Epicept - De okända preparaten
2010-11-18 07:38, Edited at: 2010-11-18 07:38Please note: Community posts are written by its members and not by Redeye’s research department. As a reader you’re always encouraged to critically analyze the content.
Igår publicerade jag en pipeline för bolaget EpiCept som kan tyckas vara främmande för en del. Med lite modifiering av webb adresserna på EpiCepts hemsida kan man komma åt information som inte är länkade till på hemsidan. Så här kommer informationen av dessa halv okända preparaten.
EP2167 is the lead compound from a family of compounds whose apoptosis-inducing anti-tumor activities are mediated through the transferrin receptor via a rapid and novel molecular mechanism. Transferrin receptor is a known and validated oncology target, but in 2005 EpiCept published (Proc. Nat. Acad. Sci. USA, 102:12095-12100, 2005) the first evidence describing its role as a rapid inducer of apoptosis, a unique and different mechanism of its use as an oncology target. The transferrin receptor is located on the surface of cells and is over expressed in several types of cancer. In preclinical testing, EP2167 has been shown to induce apoptosis in multiple cancer cell types, including prostate, breast, colorectal, non-small cell and small cell lung cancers and leukemia, and has been shown to inhibit tumor growth in xenograft tumor cancer models of differert types.
EP128504 is a novel inducer of apoptosis that has been shown to be selective for breast and colorectal cancer cells in preclinical testing. It does not appear to be active in killing normal cells. EP128504 targets a novel cytoplasmic protein affecting the IGF growth signaling pathways. EpiCept has published (Mol. Cancer Ther. 4:761-771, 2005) the mechanism of action and the role of this protein in apoptosis induction and cancer treatment, which were previously unknown until discovered by our researchers.
EP192112 is a novel inducer of apoptosis that is selective for Myc-oncogene dysregulated cells and tumors. Myc-oncogene, one of the earliest oncogenes identified, is dysregulated in a wide variety of different tumors, both hematopoietic and solid types. On-going studies indicate that the activity of the compound appears to be mediated through a novel oncology target. This compound was identified through a modification of our ASAP technology, which we term Targeted ASAP, to identify compounds that are selective in killing cells that are dysregulated for a specified molecular target while sparing normal regulated cells.
/Pfenix