells that express PAP.
Prostin E2: (Other name for: dinoprostone)
PROSTVAC: (Other name for: rilimogene galvacirepvec/rilimogene glafolivec)
protease inhibitor formulation LB1148: A proprietary formulation comprised of the serine protease inhibitor tranexamic acid (TXA), polyethylene glycol (PEG), electrolytes, and sugar, with potential GI protective activity. After reconstitution in water and upon oral or enteral administration before abdominal surgery, TXA in the protease inhibitor formulation LB1148 targets and inhibits several serine proteases in the gastrointestinal (GI) tract, thereby preventing and protecting the intestinal mucosa against degradation, which preserves gastrointestinal (GI) integrity, function and motility. By inhibiting digestive proteases, the intestinal mucosal barrier is preserved during acute physiologic shock, which may prevent multi-organ failure, postoperative ileus and surgical intra-abdominal adhesions. PEG enhances transport of TXA through the GI tract. The other components provide energy and balance dietary electrolytes, thereby promoting healing of the GI barrier.
protease-activated anti-EGFR/anti-CD3 bispecific antibody prodrug CX-904: A recombinant bispecific antibody prodrug composed of a bispecific antibody directed against the tumor-associated antigen (TAA) human epidermal growth factor receptor (EGFR; HER1; ErbB1) and the human T-cell surface antigen CD3 that is linked to a proprietary masking peptide through a protease-cleavable linker, with potential immunostimulating and antineoplastic activities. Upon administration of protease-activated anti-EGFR/anti-CD3 bispecific antibody prodrug CX-904, the linkage system is stable in the circulation and, upon extravasation into the tumor microenvironment (TME), the peptide mask is cleaved by tumor-associated proteases. These proteases are present in high concentrations and aberrantly activated in the TME, while expressed as inactive forms, at much lower concentrations, in normal, healthy tissue. Protease cleavage of the linker enables binding of the unmasked, fully active bispecific antibody moiety of CX-904 to both CD3 on cytotoxic T lymphocytes (CTLs) and EGFR on EGFR-expressing tumor cells. This activates and redirects CTLs to EGFR-expressing tumor cells, leading to CTL-mediated killing of EGFR-expressing tumor cells. EGFR, upregulated and/or mutated in a variety of tumor cell types, plays a key role in tumor cell proliferation and survival.
protease-activated anti-PD-L1 antibody prodrug CX-072: A recombinant antibody prodrug composed of a monoclonal antibody directed against the tumor-associated antigen (TAA) programmed cell death 1 ligand 1 (PD-L1; B7-H1; CD274) that is linked to a proprietary masking peptide through a protease-cleavable linker on the amino terminus of the light chain domain of the antibody, with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, the linkage system is stable in the circulation and, upon extravasation into the tumor microenvironment, the peptide mask is cleaved by tumor-associated proteases. These proteases are present in high concentrations and aberrantly activated in the tumor microenvironment, while expressed as inactive forms, at much lower concentrations, in normal, healthy tissue. Protease cleavage of the linker enables binding of the unmasked, fully active monoclonal antibody moiety of CX-072 to PD-L1, which is over expressed on certain cancer cells. This blocks the binding to and activation of its receptor programmed cell death 1 (PD-1) on T lymphocytes, thereby enhancing the T-cell-mediated anti-tumor immune response and reversing PD-L1/PD-1-mediated T-cell suppression. PD-L1 binding to PD-1 on T cells suppresses the immune system and results in immune evasion. Compared to the unmodified PD-L1 antibody, peptide masking of CX-072 minimizes binding to PD-L1 in normal tissues, thereby decreasing autoimmune-based side effects while retaining anti-tumor activity.
proteasome inhibitor TQB3602: An orally bioavailable proteasome inhibitor (PI) with potential antineoplastic activity. Upon oral administration, proteasome inhibitor TQB3602 inhibits the activity of the proteasome, blocking the targeted proteolysis normally performed by the proteasome, which leads to an accumulation of unwanted or misfolded proteins, the disruption of various cell signaling pathways, and resulting in the induction of apoptosis. Proteasomes are large protease complexes that degrade unneeded or damaged proteins that have been ubiquinated.
protein arginine methyltransferase 5 inhibitor GSK3326595: An orally available, selective small molecule inhibitor of protein arginine methyltransferase 5 (PRMT5), with potential antiproliferative and antineoplastic activities. Although the mechanism of action has not been completely determined, PRMT5 inhibitor GSK3326595 binds to the substrate recognition site of PRMT5 following oral administration and inhibits its methyltransferase activity, which decreases the levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 and modulates the expression of genes involved in several cellular processes, including cell proliferation. Therefore, this agent may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation and may lead to decreased growth of rapidly proliferating cells, including cancer cells. PRTM5, an arginine methyltransferase that can catalyze the formation of both omega-N monomethylarginine (MMA) and symmetrical dimethylarginine (sDMA) on histones and a variety of other protein substrates, is overexpressed in several neoplasms.
protein arginine methyltransferase 5 inhibitor PF-06939999: An orally available inhibitor of protein arginine N-methyltransferase 5 (histone-arginine N-methyltransferase PRMT5; PRMT5) with potential antiproliferative and antineoplastic activities. Although the mechanism of action has not yet been fully elucidated, orally administered PRMT5 inhibitor PF-06939999 inhibits the methyltransferase activity of PRMT5, thereby decreasing the levels of monomethylated and dimethylated arginine residues in histones H2A, H3, and H4, and modulating the expression of genes involved in several cellular processes including cell proliferation. This may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, and may decrease the growth of rapidly proliferating cells, including cancer cells. PRTM5, an arginine methyltransferase that can catalyze the formation of both omega-N monomethylarginine (MMA) and symmetrical dimethylarginine (sDMA) on histones and a variety of other protein substrates, is overexpressed in several neoplasms.
