ABT 737

Chemical properties

Yellow Solid

The Uses of ABT 737

A selective inhibitor of BCL-2, in small cell lung cancer. ABT-737 induced dramatic regressions in tumors derived from some SCLC cell lines.

The Uses of ABT 737

ABT-737 is a BH3 mimetic inhibitor of Bcl-xL, Bcl-2 and Bcl-w with EC50 of 78.7 nM, 30.3 nM and 197.8 nM, respectively.

What are the applications of Application

ABT 737 is a selective inhibitor of Bcl-2

Definition

ChEBI: ABT-737 is a biphenyl that is 4-chloro-1,1'-biphenyl substituted by a (4-{4-[(4-{[(2R)-4-(dimethylamino)-1-(phenylsulfanyl)butan-2-yl]amino}-3-nitrobenzene-1-sulfonyl)carbamoyl]phenyl}piperazin-1-yl)methyl group at position 2'. It is a BH3-mimetic drug which targets the anti-apoptotic B-cell lymphoma-2 (BCL-2) family proteins, including BCL-2, BCL-xL, and BCL-w, and induces apoptosis in cancer cells. It has a role as an anti-allergic agent, an anti-inflammatory agent, an antineoplastic agent, an apoptosis inducer and a B-cell lymphoma 2 inhibitor. It is a member of biphenyls, a member of monochlorobenzenes, a C-nitro compound, an aromatic amine, a N-arylpiperazine, a N-sulfonylcarboxamide, an aryl sulfide, a secondary amino compound and a tertiary amino compound.

Biological Functions

ABT-737 is a BH3 mimetic inhibitor of Bcl-xL, Bcl-2 and Bcl-w with EC50 of 78.7 nM, 30.3 nM and 197.8 nM in cell-free assays, respectively; no inhibition observed against Mcl-1, Bcl-B or Bfl-1. ABT-737 induces mitochondrial pathway apoptosis and mitophagy. Phase 2.

Biological Activity

abt-737 is a novel and potent inhibitor of b-cell lymphoma 2 (bcl-2) family proteins, which are critical for cell survival and overexpressed in many tumor cells, with high affinity towards bcl-xl, bcl-2, and bcl-w but no affinity towards less homologous proteins, such as bcl-b, mcl-1, and a1. abt-737 has shown single-agent activity against lymphoma and small-cell lung cancer as well as substantial antimyeloma activity both in vitro and in vivo. in recent studies, acute myeloid leukemia blast, origenitor, and stem cells are effectively killed by abt-737 with normal hematopoietic cells intact. the disruption of the bcl-2/bax complex and bak-dependent but bim-independent activation of the intrinsic apoptotic pathway could also be induced by abt-737.marina konopleva, rooha contractor, twee tsao, ismael samudio, peter p. ruvolo, shinichi kitada, xingming deng, dayong zhai, yue-xi shi, thomas sneed, monique verhaegen, maria soengas, vivian r. ruvolo, teresa mcqueen, wendy d. schober, julie c. watt, tilahun jiffar, xiaoyang ling, frank c. marini, david harris, martin dietrich, zeev estrov, james mccubrey, w. stratford may, john c. reed, and michael andreeff. mechanisms of apoptosis sensitivity and resistance to the bh3 mimetic abt-737 in acute myeloid leukemia. cancer cell 2006: 10; 375-388suzanne trudel, a. keith stewart, zhihua li, yanjun shu, sheng-ben liang, young trieu, donna reece, josh paterson, dingyan wang, and xiao-yan wen. the bcl-2 family protein inhibitor,abt-737, has substantial antimyeloma activity and shows synergistic effect with dexamethasone and melphalan. clin cancer res 2007; 13 (2) 621-629

storage

Store at -20°C