Capivasertib

SKU: orb1307109

描述

Capivasertib (AZD5363) is an orally active, pan-AKT inhibitor targeting Akt1, Akt2, and Akt3 with low nanomolar potency. It demonstrates antitumor efficacy in preclinical models of breast cancer and is widely used in research exploring AKT signaling in oncology, supported by both in vitro and in vivo studies.

研究领域

Cell Biology, Signal Transduction

图片与验证

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关键属性

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CAS 号	1143532-39-1
MW	428.92
纯度	99.68% (May vary between batches)
分子式	C₂₁H₂₅ClN₆O₂
SMILES	NC1(CCN(CC1)c1ncnc2[nH]ccc12)C(=O)N[C@@H](CCO)c1ccc(Cl)cc1
靶点	Akt,mTOR,Autophagy,PKA
溶解性	DMSO:130 mg/mL (303.09 mM);Ethanol:1 mg/mL (2.33 mM);10% DMSO+40% PEG300+5% Tween 80+45% Saline:8 mg/mL (18.65 mM);H2O:Insoluble

生物活性

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靶点 IC50	ROCK2:60 nM\|Akt3:7 nM (cell free)\|ROCK1:470 nM\|p70 S6K:6 nM (cell free)\|Akt1:3 nM (cell free)\|PKA:7 nM (cell free)\|Akt2:7 nM (cell free)
体内	METHODS: To assay antitumor activity in vivo, Capivasertib (100-300 mg/kg, 10% DMSO 25% w/v Kleptose HPB buffer) was administered by gavage twice daily for two weeks to nude mice harboring mammary cancer tumor BT474c. RESULTS: Capivasertib dose-dependently inhibited the growth of human tumor xenografts in vivo. METHODS: To assay antitumor activity in vivo, Capivasertib (100-300 mg/kg, 10% DMSO 25% w/v Kleptose HPB buffer) was administered by gavage to a PDGCX mouse model twice daily for twenty days. RESULTS: Capivasertib monotherapy resulted in 60% tumor growth inhibition.
体外	METHODS: Six strains of human gastric cancer cells were treated with Capivasertib (40 nM-50 µM) for 72 h. Cell viability was measured by SRB Assay. RESULTS: The IC50 of Capivasertib on HGS27, AGS, N87, SNU-1, MKN45, and MGC803 cells were 4.6/0.1/14.18/24.04/30.0/44.4 µM, respectively. METHODS: Breast cancer cells BT474c and prostate cancer cells LNCaP were treated with Capivasertib (0.03-10 µmol/L) for 2 h, and the expression levels of target proteins were detected by Western Blot. RESULTS: Capivasertib effectively inhibited the phosphorylation of S6 and 4E-BP1 in the cell lines, while it increased the phosphorylation of AKT at ser473 and thr308.
细胞研究	A high-throughput screening cell-based assay was developed to measure cellular AKT activity using the MDA-MB-468 breast cancer cell line. Cells were exposed to AZD5363 at concentrations ranging from 3 to 0.003 μmol/L. After a 2-hour treatment, cells were fixed with formaldehyde, washed, permeabilized with 0.5% polysorbate 20 and then probed with a phospho-specific antibody against GSK3βser9. Levels of phosphorylated GSK3βser9 were measured with an Acumen Explorer laser scanning cytometer and IC50 values estimates by fitting data in Origin 7.0.
动物研究	When mean tumor sizes reached approximately 0.2 cm^3, the mice were randomized into control and treatment groups. The treatment groups received varying dose schedules of AZD5363 solubilized in a 10% DMSO 25% w/v Kleptose HPB buffer by oral gavage, docetaxel solubilized in 2.6% ethanol in injectable water by intravenous injection once on day 1 at 15 or 5 mg/kg once weekly. When administered in combination, docetaxel was administered 1 hour before the oral dose of AZD5363. The control group received the DMSO/Kleptose buffer alone, twice daily by oral gavage. Tumor volumes (measured by caliper), animal body weight, and tumor condition were recorded twice weekly for the duration of the study. Mice were sacrificed by CO2 euthanasia. The tumor volume was calculated (taking length to be the longest diameter across the tumor and width to be the corresponding perpendicular diameter) using the formula: (length × width) × √(length × width) × (π/6). Growth inhibition from the start of treatment was assessed by comparison of the differences in tumor volume between control and treated groups. Because the variance in mean tumor volume data increases proportionally with volume (and is therefore disproportionate between groups), data were log transformed to remove any size dependency before statistical evaluation. Statistical significance was evaluated using a one-tailed, 2-sample t-test.

储存与操作

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储存	-20°C
有效期	12 months from date of receipt.
免责声明	For research use only

别名

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Inhibitor, inhibit, mTOR (p70S6K), Akt, AZD 5363, Autophagy, AZD5363, AZD-5363, Akt1, Akt2, Akt3, Capivasertib, Protein kinase B, PKB, PKA

相似产品

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(R)-Capivasertib [orb3143389]
CAS 号：
1143532-51-7
MW:
428.92
分子式：
C₂₁H₂₅ClN₆O₂
可选规格： 50 mg, 10 mg
DHRS11-IN-1 [orb3211420]
可选规格： 10 mg, 50 mg
Capivasertib [orb3229770]
纯度：
>98%
CAS 号：
1143532-39-1
MW:
428.9
分子式：
C₂₁H₂₅ClN₆O₂
可选规格： 5 mg, 25 mg
AZD-5363 [orb1226921]
纯度：
>98% (HPLC)
CAS 号：
1143532-39-1
MW:
428.92
分子式：
C₂₁H₂₅ClN₆O₂
可选规格： 5 mg, 10 mg, 25 mg, 50 mg, 100 mg, 200 mg, 500 mg, 1 g, 2 mg

质量保证

Explore bioreagents carefree to elevate your research. All our products are rigorously tested for performance. If a product does not perform as described on its datasheet, our scientific support team will provide expert troubleshooting, a prompt replacement, or a refund. For full details, please see our 条款与条件和选购指南.

化合物标识

PubChem CID

25227436 ↗

关键属性

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暂无计算属性。

实验方案信息

查看更多实验方案

Petros A Tyrakis 1, Domen Kampjut 1, Georgina F Steele 1, H Jonathan G Lindström 1, Deborah Chirnomas 1, Benjamin D Hopkins 2, Marcus D Goncalves 3, Siddhartha Mukherjee 4, Lewis C Cantley 5, Oliver D K Maddocks 6 Multi-node inhibition targeting mTORC1, mTORC2 and PI3Kα potently inhibits the PI3K/AKT/mTOR pathway in endometrial and breast cancer models Br J Cancer ., (2025)

PubMed: 40360883

CAS 号：	1143532-51-7
MW:	428.92
分子式：	C₂₁H₂₅ClN₆O₂

纯度：	>98%
CAS 号：	1143532-39-1
MW:	428.9
分子式：	C₂₁H₂₅ClN₆O₂

纯度：	>98% (HPLC)
CAS 号：	1143532-39-1
MW:	428.92
分子式：	C₂₁H₂₅ClN₆O₂

Capivasertib

描述

研究领域

图片与验证

关键属性

生物活性

储存与操作

别名

相似产品

(R)-Capivasertib [orb3143389]

DHRS11-IN-1 [orb3211420]

Capivasertib [orb3229770]

AZD-5363 [orb1226921]

质量保证

化合物标识

关键属性

实验方案信息

可选规格