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Ascenta Therapeutics Announces Results of Preclinical Evaluation of AT-406 in Multiple Cancer Models
Date:4/21/2009

by blocking the activity of at least three "inhibitors of apoptosis proteins" or IAPs (including XIAP, c-IAP1, and c-IAP2) to create conditions in which apoptosis can proceed. As such, AT-406 is considered a multi-IAP antagonist. IAPs are key components of the complex cascade of protein signaling that activates enzymes called caspases to initiate breakdown of the cancer cell. AT-406 is thought to mimic the activity of Smac (second mitochondria-derived activator of caspases) by binding to XIAP and preventing it from inhibiting caspase activation. Upon binding, AT-406 induces rapid degradation of cIAP-1/2 proteins and promotes apoptosis through activation of caspase-8 and the death-receptor complex.

AT-406 is in late-stage preclinical development and has demonstrated strong single-agent antitumor activity in multiple xenograft models of human cancer, including breast cancer, pancreatic cancer, prostate cancer, and lung cancer. AT-406 has also been shown to work synergistically with conventional chemotherapeutic and targeted agents (such as tyrosine kinase inhibitors) in preclinical tumor models.

Other Research Including AT-101

Ascenta Therapeutics also announced that researchers from the University of Pennsylvania presented results at AACR from an independent laboratory study examining the role of Bcl-2 homology (BH) family proteins in the development of chemotherapy resistance in neuroblastoma (Abstract # 3269). Using human-derived neuroblastoma cell lines, these investigators demonstrated differential resistance patterns to inhibitors of the Bcl-2 family proteins based on the relative BH proteins expressed (specifically, Mcl-1 or Bcl-2). They showed that Ascenta's small molecule pan-Bcl-2 inhibitor, AT-101, had preferential inhibition in Mcl-1 predominant lines. They concluded that compounds with activity against Mcl-1 may be useful in the treatment of high-risk neuroblastoma and warrant further stu
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SOURCE Ascenta Therapeutics, Inc.
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