BDA-366 是一种有效的 BCL2 拮抗剂，以高亲和力和选择性 (Ki = 3.3 nM) 结合 BCL2-BH4 结构域。 BDA-366 诱导 BCL2 的构象变化，从而消除其抗凋亡功能，将其从存活分子转变为细胞死亡诱导剂。 BDA-366 抑制肺癌细胞的生长。

BDA-366 is a potent Bcl2 antagonist, binding Bcl2-BH4 domain with high affinity and selectivity (Ki = 3.3 nM). BDA-366 induces conformational change in Bcl2 that abrogates its antiapoptotic function, converting it from a survival molecule to a cell death inducer. BDA-366 suppresses growth of lung cancer cells[1].

NSC 228155 promotes transactivation of several RTKs, including ErbB2 and ErbB3, Insulin R and IGF-1 R receptors in the cells. It stimulates dimerization of sEGFR domain II[1]. NSC 228155 can rapidly move across cell membranes and disperse within both cytoplasmic and nuclear compartments. It rapidly generates hydrogen peroxide within cells[2]. NSC 228155 is also a potent inhibitor of KIX-KID interaction(IC50 = 0.36 μM), but it is not particularly selective against CREB-mediated gene transcription in HEK 293T cells[3].

1909226-00-1

C24H29N3O4

423.5

Ethanol:5 mg/mL (11.8 mM)
DMSO:78 mg/mL (184.2 mM)
H2O:<1 mgml
Powder: -20°C for 3 years
In solvent: -80°C for 2 years