产品
编 号：F618262
分子式：C17H14Cl2FN3OS
分子量：398.28
分子式：C17H14Cl2FN3OS
分子量：398.28
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
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5mg
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10mg
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25mg
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结构图
CAS No: 2411853-34-2
产品详情
生物活性：
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 decreases the phosphorylation level of Akt, decreases MMP2 activity, thereby reducing the ability of tumor cells to migrate and invade. JR-AB2-011 also induces non-apoptotic cell death.
体内研究：
JR-AB2-011 (20 mg/kg; i.p; 每天) 减少了 注射 B16 细胞的 C57BL/6N 小鼠的肝脏转移的大小和数量。没有严重的副作用或体重损失。JR-AB2-011 (4 mg/kg; p.o.; 每天) 显着阻断 Dioscin 诱导的 M2 巨噬细胞极化的促进作用。Animal Model:C57BL/6N mice with injection of B16 cells .
Dosage:20 mg/kg everyday
Administration:i.p.
Result:JR-AB2-011 resulted in a significant decrease in hepatic tumor burden and metastasis load, as assessed by MRI and BLI. Histological analysis confirmed the presence of fewer and smaller metastases in the liver of treated mice. MMP2 expression was also significantly reduced.
Animal Model:DSS (dextran sulfate sodium) induced colitis in mice
Dosage:4 mg/kg; Dioscin 160 mg/kg; daily
Administration:p.o.
Result:JR-AB2-011 significantly blocked the Dioscin-induced promotion of M2 macrophage polarization.JR-AB2-011 inhibited the mTORC2/PPAR-γ signaling pathway, attenuating the regulatory effects of Dioscin on macrophage metabolism and polarization. The decrease in inflammation-related biomarkers (e.g., TNF-α, IL-6, IFN-γ, etc.) was partially reversed, indicating that the anti-inflammatory effects of Dioscin were suppressed.
体外研究：
JR-AB2-011 (10 μM - 250 μM; 48h) 显著降低了不同黑素瘤细胞系 （MelJu, MelJuso, MelIm, B16） 的存活率和增殖能力。 JR-AB2-011 (50 μM, 250 μM; 48 h) MelIm 细胞中 Akt 的磷酸化水平降低，说明 mTORC2 的抑制减弱了 Akt 信号通路。JR-AB2-011 (50 μM, 250 μM; 48-78 h) 处理后细胞存活分数 SF 显著减少，黑素瘤细胞的迁移和侵袭能力显著减少，主要通过降低 MMP2 的活性实现。
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 decreases the phosphorylation level of Akt, decreases MMP2 activity, thereby reducing the ability of tumor cells to migrate and invade. JR-AB2-011 also induces non-apoptotic cell death.
体内研究：
JR-AB2-011 (20 mg/kg; i.p; 每天) 减少了 注射 B16 细胞的 C57BL/6N 小鼠的肝脏转移的大小和数量。没有严重的副作用或体重损失。JR-AB2-011 (4 mg/kg; p.o.; 每天) 显着阻断 Dioscin 诱导的 M2 巨噬细胞极化的促进作用。Animal Model:C57BL/6N mice with injection of B16 cells .
Dosage:20 mg/kg everyday
Administration:i.p.
Result:JR-AB2-011 resulted in a significant decrease in hepatic tumor burden and metastasis load, as assessed by MRI and BLI. Histological analysis confirmed the presence of fewer and smaller metastases in the liver of treated mice. MMP2 expression was also significantly reduced.
Animal Model:DSS (dextran sulfate sodium) induced colitis in mice
Dosage:4 mg/kg; Dioscin 160 mg/kg; daily
Administration:p.o.
Result:JR-AB2-011 significantly blocked the Dioscin-induced promotion of M2 macrophage polarization.JR-AB2-011 inhibited the mTORC2/PPAR-γ signaling pathway, attenuating the regulatory effects of Dioscin on macrophage metabolism and polarization. The decrease in inflammation-related biomarkers (e.g., TNF-α, IL-6, IFN-γ, etc.) was partially reversed, indicating that the anti-inflammatory effects of Dioscin were suppressed.
体外研究：
JR-AB2-011 (10 μM - 250 μM; 48h) 显著降低了不同黑素瘤细胞系 （MelJu, MelJuso, MelIm, B16） 的存活率和增殖能力。 JR-AB2-011 (50 μM, 250 μM; 48 h) MelIm 细胞中 Akt 的磷酸化水平降低，说明 mTORC2 的抑制减弱了 Akt 信号通路。JR-AB2-011 (50 μM, 250 μM; 48-78 h) 处理后细胞存活分数 SF 显著减少，黑素瘤细胞的迁移和侵袭能力显著减少，主要通过降低 MMP2 的活性实现。
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