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商品描述
AMG232
- Catalog No.：MC1217
- Data Sheet
- MSDS
- Support
- Description
- References ( 0 )
- Protocol
- CasNo：
- 1352066-68-2
- MolecularFormula：
- C28H35Cl2NO5S
- Purity：
- >98%
- Target：
- MDM-2/p53
- IC50：
- No data
- In Vitro：
- AMG 232 (10 μM) induces p53 signaling and inhibits tumor cell proliferation in three p53 wild-type tumor cell lines (SJSA-1, HCT116, and ACHN)[1]. AMG 232 significantly inhibits the human MDM2-p53 interaction in the biochemical HTRF-based assay (IC50=0.6 nM). AMG 232 potently inhibits proliferation of non-MDM2-amplified HCT116 colorectal cells in the BrdU assay (IC50=10 nM)[3].
- In Vivo：
- AMG 232 (10, 25, 75 mg/kg, p.o.) activates p53 pathway activity in vivo. AMG 232 (100 mg/kg, p.o.) results in 86% TGI compared with control, and the ED50 is 31 mg/kg in the HCT116 colorectal cancer model (KRAS mutant), and results in 97% TGI, with an ED50 of 18 mg/kg in an A375sq2 BRAF-mutant melanoma model[1]. AMG 232 exhibits low clearance (<0.25 × qh) and="" moderate="" to="" high="" oral="" bioavailability="" in="" mice,="" rats="" and="" monkeys="" (="">42%), but high clearance (0.74 × Qh) and low oral exposure in dogs (18%)[2]. AMG 232 displays robust tumor growth inhibition compared to the vehicle, with an ED50 of 9.1 mg/kg q.d. AMG 232 causes a dose-dependent tumor growth inhibition with an ED50 of 16 mg/kg[3].
- Fields：
- AMG232 is a potent, selective and orally bioavailable inhibitor of MDM2−p53 interaction with IC50 value of 9.1 nM in EdU cells .
- Specificity：
- Target:MDM-2/p53. Fields: AMG232 is a potent, selective and orally bioavailable inhibitor of MDM2−p53 interaction with IC50 value of 9.1 nM in EdU cells .
- Source：
- Rabbit
- Dilution：
- WB 1:500-2000
- Concentration：
- >98%
- Storage Stability：
- 2 years -20°C Powder, 2 weeks4°C in DMSO,6 months-80°C in DMSO
- Other Name：
- AMG-232,AMG 232
- MolecularWeight(Da)：
- 568.55
- References：
- [1]. Canon J, et al. The MDM2 Inhibitor AMG 232 Demonstrates Robust Antitumor Efficacy and Potentiates the Activity of p53-Inducing Cytotoxic Agents. Mol Cancer Ther. 2015 Mar;14(3):649-58.[2]. Ye Q,
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