BDA366 特异性靶向 BCL2 BDA-366 的 BH4 结构域并抑制人骨髓瘤的生长。 BDA-366 通过诱导 BCL2 构象变化在 MM 细胞系和原代 MM 细胞中诱导强烈的细胞凋亡。 BDA-366 的递送显着抑制了 NOD-scid/IL2Rγnull 小鼠中人 MM 异种移植物的生长，对正常造血细胞或体重没有明显影响。

BDA-366 specifically targets the BH4 domain of Bcl2 BDA-366 and suppresses human myeloma growth. BDA-366 induces robust apoptosis in MM cell lines and primary MM cells by inducing BCL2 conformational change. Delivery of BDA-366 substantially suppressed the growth of human MM xenografts in NOD-scid/IL2Rγnull mice, without obvious effects on normal hematopoietic cells or body weight.

BDA-366 induces robust apoptosis in MM(Multiple myeloma) cell lines and primary MM cells by inducing BCL2 conformational change. BDA-366 induces a conformational change in the BCL2 molecule that converts it to a death protein, and inhibits lung cancer growth in vitro and in vivo[1]. BDA-366 did not bind to other Bcl2 family members, including Bcl-XL, Mcl-1, or Bfl-1/A1, indicating the specificity of its Bcl2 binding. BDA-366 induces apoptotic cell death in a Bax-dependent manner and induces calcium (Ca2+) release via inhibition of Bcl2/IP3R interaction[2].

Human MM cell lines RPMI8226 and U266 were treated with BDA366 at increasing concentrations (0, 0.1, 0.25, 0.5 μM) for 48hr. Cells were harvested, stained with Annexin V and propidium iodide (PI), and subjected to FACS analysis. Apoptotic cells were gated on the Annexin V positive population. Annexin V+PI? cells were early apoptotic cells, Annexin+PI+ cells were late apoptotic cells, and Annexin?PI+ cells were necrotic cells.(Only for Reference)

1821496-27-8

C24H29N3O4

423.513

BDA-366;BDA 366

Ethanol:5 mg/mL (11.8 mM)
H2O:<1 mgml
DMSO:84 mg/mL (198.34 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years