JR-AB2-011 是一种选择性 mTORC2 抑制剂，IC50 值为 0.36 μM。 JR-AB2-011 通过阻断 Rictor-mTOR 结合来抑制 mTORC2 活性（Ki:0.19 μM）。 JR-AB2-011 具有抗多形性胶质母细胞瘤 (GBM) 特性。
货号:ajcx13638
CAS:N/A
分子式:C17H14Cl2FN3OS
分子量：398.28
溶解度:DMSO : 62.5 mg/mL (156.92 mM);H2O :< 0.1 mg/mL (insoluble)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

JR-AB2-011 is a selective mTORC2 inhibitor with an IC50 value of 0.36 μM. JR-AB2-011 inhibits mTORC2 activity by blocking Rictor-mTOR association (Ki: 0.19 μM). JR-AB2-011 has anti-glioblastoma multiforme (GBM) properties[1]. mTORC2|0.36 μM (IC50)

JR-AB2-011 (1 μM; 24 hours) has good anti-GBM properties, blocks mTORC2 signaling and Rictor association with mTOR[1].JR-AB2-011 (0.5-2 μM; 48 hours) displays the least toxicity to normal neurons with no significant cytotoxic effects for concentrations up to 10 mM compared to CID613034[1]. Apoptosis Analysis[1] Cell Line: U87 GBM cells; LN229 GBM cells

Mice receiving JR-AB2-011 (4 mg/kg; daily i.p. for 10 days; 20 mg/kg; daily i.p. for 10 days) at either dosing regimen display marked inhibition of tumor growth rate (JR-AB2-011 at 4 mg/kg/d; 74% inhibition at end of dosing period; tumor growth delay 10.0 days; JR-AB2-011 at 20 mg/kg/d; 80% inhibition at end of dosing period; tumor growth delay 12.0 days) as compared to mice receiving vehicle alone[1]. Animal Model: LN229 cells in female C.B.-17-scid (Taconic) mice[1]

[1]. Benavides-Serrato A, et al. Specific blockade of Rictor-mTOR association inhibits mTORC2 activity and is cytotoxic in glioblastoma. PLoS One. 2017 Apr 28;12(4):e0176599.