protein arginine methyltransferase 5 inhibitor PRT543: An orally available small molecule inhibitor of protein arginine methyltransferase 5 (PRMT5), with potential antiproliferative and antineoplastic activities. Although the exact mechanism of action has not been completely determined, upon oral administration, PRMT5 inhibitor PRT543 selectively binds to the substrate recognition site of PRMT5 and inhibits its methyltransferase activity. This decreases the levels of both monomethylated and dimethylated arginine residues in histones H2A, H3 and H4 and modulates the expression of genes involved in several cellular processes, including cellular proliferation. As a result, PRT543 may increase the expression of antiproliferative genes and/or decrease the expression of genes that promote cell proliferation, which may lead to decreased growth of rapidly proliferating cells, including cancer cells. PRTM5, an arginine methyltransferase that catalyzes the formation of both omega-N monomethylarginine (MMA) and symmetric dimethylarginine (sDMA) on histones and a variety of other protein substrates, is overexpressed in several neoplasms.
protein phosphatase 2A inhibitor LB-100: A water soluble inhibitor of the protein phosphatase 2A (PP2A), with potential chemo- and radiotherapy enhancing activity. Upon injection, PP2A inhibitor LB-100 inhibits the removal of phosphate groups from proteins essential for cell cycle progression. When used with radio- or chemotherapy treatment, this agent prevents the activation of PP2A-mediated repair mechanisms and allows for malignant cells to progress through the cell cycle without having their damaged DNA repaired. This enhances the cytotoxic effect of the chemotherapeutic or radiotherapeutic agent and results in tumor cell apoptosis. PP2A, a serine/threonine phosphatase that plays a key role in the control of cell growth and DNA damage repair.
protein stabilized liposomal docetaxel nanoparticles: A formulation containing protein-stabilized liposome nanoparticles encapsulating the poorly water-soluble, second-generation taxane analog docetaxel with antineoplastic activity. Docetaxel binds to and stabilizes the beta-tubulin subunit, thereby inhibiting microtubule disassembly which results in cell-cycle arrest at the G2/M phase and cell death. This agent also inhibits pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and displays immunomodulatory and pro-inflammatory properties by inducing various mediators of the inflammatory response. Compared to the use of toxic carriers to increase solubilization of docetaxel, protein-stabilized liposomal docetaxel improves drug solubility while avoiding carrier-associated toxicity.
protein-engineered interleukin-12 XTX301: An engineered form of the human cytokine interleukin-12 (IL-12) in which the IL-12 is conjugated, via a tumor protease-cleavable linker, to a protein-engineered masking domain that prevents the binding of IL-12 to its receptors while in circulation and a half-life extension domain that prolongs circulating half-life, with potential immunomodulatory and antineoplastic activities. Upon administration of protein-engineered IL-12 XTX301, IL-12 is bound to the masking domain and pharmacologically inactive. Upon proteolytic cleavage by matrix metalloproteinases (MMPs) in the tumor microenvironment (TME), active IL-12 is released. IL-12 activates the immune system by promoting the secretion of interferon-gamma (IFN-g) and activating CD8+ T cells, CD4+ T cells and natural killer cells (NKs). The activation and expansion of these immune cells mediate cytolytic immune responses against tumor cells, thereby killing tumor cells and inhibiting tumor cell proliferation. The selective activation in the TME enhances the IL-12-mediated cytolytic responses against tumor cells while sparing the unwanted effects of systemic, peripheral immune activation.
protein-engineered interleukin-2 XTX202: A modified form of the recombinant form of human endogenous cytokine interleukin-2 (IL-2), that is masked with a protein domain, with potential immunoregulatory and antineoplastic activities. Upon administration of protein-engineered IL-2 XTX202, IL-2 is bound to the protein and pharmacologically inactive. IL-2 does not become active until cleaved by specific proteases in the tumor microenvironment (TME). Upon proteolytic cleavage, unbound and active IL-2 locally binds to the IL-2 receptor beta (CD122) and gamma (CD132) subunits (IL2Rb/g) that are expressed on CD8+ T-effector cells and natural killer (NK) cells, thereby activating IL2R-mediated signaling within these immune cells. The activation of T cells and NK cells mediate cytolytic immune responses against tumor cells causing tumor cell destruction and inhibition of tumor cell proliferation. XTX202 does not bind to IL-2 receptor alpha (IL-2Ra) and does not cause IL-2Ra-mediated toxicities. The selective activation in the TME enhances the IL-2-mediated cytolytic responses against tumor cells while sparing the unwanted effects of systemic, peripheral immune activation.
proteolytic enzymes: Enzymes produced and secreted by the pancreas which aid in the proteolysis of proteins in the digestive tract. Pancreatic proteolytic enzymes include trypsin, chymotrypsin and carboxypeptidase; these enzymes are secreted as zymogens, inactive precursors of the enzymes, and are activated in the lumen of the digestive canal. Another proteolytic enzyme, enteropeptidase, is associated with the brush border of enterocytes; this enzyme catalyses the conversion of trypsinogen into trypsin which, in turn, can activate a number of other pancreatic zymogens.
Protonix: (Other name for: pantoprazole sodium)
Protopic: (Other name for: tacrolimus)
protopine/nuciferine supplement: A nutritional supplement composed of the two alkaloids protopine, a benzylisoquinoline alkaloid occurring in opium poppies and other plants of the Papaveraceae family, and nuciferine, an alkaloid component of Nelumbo nucifera and Nymphaea caerulea, and in certain plants of the Papaveraceae family, with antihistamine, anticholinergic, analgesic, smooth muscle relaxing, central nervous system (CNS) suppressing and antipsychotic-like activities. Upon administration, protopine inhibits histamine H1 receptors and exerts opioid analgesic and sedative effects. As an antispasmodic, nuciferine relaxes smooth muscle cells and prevents smooth muscle contractions. It also has a calming effect. Together, protopine and nuciferine may relax the bladder and reduce urinary urgency and frequency, thereby providing relief for urge incontinence. It may also ease bladder pain and irritation.
