| Chemical Properties | Back Directory | [Boiling point ]
1144.1±65.0 °C(Predicted) | [density ]
1.41±0.1 g/cm3(Predicted) | [form ]
Solid | [pka]
6.22±0.30(Predicted) | [color ]
White to yellow | [InChIKey]
IVARZBJJMMUJHI-SSIILETPNA-N | [SMILES]
NC1N=NC(C2C=CC=CC=2O)=CC=1N1CCN(CC2C=CC(OCCOC3C=C(C4SC=NC=4C)C=CC=3CNC([C@@H]3C[C@@H](O)CN3C(=O)[C@H](C(C)(C)C)NC(C3(CC3)F)=O)=O)=CC=2)CC1 |&1:42,44,50,r| |
| Hazard Information | Back Directory | [Uses]
ACBI1 is a potent and cooperative SMARCA2, SMARCA4 and PBRM1 degrader with DC50s of 6, 11 and 32 nM, respectively. ACBI1 is a PROTAC degrader. ACBI1 shows anti-proliferative activity. ACBI1 induces apoptosis[1]. | [Definition]
ACBI1 is a potent and cooperative SMARCA2, SMARCA4 and PBRM1 degrader with DC50s of 6, 11 and 32 nM, respectively. ACBI1 is a PROTAC degrader. ACBI1 shows anti-proliferative activity and can induce apoptosis. It induced anti-proliferative effects and cell death caused by SMARCA2 depletion in SMARCA4 mutant cancer cells and acute myeloid leukemia cells dependent on SMARCA4 ATPase activity[1]. | [References]
[1] William Farnaby. “BAF complex vulnerabilities in cancer demonstrated via structure-based PROTAC design.” Nature chemical biology 15 7 (2019): 672–680.
[2] M. Koegl. “Abstract 3849: Structure-based PROTAC design demonstrates BAF complex ATPase vulnerabilities in cancer.” Experimental and Molecular Therapeutics 36 1 (2019). |
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