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BDA-366
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
BDA-366图片
CAS NO:1821496-27-8
规格:≥98%
包装与价格:
包装价格(元)
10mg电议
25mg电议
50mg电议
100mg电议
250mg电议
500mg电议

产品介绍
理化性质和储存条件
Molecular Weight (MW)423.5
FormulaC24H29N3O4
CAS No.1821496-27-8
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)DMSO: 84 mg/mL (198.3 mM)
Water: <1 mg/mL
Ethanol: 5 mg/mL (11.8 mM)
SMILES Code CCN(CC)C[C@@H](O)CNC1=CC=C(NC[C@@H]2OC2)C3=C1C(C4=C(C3=O)C=CC=C4)=O
Synonyms BDA366; BDA 366; BDA-366.
实验参考方法
In Vitro

In vitro activity: 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. 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.


Kinase Assay: BDA-366 is a potent and selective small-molecule antagonist of the Bcl2-BH4 domain, it binds to BH4 with high affinity and selectivity. The BH4 domain of Bcl2 is required for its antiapoptotic function, thus constituting a promising anticancer target. BDA-366 induced conformational change of BCL2 that exposed the BH3 domain, resulting in abrogation of its prosurvival function and conversion of BCL2 to a prodeath protein. In non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) cells, BDA-366 selectively bound to BCL2 with high affinity. BDA-366 induced apoptosis by BCL2-dependent BAX activation and cytochrome c release. In H460 cells, BDA-366 reduced Bcl2/IP3R binding, which then increased Ca2+ release.


Cell Assay: Human MM cell lines RPMI8226 and U266 were treated with BDA366 at increasing concentrations (0, 0.1, 0.25, 0.5μM) 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.

In VivoDelivery of BDA-366 substantially suppressed the growth of human MM xenografts in NOD-scid/IL2Rγ null mice, without significant cytotoxic effects on normal hematopoietic cells or body weight. Also, BDA-366 suppresses lung cancer growth via induction of apoptosis in animal models. The BH4 antagonist BDA-366 exhibits potent efficacy against human lung cancer in vivo without platelet reduction.
Animal modelNSG mice
Formulation & DosageDissolved in DMSO, diluted in PBS; 10 mg/kg; i.p.
ReferencesOncotarget. 2016 May 10;7(19):27753-63; Cancer Cell. 2015 Jun 8;27(6):852-63.