Provecta: (Other name for: PV-10)
Provenge: (Other name for: sipuleucel-T)
Proventil: (Other name for: albuterol sulfate)
Provera: (Other name for: medroxyprogesterone acetate)
Provigan: (Other name for: promethazine hydrochloride)
Provigil: (Other name for: modafinil)
proxalutamide: An orally bioavailable androgen receptor (AR) antagonist with potential antineoplastic activity. Upon oral administration, proxalutamide binds to AR in target tissues, inhibits androgen-induced receptor activation, and facilitates the formation of inactive complexes that cannot translocate to the nucleus. This prevents binding to and transcription of AR-responsive genes that regulate prostate cancer cell proliferation. In addition, proxalutamide induces AR downregulation, thereby further preventing AR-mediated signaling. This ultimately leads to an inhibition of growth in AR-expressing prostate cancer cells. AR is overexpressed in prostate cancer and plays a key role in prostate cancer cell proliferation.
prucalopride succinate: The succinate salt form of prucalopride, an orally bioavailable dihydro-benzofuran-carboxamide and selective serotonin (5-HT4) receptor agonist, with gastrointestinal (GI) prokinetic activity. Upon oral administration, prucalopride specifically targets, binds to and stimulates the 5-HT4 receptor. This alters colonic motility patterns and stimulates colonic mass movements. This may normalize bowel movements and may relief chronic constipation. In addition, by increasing esophageal and gastric motility, prucalopride may also provide relief for aspiration-associated symptoms.
prulacabtagene leucel: A preparation of a subset of allogeneic T lymphocytes that express only gamma chain and delta chain T-cell receptors (TCRs) and that are engineered to express a chimeric antigen receptor (CAR) targeting the tumor-associated antigen (TAA) CD20 (cluster of differentiation 20), with potential immunomodulating and antineoplastic activities. Upon administration, prulacabtagene leucel specifically target and bind to tumor cells expressing CD20. This induces secretion of pro-inflammatory cytokines and results in the lysis of CD20-expressing tumor cells. Gamma delta T-lymphocytes play a key role in the activation of the immune system and do not require major histocompatibility complex (MHC)-mediated antigen presentation to exert their cytotoxic effect. The CD20 antigen, a non-glycosylated cell surface phosphoprotein, is a B-cell specific cell surface antigen overexpressed in B-cell lineage malignancies.
pruvonertinib: An orally bioavailable, mutant-selective, third-generation epidermal growth factor receptor (EGFR) inhibitor, with potential antineoplastic activity. Upon oral administration, pruvonertinib targets, binds to and inhibits the activity of EGFR with exon 20 insertion (Ex20ins) activating mutations, the gatekeeper mutation T790M and some other rare mutations, thereby preventing EGFR-mediated signaling. This may both induce cell death and inhibit tumor growth in EGFR-overexpressing tumor cells. EGFR, a receptor tyrosine kinase mutated in many tumor cell types, plays a key role in tumor cell proliferation and tumor vascularization.
PSA prostate cancer vaccine: A peptide vaccine containing the prostate specific antigen (PSA) with potential antineoplastic activity. PSA, a glycoprotein secreted by prostatic epithelial and ductal cells, is overexpressed in prostate cancer cells and is used as a tumor marker for both diagnosis and treatment evaluation. Vaccination with PSA peptide vaccine may produce anti-PSA antibodies as well as elicit a cytotoxic T-cell (CTL) response against prostate cancer cells expressing this antigen, thereby decreasing tumor cell growth.
PSA RNA-pulsed dendritic cell vaccine: An autologous dendritic cell vaccine with potential immunostimulatory activity. Dendritic cells harvested from a prostate cancer patient are transfected with the mRNA encoding for prostate specific antigen (PSA), a tumor marker secreted by prostatic epithelial and ductal cells. When reintroduced back to the patient, these PSA RNA pulsed autologous dendritic cells may elicit a cytotoxic T-cell (CTL) response against PSA-positive prostate cancer cells.
PSA-PAP/KLH-pulsed autologous dendritic cell vaccine: A cell-based cancer vaccine composed of autologous dendritic cells (DCs) pulsed with the prostate-specific tumor associated antigens (TAAs) prostate specific antigen (PSA) and prostate acid phosphatase (PAP), and conjugated to the immunostimulant keyhole limpet hemocyanin (KLH), with potential immunostimulatory and antineoplastic activities. Upon administration, prostate cancer antigen/KLH-pulsed autologous dendritic cell vaccine may stimulate the immune system to mount anti-tumoral cytotoxic T lymphocyte (CTL) and antibody responses against prostate cancer cells expressing PSA and PAP, which may result in prostate cancer cell lysis. KLH is an immunogenic carrier and serves as an immunostimulant to improve antigenic immune recognition and T-cell responses and can be used to evaluate vaccine efficacy.
PSA/IL-2/GM-CSF vaccine: A prostate cancer vaccine containing prostate specific antigen (PSA) combined with the cytokines, interleukin-2 (IL-2) and granulocyte macrophage-colony-stimulating factor (GM-CSF), with potential antineoplastic activity. Upon intradermal vaccination, PSA/IL-2/GM-CSF vaccine may activate the immune system to induce a cytotoxic T-cell (CTL) response against prostate cancer cells expressing this antigen, thereby decreasing tumor cell growth. PSA, a glycoprotein secreted by prostatic epithelial and ductal cells, is overexpressed by prostate cancer cells. IL-2 stimulates natural killer (NK) cells and cytotoxic T-cells against the PSA-expressing tumor cells. GM-CSF promotes antigen presentation to dendritic cells and further stimulates a tumor-specific cytotoxic T-lymphocyte (CTL) response.
