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抑制剂/激活剂

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凋亡与自噬

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Capivasertib AZD5363

Capivasertib (AZD5363)有效抑制Akt(Akt1/Akt2/3)的所有亚型，在无细胞试验中IC50为3 nM/8 nM/8 nM，对P70S6K/PKA也具有相似的抑制效果，而对ROCK1/2抑制活性较低。Phase 2

货号：
TK0405
规格：

1mg

2mg

5mg

10mg

50mg
价格：
￥0.00

产品参数

CAS No.	1143532-39-1
生物活性	Capivasertib (AZD5363) is an orally active and potent pan-AKT kinase inhibitor with IC50 of 3, 7 and 7 nM for Akt1,Akt2 and Akt3, respectively.
分子式	C21H25ClN6O2
分子量	428.92
储存条件	Powder -20℃ 3 years
溶解性数据	DMSO : 125 mg/mL (291.43 mM; Need ultrasonic)
体内研究	Oral dosing of Capivasertib (AZD5363) to nude mice causes dose- and time-dependent reduction of PRAS40, GSK3β, and S6 phosphorylation in BT474c xenografts (PRAS40 phosphorylation EC50 ~0.1 μM total plasma exposure), reversible increases in blood glucose concentrations, and dose-dependent decreases in 2[F]fluoro-2-deoxy-D-glucose (F-FDG) uptake in U87-MG xenografts. Chronic oral dosing of Capivasertib caused dose-dependent growth inhibition of xenografts derived from various tumor types, including HER2 breast cancer models. Capivasertib also significantly enhances the antitumor activity of RP-56976 and GW572016 in breast cancer xenografts.
体外研究	Capivasertib, a novel pyrrolopyrimidine-derived compound, inhibits all AKT isoforms with a potency of 10 nM or less. Capivasertib inhibits phosphorylation of these substrates with an IC50 value of 0.06 to 0.76 μM in the 3 cell lines. Capivasertib effectively inhibits phosphorylation of S6 and 4E-BP1 in these cell lines, whereas it increases phosphorylation of AKT at both ser and thr. In BT474c cells, Capivasertib induces FOXO3a nuclear translocation with EC50 value of 0.69 μM; a concentration of 3 μM is sufficient to almost completely localize FOXO3a to the nucleus. AZD5363Capivasertibhibitor MK-2206 is much less active (IC50>30 μM).
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纯度及产品资料	98%

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