New Nanotech Design Improves Drug Efficacy, Lowers Toxicity
Researchers at the Massachusetts Institute of Technology (MIT) and Brigham and Women's Hospital have revealed a nanoscale molecular design that increases the efficacy of the chemotherapy agent docetaxel against prostate tumors while reducing its toxic side effects in mice. The study, which appeared April 18 in the Proceedings of the National Academy of Sciences and was funded in part by NCI, is the first case where aptamers - short strands of nucleic acids - have been used successfully for the targeted delivery of a cancer drug in vivo.
"The greatest advantage of our study is in the combination of materials that we used," says Dr. Robert Langer of MIT, who directed the project with Dr. Omid Farokhzad of Harvard Medical School. Their team chose prostate cancer because it is often diagnosed early, when treatment prognosis is good, hoping that a need for safer localized treatments may facilitate the translation of their work to patient care. They designed their drug-delivery vehicle from poly (D,L-lactic-co-glycolic acid) (PLGA) because of the material's demonstrated safety in other FDA-approved medical devices, such as sutures. Read more
Promoting the Development and Delivery of Targeted Therapies
Earlier this month at the American Association of Cancer Research annual meeting, impressive data were presented from a phase II trial testing the multitargeted kinase inhibitor dasatinib (BMS-354825) in patients with chronic myeloid leukemia (CML) who had failed to respond to or had developed resistance to imatinib (Gleevec). In chronic-phase CML patients, for instance, 93 percent had a complete hematologic response, meaning normal blood counts and no CML-related symptoms.
Imatinib has rightfully been heralded as a breakthrough drug. Dasatinib is an excellent example, though, of how cancer researchers are learning from the successes and failures of targeted therapies like imatinib to make important advances in the development of next-generation targeted agents. Not only does dasatinib have a 325-fold stronger affinity for its gene target, BCR-ABL, than imatinib, it also appears to be effective against 18 of the 19 identified mutated forms of BCR-ABL - the very mutations that drive imatinib resistance. Read more