PSA/PSMA DNA plasmid INO-5150: A plasmid DNA vaccine encoding the tumor-associated antigens (TAAs) prostate-specific antigen (PSA) and prostate-specific membrane antigen (PSMA), with potential immunoactivating and antineoplastic activities. Upon intramuscular delivery and electroporation of the PSA/PSMA DNA plasmid INO-5150, both PSA and PSMA are translated in cells which then activate the immune system. This induces cytotoxic T-lymphocyte (CTL) responses against tumor cells expressing PSA and PSMA. This may result in both immune-mediated tumor cell death and the inhibition of tumor cell proliferation. PSA and PSMA are overexpressed on a variety of cancer cell types. The DNA encoding the TAAs in INO-5150 is based on both human and other primate antigen gene sequences. As the plasmid genes differ from the human gene sequences encoding these antigens, INO-5150 may overcome immune tolerance to human TAAs.
PSA/PSMA/PSCA-encoding DNA plasmid vaccine PF-06755990: A DNA vaccine consisting of plasmids encoding the tumor-associated antigens (TAAs) human prostate-specific antigen (PSA), prostate-specific membrane antigen (PSMA) and prostate stem cell antigen (PSCA), with potential immunostimulating and antineoplastic activities. Upon administration via intramuscular electroporation, the PSA/PSMA/PSCA-encoding DNA Plasmid Vaccine PF-06755990 expresses PSA, PSMA and PSCA, which may elicit a cytotoxic T-lymphocyte (CTL) response against tumor cells that are expressing PSA, PSMA and PSCA, resulting in tumor cell lysis. PSA, PSMA and PSCA are overexpressed on a variety of cancer cell types.
PSA:154-163(155L) peptide vaccine: A cancer vaccine comprised of a synthetic peptide with an amino acid sequence corresponding to positions 154-163 of the amino acid sequence for prostate-specific antigen (PSA) with a leucine substitution at position 155. Upon administration, PSA:154-163(155L) peptide vaccine may elicit a cytotoxic T-cell response against tumor cells that express PSA.
Pseudomonas aeruginosa preparation: A preparation containing the inactivated Pseudomonas aeruginosa with potential immunomodulating activity. Upon inoculation, Pseudomonas aeruginosa preparation may stimulate the immune system, increasing macrophage and natural killer cell activity; it may be used thereby in cancer adjuvant treatments, and it may reduce the incidence of infection.
psilocybine: A tryptamine alkaloid, isolated from various genera of fungi including the genus Psilocybe, with hallucinogenic, anxiolytic, and psychoactive activities. In vivo, psilocybine is rapidly dephosphorylated into the active compound psilocin, which activates serotonin 2A (5-HT2A) receptors in the central nervous system (CNS), mimicking the effects of serotonin.
PSMA-specific targeting module TMpPSMA: A preparation of soluble adapter molecules consisting of an antigen-binding moiety targeting the tumor-associated antigen (TAA) human prostate-specific membrane antigen (PSMA), linked to a peptide motif recognizable by UniCAR02-T, that may be used to activate UniCAR02-T. Upon administration of PSMA-specific targeting module (TM) TMpPSMA, and upon co-administration of UniCAR02-T, the antigen-binding moiety of TMpPSMA targets and binds to cancer cells expressing PSMA, and the binding domain of UniCAR02-T binds to the nuclear antigen motif of TMpPSMA. This activates UniCAR02-T, and induces selective toxicity in and causes lysis of PSMA-expressing tumor cells. PSMA is overexpressed on the surface of metastatic and hormone-refractory prostate cancer cells.
PSMA-targeted docetaxel nanoparticles BIND-014: A proprietary preparation of polymeric nanoparticles containing the second-generation taxane docetaxel, targeted to prostate-specific membrane antigen (PSMA), with antineoplastic activity. PSMA-targeted docetaxel nanoparticles BIND-014 carry docetaxel within a matrix of polylactic acid covered with a coating of polyethylene glycol; embedded on the surface of the polyethylene glycol coating are ligands targeted to PSMA. BIND-014 allows gradual release of docetaxel upon degradation of the polylactic acid, and the PEG encapsulation escapes the host immune response while PSMA ligands on the surface restrict the cytotoxic effect to PSMA-expressing cells. Docetaxel binds to and stabilizes the beta-tubulin subunit, thereby inhibiting microtubule disassembly which results in cell-cycle arrest at the G2/M phase and cell death. PSMA is a cell-surface antigen that is abundantly present on the surface of cancer cells and on the neovasculature that feeds a wide variety of tumor types.
PSMA-targeted PET imaging agent fluorine F 18 CTT-1057: A radioconjugate composed of the phosphoramidate agent CTT1057, a human prostate specific membrane antigen (PSMA) inhibitor, and labeled with the radioisotope fluorine F 18, with potential use as a tracer for PSMA-expressing tumors during positron emission tomography (PET). Upon intravenous administration of PSMA-targeted PET imaging agent fluorine F 18 CTT-1057, the CTT-1057 moiety targets and irreversibly binds to the extracellular domain of PSMA-expressing tumor cells. Upon rapid internalization, and following PET imaging, PSMA-expressing tumor cells can be detected. PSMA, a tumor-associated antigen (TAA) and type II transmembrane protein, is expressed on the membrane of prostatic epithelial cells and overexpressed on prostate tumor cells.
