产品
编 号：F744908
分子式：C35H41Cl3N8O
分子量：696.11
分子式：C35H41Cl3N8O
分子量：696.11
产品类型
规格
价格
是否有货
1mg
询价
询价
5mg
询价
询价
10mg
询价
询价
50mg
询价
询价
结构图
CAS No: 1416775-08-0
产品详情
生物活性：
Vevorisertib (ARQ 751) trihydrochloride is a selective, allosteric, pan-AKT and AKT1-E17K mutant inhibitors. Vevorisertib trihydrochloride potently inhibit phosphorylation of AKT. Vevorisertib trihydrochloride has Kd values of 1.2 nM and 8.6 nM for AKT1 and AKT1-E17K, respectively. Vevorisertib trihydrochloride has IC50 values of 0.55, 0.81, and 1.3 nM for AKT1, AKT2, and AKT3, respectively. Vevorisertib trihydrochloride can be used for the research of cancer.
体内研究：
Vevorisertib trihydrochloride (25, 50 and 75 mg/kg; p.o.; 5 days dosing followed by a 4 day dosing holiday for 20 days) shows potent tumor growth inhibition of 68, 78 and 98%, respectively.Vevorisertib trihydrochloride (5, 10, 20, 40, 80, and 120 mg/kg; p.o. daily for ten days) shows tumor growth inhibition of 29, 33, 50, 73, 83, and 92%, respectively.Vevorisertib trihydrochloride reachs Cmax plasma concentrations of ≥2 μM.Vevorisertib trihydrochloride is generally well-tolerated at dose levels up to 120 mg/kg.Vevorisertib trihydrochloride (MK-4440)/IM combination shows superior efficacy in an IM-sensitive preclinical model of GIST compared with either single agent.Animal Model:Endometrial PDX mouse xenograft models (AKT1-E17K mutation tumor fragments subcutaneously implanted in athymic nude mice; tumor volume of approximately 200 mm3)
Dosage:25, 50 and 75 mg/kg
Administration:p.o.; 5 days dosing followed by a 4 day dosing holiday for 20 days
Result:Showed potent tumor growth inhibition of 68, 78 and 98%, respectively.
Animal Model:AN3CA mouse xenograft models (female NCr nu/nu mice with 250 mm3 tumors size)
Dosage:5, 10, 20, 40, 80, and 120 mg/kg
Administration:p.o.; daily for ten days
Result:Showed tumor growth inhibition of 29, 33, 50, 73, 83, and 92%, respectively.
体外研究：
Vevorisertib trihydrochloride (0, 12, 33, 111, 333, 1000 nM, 2 hours) inhibits phosphorylation of AKT1-E17K.Vevorisertib trihydrochloride (1 μM for 2 hours; NIH 3T3 cells are transfected with either pcDNAAKT-WT-GFP or pcDNA-E17K-GFP) inhibits plasma membrane translocation of AKT-WT and AKT1-E17K irrespective of the presence of growth factors.Vevorisertib trihydrochloride (5 μM) exhibites 57% inhibition of full-length AKT1.Vevorisertib trihydrochloride (0, 0.012, 0.037, 0.11, 0.33, 1 μM; 2 hours) shows a dose-dependent effect on mTORC1 and AKT direct substrates including PRAS40, GSK3β, FOXO, BAD, and AS160 in cancer cell lines.Vevorisertib trihydrochloride has anti-proliferative effect on esophageal, breast, and head and neck cancer cells (GI50 Vevorisertib trihydrochloride 相关抗体:Western Blot AnalysisCell Line:293T cells (transiently transfected with pcDNA-E17K-GFP)
Concentration:0, 12, 33, 111, 333, 1000 nM
Incubation Time:2 hours
Result:Inhibited phosphorylation of AKT1-E17K.
Western Blot AnalysisCell Line:Cancer cell lines: MDA-MB 453 (PIK3CAH1047R; Her2 amp), NCI-H1650 (PTEN null), KU-19-19 (AKT1-E17K&E49K; NRas Q61R)
Concentration:0, 0.012, 0.037, 0.11, 0.33, 1 μM
Incubation Time:2 hours
Result:Showed a dose-dependent effect on mTORC1 and AKT direct substrates including PRAS40, GSK3β, FOXO, BAD, and AS160.
