Cytoskeletal Signaling Akt Capivasertib


Catalog No. T1920   CAS 1143532-39-1
Synonyms: AZD5363

Capivasertib (AZD5363) is a new-type orally available inhibitor of the serine/threonine protein kinase AKT (IC50s: 3/7/7 nM for Akt1/2/3).

Capivasertib, CAS 1143532-39-1
Pack Size Availability Price/USD Quantity
1 mg In stock 43.00
2 mg In stock 52.00
5 mg In stock 72.00
10 mg In stock 112.00
25 mg In stock 190.00
50 mg In stock 288.00
100 mg In stock 480.00
1 mL * 10 mM (in DMSO) In stock 72.00
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Purity 97.59%
Purity 99.60%
Purity 99.48%
Purity 98.00%
Purity 99.29%
Biological Description
Chemical Properties
Storage & Solubility Information
Description Capivasertib (AZD5363) is a new-type orally available inhibitor of the serine/threonine protein kinase AKT (IC50s: 3/7/7 nM for Akt1/2/3).
Targets&IC50 Akt1 ,   Akt2 ,   Akt3 ,   ROCK2
Kinase Assay Caliper Off-Chip Incubation Mobility Shift assay: The ability of AZD5363 and other compounds to inhibit the activity of AKT1, AKT2, and AKT3 is evaluated by the Caliper Off-Chip Incubation Mobility Shift assay. Active recombinant AKT1, AKT2, or AKT3 are incubated with a 5-FAM-labeled custom-synthesized peptide substrate together with increasing concentrations of inhibitor. Final reactions contained 1 to 3 nM AKT1, AKT2, or AKT3 enzymes; 1.5 mM peptide substrate; ATP at K m for each AKT isoform; 10 mM MgCl2, 4 mM DTT, 100 mM HEPES, and 0.015% Brij-35. The reactions are incubated at room temperature for 1 hour and stopped by the addition of buffer containing 100 mM HEPES, 0.015% Brij-35 solution, 0.1% coating reagent, 40 mM EDTA, and 5% DMSO. Plates are then analyzed using a Caliper LC3000, allowing for separation of peptide substrate and phosphorylated product by electrophoresis with subsequent detection and quantification of laser induced fluorescence.
Cell Research
Cell proliferation assay is determined by 2 methods, MTS and Sytox Green. Briefly, cells are seeded in 96-well plates and incubated overnight at 37 ℃, 5% CO2. Cells are then exposed to concentrations of AZD5363 ranging from 30 to 0.003μM for 72 hours. For the MTS endpoint, cell proliferation is measured by the CellTiter AQueous Non-Radioactive Cell Proliferation Assay reagent in accordance with the manufacturer's protocol. For the Sytox Green endpoint, Sytox Green nucleic acid dye diluted in TBS-EDTA buffer is added to cells (final concentration of 0.13 μM) and the number of dead cells detected using an Acumen Explorer. Cells are then permeabilized by the addition of saponin (0.03% final concentration, diluted in TBS-EDTA buffer), incubated overnight and a total cell count measured. Predose measurements are made for both MTS and Sytox Green endpoints, and concentration needed to reduce the growth of treated cells to half that of untreated cells values are determined using absorbance readings (MTS) or live cell counts.(Only for Reference)
Cell lines: 182 solid and hematologic tumor cell lines
Synonyms AZD5363
Purity 97.59%
Molecular Weight 428.92
Formula C21H25ClN6O2
CAS No. 1143532-39-1


0-4℃ for short term (days to weeks), or -20℃ for long term (months).

Solubility Information

DMSO: 80 mg/mL (186.5 mM)

Ethanol: 1 mg/mL

Water: Insoluble

( < 1 mg/ml refers to the product slightly soluble or insoluble )


References and Literature
1. Davies BR, et al. Preclinical pharmacology of AZD5363, an inhibitor of AKT: pharmacodynamics, antitumor activity, and correlation of monotherapy activity with genetic background. Mol Cancer Ther. 2012 Apr;11(4):873-87. 2. Wang J, Xu X, Wang T, et al. Ceritinib increases sensitivity of AKT inhibitors to gastric cancer[J]. European Journal of Pharmacology. 2021: 173879. 3. Luo Q, Wu X, Nan Y, et al. TRIM32/USP11 Balances ARID1A Stability and the Oncogenic/Tumor-Suppressive Status of Squamous Cell Carcinoma[J]. Cell Reports. 2020, 30(1): 98-111. e5. 4. Weng Q, Zhao M, Zheng J, et al. STAT3 dictates β-cell apoptosis by modulating PTEN in streptozocin-induced hyperglycemia[J]. Cell Death & Differentiation. 2020, 27(1): 130-145.

Related compound libraries

This product is contained In the following compound libraries:
Bioactive Compound Library Inhibitor Library Anti-cancer Compound Library Clinical Compound Library Anti-diabetic Compound Library Stem cell Differentiation Compound Library Autophagy Compound Library Oxidation-Reduction Compound Library PI3K-AKT-mTOR Compound Library Kinase Inhibitor Library Anti-cancer Clinical Compound Library Anti-cancer Metabolism Compound Library Preclinical Compound Library TGF-beta/Smad Compound Library Cell cycle related Compound Library Promoting Cancer Cell Differentiation Compound Library Anti-obesity Compound Library Neural Regeneration Compound Library Anti-aging Compound Library Anti-cancer Active Compound library Anti-cancer Drug library Drug Repurposing Library HIF-1 Signaling Pathway Compound Library Anti-Lung Cancer Compound Library Glycometabolism Compound Library Anti-Breast Cancer Compound Library Anti-Pancreatic Cancer Compound Library Cytoskeletal Signaling Pathway Compound Library Glutamine Metabolism Compound Library

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