PSMA-targeted tubulysin B-containing conjugate EC1169: An injectable, water soluble, small molecule drug conjugate (SMDC) containing a ligand specific for prostate-specific membrane antigen (PSMA), conjugated via a stable, enzyme-cleavable linker to the cytotoxic agent tubulysin B hydrazide (TubBH), with potential antineoplastic activity. Upon administration of PSMA-targeted tubulysin B-containing conjugate EC1169, the PSMA ligand specifically targets and binds to PSMA, a protein which is abundantly expressed on the surface of metastatic and hormone-refractory prostate cancer cells as well as on the neovasculature of many solid tumors. This allows for the specific delivery of TubBH to PSMA-expressing cancer cells. Upon internalization and cleavage, tubulysin B binds to tubulin and inhibits microtubule polymerization, which blocks cell division and results in G2/M phase arrest, tumor cell apoptosis and a decrease in PSMA-expressing tumor cells.
PSMA-targeting agent-technetium Tc99m EC0652: A radioconjugate composed of 2-[3-(1, 3-dicarboxy propyl)-ureido] pentanedioic acid (DUPA), a prostate-specific membrane antigen (PSMA)-targeting ligand, linked to the radioisotope technetium Tc 99m (Tc99m), that can potentially be used as a radioimaging agent for PSMA-overexpressing tumor cells. Upon administration, the PSMA-targeting moiety of EC0652 targets and binds to PSMA-expressing tumors. Upon uptake and single-photon emission computed tomography (SPECT) imaging, PSMA-expressing tumors can be visualized and identified. In turn, PSMA-overexpression can be used to evaluate both the efficacy of and response to certain PSMA-targeting cytotoxic agents. PSMA, a tumor-associated antigen (TAA), is overexpressed by most prostate cancers.
PSMA-targeting fluorescent imaging agent IS-002: A near-infrared (NIR) fluorescent imaging agent targeting the tumor-associated antigen (TAA) prostate-specific membrane antigen (PSMA), that can potentially be used as a tumor-selective fluorescent imaging agent during NIR fluorescence imaging-guided surgery. Upon intravenous administration, the PSMA-targeting fluorescent imaging agent IS-002 targets and binds to PSMA on PSMA-expressing tumor cells. Upon fluorescent imaging, PSMA-expressing tumors can be visualized and identified, and surgically removed. PSMA is overexpressed by most prostate cancers.
PSMA/CD3 tri-specific T-cell activating construct HPN424: A recombinant antibody derivative composed of tri-specific T-cell activating construct (TriTAC) directed against the human tumor-associated antigen (TAA) prostate-specific membrane antigen (PSMA; FOLH1) and the CD3 antigen found on T lymphocytes and an albumin-binding domain, with potential immunostimulating and antineoplastic activities. Upon administration, PSMA/CD3 tri-specific T-cell antibody construct HPN424 targets and binds PSMA on tumor cells and CD3 on cytotoxic T lymphocytes (CTLs), thereby bringing PSMA-expressing tumor cells and CTLs together, which results in the CTL-mediated cell death of PSMA-expressing tumor cells. The albumin-binding domain targets and binds to serum albumin, thereby extending the serum half-life of HPN424. PSMA is overexpressed on the surface of metastatic and hormone-refractory prostate tumor cells.
PSMA/TARP peptide vaccine: A peptide-based cancer vaccine containing epitopes of T cell receptor gamma-chain alternate reading frame protein (TARP) and prostate-specific membrane antigen (PSMA) in combination with a Poly IC-LC immunoadjuvant, with potential antineoplastic activity. Upon administration, PSMA/TARP peptide vaccine may stimulate a host cytotoxic T-cell (CTL) response against TARP- and PSMA-expressing tumor cells, resulting in tumor cell cytotoxicity. The nuclear protein TARP and PSMA are commonly expressed in prostate cancer cells.
psoralen: A furocoumarin that intercalates with DNA, inhibiting DNA synthesis and cell division. Psoralen is used in Photochemotherapy with high-intensity long-wavelength UVA irradiation. Psoralens are tricyclic furocumarins and have a strong tendency to intercalate with DNA base pairs. Irradiation of nucleic acids in the presence of psoralen with long wave UV (~360 nm) results in the 2+2 cyclo- addition of either of its two photoreactive sites with 5,6-carbon bonds of pyrimidines resulting in crosslinking double-stranded nucleic acids.
Psoria-Gold: (Other name for: curcumin-based gel)
PTEF-b/CDK9 inhibitor VIP152: An inhibitor of cyclin-dependent kinase 9 (CDK9), the catalytic subunit of the RNA polymerase II (RNA Pol II) elongation factor positive transcription elongation factor b (PTEF- b; PTEFb), with potential antineoplastic activity. Upon administration, VIP152 binds to and blocks the phosphorylation and kinase activity of CDK9, thereby preventing PTEFb-mediated activation of RNA Pol II and leading to the inhibition of gene transcription of various anti-apoptotic proteins. This may cause cell cycle arrest and induce apoptosis, which may lead to a reduction in tumor cell proliferation. The protein complex PTEF-b, a heterodimer consisting of CDK9 and a regulatory cyclin subunit of the T family, is over-activated in various tumor cell types; it plays a key role in the regulation of Pol II-mediated transcription of anti-apoptotic proteins. Tumor cells are dependent on anti-apoptotic proteins for their survival.
pterostilbene: A naturally-derived stilbenoid structurally related to resveratrol, with potential antioxidant, anti-inflammatory, pro-apoptotic, antineoplastic and cytoprotective activities. Upon administration, pterostilbene exerts its antioxidant activity by scavenging reactive oxygen species (ROS), thereby preventing oxidative stress and ROS-induced cell damage. It may also activate the nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated pathway and increase the expression of various antioxidant enzymes, such as superoxide dismutase (SOD). In addition, pterostilbene is able to inhibit inflammation by reducing the expression of various inflammatory mediators, such as interleukin (IL) 1beta, tumor necrosis factor alpha (TNF-a), inducible nitric oxide synthase (iNOS), cyclooxygenases (COX), and nuclear factor kappa B (NF-kB). It also inhibits or prevents the activation of many signaling pathways involved in carcinogenesis, increases expression of various tumor suppressor genes while decreasing expression of certain tumor promoting genes and directly induces apoptosis in tumor cells.
