ABT-737 is a small molecule drug that inhibits Bcl-2 and Bcl-xL, two members of the Bcl-2 family of evolutionarily-conserved proteins that share B cl-2 H omology (BH) domains.

May 15, 2005 · ABT-737 exhibits single-agent-mechanism-based killing of cells from lymphoma and small-cell lung carcinoma lines, as well as primary patient-derived cells, and in animal models,...

ABT-737 binds to the hydrophobic groove of multiple members of the anti-apoptotic Bcl-2 protein family, including Bcl-2, Bcl-xl and Bcl-w. This inhibits the activity of these pro-survival proteins and restores apoptotic processes in tumor cells, via activation of Bak/Bax-mediated apoptosis.

ABT-737, a small-molecule inhibitor used in the current study, is a BH3 simulator developed by the IDUT laboratory and Abbott Laboratory, and is the first class of small molecule inhibitors (SMIs) that causes tumour-specific killing (30).

Feb 8, 2006 · We show that resistant cells can be sensitized to ABT-737 by approaches that downregulate, destabilize, or inactivate Mcl-1. Our studies provide a rational basis for designing clinical trials of this highly promising agent and a benchmark for systematically evaluating BH3 mimetic compounds.

ABT-737 is a small molecule that binds to Bcl-2/Bcl-xL (but not Mcl-1) with high affinity and disrupts their interaction with pro-apoptotic Bax/Bak, thus enhancing apoptosis.

Aug 9, 2012 · The novel anticancer drug ABT-737 is a Bcl-2 Homology 3 (BH3)-mimetic that induces apoptosis by inhibiting pro-survival Bcl-2 proteins. ABT-737 binds with equal affinity to Bcl-2, Bcl-xL and...

ABT-737, a Bcl-2/Bcl-x L inhibitor with affinity in the nanomolar range, has shown activity against several hematopoietic and solid tumor cell lines and xenografts (12 – 15).

Apr 26, 2007 · ABT-737 is a BH3 mimetic small-molecule inhibitor that binds with high affinity to Bcl-2 and Bcl-xL, preventing the sequestration of proapoptotic molecules and shifting the cell...

Sep 30, 2021 · We have reported the efficacy of the BCL-2 inhibitor, ABT-737, on the AML post-MDS model; here, we report that this BCL-2 inhibitor also significantly extended survival of the HR-MDS mouse model, with reductions of BM blasts and …