Vevorisertib (ARQ 751) trihydrochloride is a selective, allosteric, pan-AKT and AKT1-E17K mutant inhibitors. Vevorisertib trihydrochloride potently inhibit phosphorylation of AKT. Vevorisertib trihydrochloride has Kd values of 1.2 nM and 8.6 nM for AKT1 and AKT1-E17K, respectively. Vevorisertib trihydrochloride has IC50 values of 0.55, 0.81, and 1.3 nM for AKT1, AKT2, and AKT3, respectively. Vevorisertib trihydrochloride can be used for the research of cancer.
体内研究：
Vevorisertib trihydrochloride (25, 50 and 75 mg/kg; p.o.; 5 days dosing followed by a 4 day dosing holiday for 20 days) shows potent tumor growth inhibition of 68, 78 and 98%, respectively.Vevorisertib trihydrochloride (5, 10, 20, 40, 80, and 120 mg/kg; p.o. daily for ten days) shows tumor growth inhibition of 29, 33, 50, 73, 83, and 92%, respectively.Vevorisertib trihydrochloride reachs Cmax plasma concentrations of ≥2 μM.Vevorisertib trihydrochloride is generally well-tolerated at dose levels up to 120 mg/kg.Vevorisertib trihydrochloride (MK-4440)/IM combination shows superior efficacy in an IM-sensitive preclinical model of GIST compared with either single agent.Animal Model:Endometrial PDX mouse xenograft models (AKT1-E17K mutation tumor fragments subcutaneously implanted in athymic nude mice; tumor volume of approximately 200 mm3)
Dosage:25, 50 and 75 mg/kg
Administration:p.o.; 5 days dosing followed by a 4 day dosing holiday for 20 days
Result:Showed potent tumor growth inhibition of 68, 78 and 98%, respectively.
Animal Model:AN3CA mouse xenograft models (female NCr nu/nu mice with 250 mm3 tumors size)
Dosage:5, 10, 20, 40, 80, and 120 mg/kg
Administration:p.o.; daily for ten days
Result:Showed tumor growth inhibition of 29, 33, 50, 73, 83, and 92%, respectively.
体外研究：
Vevorisertib trihydrochloride (0, 12, 33, 111, 333, 1000 nM, 2 hours) inhibits phosphorylation of AKT1-E17K.Vevorisertib trihydrochloride (1 μM for 2 hours; NIH 3T3 cells are transfected with either pcDNAAKT-WT-GFP or pcDNA-E17K-GFP) inhibits plasma membrane translocation of AKT-WT and AKT1-E17K irrespective of the presence of growth factors.Vevorisertib trihydrochloride (5 μM) exhibites 57% inhibition of full-length AKT1.Vevorisertib trihydrochloride (0, 0.012, 0.037, 0.11, 0.33, 1 μM; 2 hours) shows a dose-dependent effect on mTORC1 and AKT direct substrates including PRAS40, GSK3β, FOXO, BAD, and AS160 in cancer cell lines.Vevorisertib trihydrochloride has anti-proliferative effect on esophageal, breast, and head and neck cancer cells (GI50 Vevorisertib trihydrochloride 相关抗体:Western Blot AnalysisCell Line:293T cells (transiently transfected with pcDNA-E17K-GFP)
Concentration:0, 12, 33, 111, 333, 1000 nM
Incubation Time:2 hours
Result:Inhibited phosphorylation of AKT1-E17K.
Western Blot AnalysisCell Line:Cancer cell lines: MDA-MB 453 (PIK3CAH1047R; Her2 amp), NCI-H1650 (PTEN null), KU-19-19 (AKT1-E17K&E49K; NRas Q61R)
Concentration:0, 0.012, 0.037, 0.11, 0.33, 1 μM
Incubation Time:2 hours
Result:Showed a dose-dependent effect on mTORC1 and AKT direct substrates including PRAS40, GSK3β, FOXO, BAD, and AS160.
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