PTPN2 inhibitor ABBV-CLS-484: An orally bioavailable inhibitor of the T-cell specific tyrosine-protein phosphatase non-receptor type 2 (PTPN2), with potential immunomodulating and antineoplastic activities. Upon oral administration, PTPN2 inhibitor ABBV-CLS-484 specifically targets and binds to PTPN2. This prevents PTPN2-mediated signal transduction pathways and may activate anti-tumor T-cell immune responses. It may also sensitize tumor cells to immunotherapeutics. PTPN2 negatively regulates TCR and cytokine signaling needed for T-cell function, homeostasis and differentiation.
PTTC topical ointment ACU-D1: A topical ointment formulation containing pentaerythritol tetrakis (3-(3,5-di-tert-butyl-4-hydroxyphenyl) propionate) (PTTC), an inhibitor of the 26S proteasome, with potential antiangiogenic and antineoplastic activities. Upon topical administration of the PTTC topical ointment ACU-D1, PTTC inhibits the activity of the 26S proteasome, blocking the targeted proteolysis normally performed by the proteasome and resulting in an accumulation of unwanted or misfolded proteins. This disrupts various cell signaling pathways and may lead to cell cycle arrest, apoptosis, and inhibition of angiogenesis. Proteasomes are large protease complexes that degrade unneeded or damaged proteins that have been ubiquitinated.
pTVG-HP plasmid DNA vaccine: A cancer vaccine containing plasmid DNA encoding human prostatic acid phosphatase (PAP) (pTVG-HP) with potential immunostimulatory and antineoplastic activities. Upon administration, pTVG-HP plasmid DNA vaccine may stimulate the host immune system to generate a cytotoxic T lymphocyte (CTL) response against PAP-expressing prostate cancer cells. PAP or prostatic specific acid phosphatase (PSAP) is a tumor associated antigen (TAA) that may be overexpressed in prostate cancer.
pucotenlimab: A recombinant human monoclonal antibody directed against the negative immunoregulatory human cell receptor programmed cell death protein 1 (PD-1; PDCD1; CD279), with potential immune checkpoint inhibitory and antineoplastic activities. Upon administration, pucotenlimab targets, binds to and inhibits PD-1 and its downstream signaling pathways. This may restore immune function through the activation of T cells and T-cell-mediated immune responses against tumor cells. PD-1, a transmembrane protein in the immunoglobulin superfamily (IgSF) expressed on T cells, functions as an immune checkpoint that negatively regulates T-cell activation and effector function when activated by its ligands programmed cell death-1 ligand 1 (PD-L1) or 2 (PD-L2); it plays an important role in tumor evasion from host immunity.
pudexacianinium: The chloride salt form of pudexacianinium, an optical imaging agent and derivative of indocyanine green (ICG), a nontoxic, fluorescent, tricarbocyanine dye with a peak spectral absorption at 790 nm, that can be used for near-infrared (NIR) imaging using a NIR fluorescence (NIR-F) medical device. Upon intravenous administration, pudexacianinium is primarily and rapidly excreted by the kidneys. This provides visualization of the ureter(s) during surgery upon NIR-F imaging. Ureter visualization decreases ureter injuries during abdominopelvic surgery.
Pulmicort: (Other name for: budesonide)
pulmicort turbuhaler: (Other name for: budesonide)
Pulmozyme: (Other name for: dornase alfa inhalation solution)
pulrodemstat: An orally available inhibitor of lysine specific demethylase 1 (LSD1), with potential antineoplastic activity. Upon administration, pulrodemstat binds to and inhibits LSD1, a demethylase that suppresses the expression of target genes by converting the di- and mono-methylated forms of lysine at position 4 of histone H3 (H3K4) to mono- and unmethylated H3K4, respectively. LSD1 inhibition enhances H3K4 methylation and increases the expression of tumor (remove hyphen) suppressor genes. This may lead to an inhibition of cell growth in LSD1-overexpressing tumor cells. In addition, LSD1 demethylates mono- or di-methylated H3K9 which increases gene expression of tumor promoting genes; inhibition of LSD1 promotes H3K9 methylation and decreases transcription of these genes. LSD1, an enzyme belonging to the flavin adenine dinucleotide (FAD)-dependent amine oxidase family that is overexpressed in certain tumor cells, plays a key role in tumor cell growth and survival.
pUMVC3-hIGFBP-2 multi-epitope plasmid DNA vaccine: A plasmid DNA vaccine containing mammalian expression vector pUMVC3, encoding epitopes of human insulin-like growth factor-binding protein 2 (hIGFBP-2) with potential immunostimulating and antineoplastic activities. Upon vaccination, pUMVC3-hIGFBP-2 multi-epitope plasmid DNA vaccine may activate the immune system to mount a cytotoxic T-lymphocyte (CTL) response against hIGFBP-2-expressing cells. The tumor associated antigen (TAA) hIGFBP-2, a member of the insulin like growth factor receptor family, is overexpressed in a number of cancer cell types and its expression has been associated with increased invasiveness.
pUMVC3-IGFBP2-HER2-IGF1R plasmid DNA vaccine: A polyepitope plasmid DNA vaccine containing the mammalian expression vector pUMVC3 encoding epitopes derived from three tumor-associated antigens (TAAs): human insulin-like growth factor-binding protein 2 (IGFBP2), human epidermal growth factor receptor 2 (HER2; ERBB2) and insulin-like growth factor 1 receptor (IGF1R), with potential immunostimulating and antineoplastic activities. Upon intradermal vaccination, pUMVC3-IGFBP2-HER2-IGF1R plasmid DNA vaccine transfects local keratinocytes, which process the plasmid, express the epitopes and present them to antigen-presenting cells (APCs). This activates the immune system to mount a combined response from specific T helper type 1 (Th1) cells, memory T cells and cytotoxic T lymphocytes (CTL) against IGFBP2-, HER2-, and IGF1R-expressing tumor cells. IGFBP2, HER2, and IGF1R are tumor-associated proteins overexpressed in certain tumor cell types, and play key roles in cellular proliferation and survival.
