| Identification | Back Directory | [Name]
BDA-366 | [CAS]
1909226-00-1 | [Synonyms]
1-[[(2S)-3-(Diethylamino)-2-hydroxypropyl]amino]-4-[[(2S)-2-oxiranylmethyl]amino]-9,10-anthracenedione | [Molecular Formula]
C24H29N3O4 | [MOL File]
1909226-00-1.mol | [Molecular Weight]
423.5 |
| Chemical Properties | Back Directory | [Boiling point ]
669.4±55.0 °C(Predicted) | [density ]
1.313±0.06 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
Soluble in DMSO | [form ]
A solid | [pka]
14.21±0.20(Predicted) |
| Hazard Information | Back Directory | [Uses]
BDA-366 is a potent Bcl2 antagonist (Ki = 3.3 nM), binding Bcl2-BH4 domain with high affinity and selectivity. 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]. | [Definition]
ChEBI: BDA-366 is a member of the class of anthraquinone that is 1,4-diamino-9,10-anthraquinone in which the two amino groups are carrying 3-(diethylamino)-2-hydroxypropyl and (oxiran-2-yl)methyl substituents. It exhibits anti-cancer properties. It has a role as an antineoplastic agent and an apoptosis inducer. It is an anthraquinone, an epoxide, a tertiary amino compound, a secondary amino compound and a secondary alcohol. It is functionally related to a 9,10-anthraquinone. | [Biological Activity]
bda-366 is a selective antagonist of bcl2 bh4 domain with ki value of 3.3 nm [1].bcl2 is an important anti-apoptotic protein. bcl2 homology 4 (bh4) domain is required for its antiapoptotic function, thus acts as a promising anticancer target [1].bda-366 is a selective bcl2 inhibitor. 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 [1].in mice bearing h460 lung cancer xenografts, treatment with bda-366 (0, 10, 20, and 30 mg/kg/day) via i.p. route for 14 days induced apoptosis and potently inhibited tumor growth in a dose-dependent way. there was no significant toxicity at the maximum therapeutic dose. in tumor tissue from patients with nsclc, bda-366 synergized with rad001 and resulted in significantly greater inhibition of lung cancer growth compared with either agent alone [1]. | [IC 50]
Bcl-2: 3.3 nM (Ki) | [storage]
Store at -20°C | [References]
[1]. han b, park d, li r, et al. small-molecule bcl2 bh4 antagonist for lung cancer therapy. cancer cell, 2015, 27(6): 852-863. |
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