Puricase: (Other name for: pegloticase)
Purinethol: (Other name for: mercaptopurine)
purinostat mesylate: The mesylate salt form of purinostat, an inhibitor of histone deacetylase (HDAC) classes I and IIb, with potential antineoplastic activities. Upon administration, purinostat selectively inhibits the catalytic activity of class I and IIb HDACs, which results in an accumulation of highly acetylated chromatin histones, the induction of chromatin remodeling and an altered pattern of gene expression. This leads to the inhibition of tumor oncogene transcription, and the selective transcription of tumor suppressor genes, which inhibits tumor cell division and induces tumor cell apoptosis. HDAC, an enzyme upregulated in many tumor types, deacetylates chromatin histone proteins. Class I HDACs are located in the nucleus and include HDACs 1, 2, 3, and 8; class IIb HDACs include HDAC 6 and 10 and are located in both the nucleus and the cytoplasm.
Purixan: (Other name for: mercaptopurine)
Purixan: (Other name for: mercaptopurine oral suspension)
Purlytin: (Other name for: rostaporfin)
purple grape juice: Juice made form dark, purple grapes that contain polyphenols with antioxidant and potential cardiovascular protecting activities. Purple grape juice contains high amounts of flavonoids that may increase antioxidant activity and reduce oxidative stress, reduce low-density lipoprotein (LDL), and improve nitric oxide formation, endothelial function and vasodilation.
PV-10: An injectable ten percent solution of rose bengal disodium, an iodinated fluorescein derivative, with potential antineoplastic and radiosensitizing activities. When injected into tumor tissue, PV-10 specifically targets and concentrates in tumor cells, producing cytotoxic singlet oxygen when exposed to ionizing radiation. In addition, PV-10 may stimulate an anti-tumor immune response.
PV701: An attenuated, replication-competent, oncolytic strain of Newcastle disease virus. PV701 selectively lyses tumor cells. The selectivity of this agent is related to defects in the interferon-mediated antiviral response found in tumor cells.
PVA microporous hydrospheres: An embolic material composed of microspheres of polyvinyl alcohol (PVA) polymers. These water-soluble, compressible microspheres may be used to encapsulate various therapeutic agents; drug-loaded microspheres can then be used as a drug delivery vehicle during embolization of tumor vasculature.
PVA microporous hydrospheres/doxorubicin hydrochloride: An embolic material composed of microspheres of polyvinyl alcohol (PVA) polymers loaded with doxorubicin hydrochloride with antineoplastic activity. Doxorubicin hydrochloride-loaded microspheres may be used as a drug delivery vehicle during embolization of tumor vasculature. Doxorubicin intercalates DNA, interferes with catalytic activity of topoisomerase II, and causes DNA adducts and other DNA damage, resulting in tumor cell growth inhibition and apoptosis. When used in tumor vasculature embolization, this preparation may provide more tumor-specific treatment with doxorubicin compared to the systemic administration of doxorubicin, thereby reducing the systemic toxicity of doxorubicin.
pVAXrcPSAv53l vaccine: A cancer vaccine containing xenogenic DNA from rhesus macaque (Macaca mulatta) that encodes prostate specific antigen (PSA) with potential immunostimulating and antineoplastic activities. Upon repeated intradermal administration via electroporation, pVAXrcPSAv53l vaccine may induce a cytotoxic T-lymphocyte (CTL) response against PSA-expressing prostate cancer cells. Rhesus PSA is 89% homologous to human PSA.
PVDF/sirolimus topical: A topical formulation consisting of a polyvinylidene fluoride (PVDF) polymer resin containing the macrolide sirolimus (rapamycin), produced by the organism Streptomyces hygroscopicus, with immunosuppressive activity. Upon application of topical PVDF/sirolimus, sirolimus migrates from the PVDF polymer resin into the skin. Once inside cells, sirolimus binds to the immunophilin FK binding protein-12 (FKBP-12) and forms a sirolimus:FKBP-12 complex. This complex binds to and inhibits the activity of the serine/threonine kinase mammalian target of rapamycin (mTOR), which may result in the suppression of cytokine-driven T-cell activation and proliferation.
Pycnogenol: (Other name for: French maritime pine bark extract)
Pylarify: (Other name for: fluorine F 18 piflufolastat)
pyrazinamide: A synthetic pyrazinoic acid amide derivative with bactericidal property. Pyrazinamide is particularly active against slowly multiplying intracellular bacilli (unaffected by other drugs) by an unknown mechanism of action. Its bactericidal action is dependent upon the presence of bacterial pyrazinamidase, which removes the amide group to produce active pyrazinoic acid. Pyrazinamide is an important component of multidrug therapy for tuberculosis.
pyrazine diazohydroxide: A congener of pyridine 2-diazohydroxide. Pyrazine diazohydroxide forms DNA adducts via the reactive pyrazine diazonium ion, thereby inhibiting DNA synthesis.
pyrazofurin: A nucleoside analog. Pyrazofurin potently inhibits orotidine 5'-monophosphate (OMP) decarboxylase, thereby interfering with de novo synthesis of uridine nucleotides and resulting in cytotoxicity. This agent also causes a rapid depletion of the pyrimidine deoxynucleotide pool, thereby inhibiting DNA synthesis and cell replication.
pyrazoloacridine: A 9-methoxy acridine compound containing a reducible 5-nitro substituent. Pyrazoloacridine appears to intercalate into DNA and inhibit RNA synthesis, DNA synthesis, and the activities of topoisomerases I and II, thereby causing cytotoxicity.
pyridoxal phosphate: The active form of vitamin B6 and a coenzyme for many pyridoxal phosphate (PLP)-dependent enzymes. PLP is involved in numerous enzymatic transamination, decarboxylation and deamination reactions; it is necessary for the synthesis of amino acids and amino acid metabolites, and for the synthesis and/or catabolism of certain neurotransmitters, including the conversion of glutamate into gamma-aminobutyric acid (GABA) and levodopa into dopamine. PLP can be used as a dietary supplement in cases of vitamin B6 deficiency. Reduced levels of PLP in the brain can cause neurological dysfunction.
pyridoxine hydrochloride: The hydrochloride salt of pyridoxine, a water-soluble B vitamin. Pyridoxine is converted in the liver into the metabolically active coenzyme form pyridoxal 5'-phosphate (P5P), an essential cofactor in many enzymatic reactions in amino acid metabolism, including transamination, deamination, and decarboxylation. P5P is required for glycogenolysis and the synthesis of sphingolipids and is essential to red blood cell, nervous system, and immune system functions.
pyrimethamine: A synthetic derivative of ethyl-pyrimidine with potent antimalarial properties. Pyrimethamine is a competitive inhibitor of dihydrofolate reductase (DHFR). DHFR is a key enzyme in the redox cycle for production of tetrahydrofolate, a cofactor that is required for the synthesis of DNA and proteins. This agent is often used in combination with other antimalarials for the treatment of uncomplicated falciparum malaria.
pyrotinib: An orally bioavailable, dual kinase inhibitor of the epidermal growth factor receptor (EGFR or HER-1) and the human epidermal growth factor receptor 2 (ErbB2 or HER-2), with potential antineoplastic activity. Upon oral administration, pyrotinib binds to and inhibits both EGFR and HER2, which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumor cells. EGFR and HER2 are receptor tyrosine kinases that are upregulated in various tumor cell types and play major roles in tumor cell proliferation and tumor vascularization.
pyrotinib dimaleate: The dimaleate ester of pyrotinib, an orally bioavailable, dual kinase inhibitor of the epidermal growth factor receptor (EGFR, ErbB1 or HER-1) and the human epidermal growth factor receptor 2 (ErbB2 or HER-2), with potential antineoplastic activity. Upon oral administration, pyrotinib binds to and inhibits both EGFR and HER2, which may result in the inhibition of tumor growth and angiogenesis, and tumor regression in EGFR/HER2-expressing tumor cells. EGFR and HER2 are receptor tyrosine kinases that are upregulated in various tumor cell types and play major roles in tumor cell proliferation and tumor vascularization.
pyroxamide: A synthetic derivative of hydroxamic acid with antineoplastic properties, Pyroxamide inhibits histone deacetylases involved in transcription; induces hyperacetylation of core histones, modulating chromatin structure and affecting transcription of some genes that inhibit tumor growth; and induces growth arrest and apoptosis. Pyroxamide is used in clinical studies for cancer chemotherapy.
pyruvate kinase inhibitor TLN-232: A synthetic cyclic heptapeptide with potential antineoplastic activity. Pyruvate kinase (PK) inhibitor TLN-232 targets pyruvate kinase M2 (M2PK), which may disrupt tumor cell anaerobic glycolysis. M2PK is a dimeric isoform of PK and the predominant PK isoform found in tumor cells.
pyruvate kinase M2 isoform activator TP-1454: An orally bioavailable activator of pyruvate kinase M2 isoform (PKM2), with potential immunomodulating and antineoplastic activities. Upon oral administration, PKM2 activator TP-1454 locks PKM2 into the active tetrameric form. This may prevent the production of glycolytic intermediates by the less active dimer form of PKM2, depleting the supply of glycolytic intermediates which are needed for tumor cell growth. This may also inhibit immune suppression mediated by the dimer form of PKM2. Altogether, this may slow tumor cell growth and enhance anti-tumor immune responses, thereby inhibiting tumor cell proliferation. PKM2, the predominant PK isoform found in tumor cells, is responsible for catalyzing the last step of glycolysis. PKM2 plays a critical role in the metabolic changes observed in cancer and immune cells and establishes a metabolic advantage for tumor cells over the tumor immune microenvironment.
pyruvate kinase-R activator AG-946: An orally available activator of the red cell isoform of pyruvate kinase (PK-R; PKR), with potential to improve hemolytic anemia and related-symptoms in patients with pyruvate kinase deficiency (PKD). Upon oral administration, PKR activator AG-946 binds to and activates PKR, thereby enhancing glycolytic pathway activity in red blood cells (RBCs), improving adenosine triphosphate (ATP) levels and reducing 2,3-diphosphoglycerate (2,3-DPG) levels. This may result in increased oxygen affinity, improved RBC deformability, decreased sickle RBC hemolysis, increased hemoglobin (Hb) levels and improved RBC membrane function. Mutations in PKR cause deficiency in PKR which prevents adequate RBC glycolysis, leading to a build-up of the upstream glycolytic intermediate 2,3-DPG and deficiency in the PKR product ATP.
pyrvinium pamoate: The pamoate salt of pyrvinium, a quinoline-derived cyanine dye and an mitochondrial oxidative phosphorylation (OxPhos) inhibitor, with anthelmintic and potential antineoplastic activities. Upon administration, pyrvinium pamoate may inhibit mitochondrial OxPhos and mitochondrial respiration, decreases mitochondrial function, prevents tumor cell metabolism and deprives tumor cells of energy, thereby preventing tumor cell proliferation and leading to tumor cell death in some types of cancer cells. Mitochondrial OxPhos is overactivated in cancer cells and plays a key role in tumor cell proliferation. Drug resistant tumor cells are very susceptible to decreased mitochondrial OxPhos as they cannot easily compensate for the decrease in mitochondrial function by increasing glycolysis.