1. PI3K/Akt/mTOR
  2. Akt

AZD5363 (Synonyms: Capivasertib)

Cat. No.: HY-15431 Purity: 99.71%
Handling Instructions

AZD5363 is a potent pan-AKT kinase inhibitor with IC50 of 3, 7 and 7 nM for Akt1,Akt2 and Akt3, respectively.

For research use only. We do not sell to patients.
AZD5363 Chemical Structure

AZD5363 Chemical Structure

CAS No. : 1143532-39-1

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Free Sample (0.5-1 mg)   Apply now  
10 mM * 1 mL in DMSO USD 106 In-stock
5 mg USD 96 In-stock
10 mg USD 144 In-stock
50 mg USD 360 In-stock
100 mg USD 600 In-stock
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    AZD5363 purchased from MCE. Usage Cited in: Oncotarget. 2016 May 17;7(20):29131-42.

    A674563 selectively inhibits FLT3-ITD. Inhibitory Effects of A674563 against auto-phosphorylation of FLT3 wt/mt kinases in the FLT3 wt/mt transformed BaF3 isogenic cell lines.

    View All Akt Isoform Specific Products:

    • Biological Activity

    • Protocol

    • Technical Information

    • Purity & Documentation

    • References


    AZD5363 is a potent pan-AKT kinase inhibitor with IC50 of 3, 7 and 7 nM for Akt1,Akt2 and Akt3, respectively.

    IC50 & Target[1]


    3 nM (IC50)


    7 nM (IC50)


    7 nM (IC50)


    6 nM (IC50)


    7 nM (IC50)


    60 nM (IC50)


    470 nM (IC50)



    In Vitro

    AZD5363, a novel pyrrolopyrimidine-derived compound, inhibits all AKT isoforms with a potency of 10 nM or less and inhibits phosphorylation of AKT substrates in cells with a potency of approximately 0.3 to 0.8 μM. AZD5363 inhibits phosphorylation of these substrates with an IC50 value of 0.06 to 0.76 μM in the 3 cell lines. AZD5363 effectively inhibits phosphorylation of S6 and 4E-BP1 in these cell lines, whereas it increases phosphorylation of AKT at both ser473 and thr308. In BT474c cells, AZD5363 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. AZD5363 inhibits S6 phosphorylation with an IC50 value of approximately 4.8 μM, whereas the allosteric inhibitor MK-2206 is much less active (IC50>30 μM)[1].

    In Vivo

    Oral dosing of 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[18F]fluoro-2-deoxy-D-glucose (18F-FDG) uptake in U87-MG xenografts. Chronic oral dosing of AZD5363 caused dose-dependent growth inhibition of xenografts derived from various tumor types, including HER2+ breast cancer models that are resistant to trastuzumab. AZD5363 also significantly enhances the antitumor activity of docetaxel, lapatinib, and trastuzumab in breast cancer xenografts[1].

    Clinical Trial
    Preparing Stock Solutions
    Concentration Volume Mass 1 mg 5 mg 10 mg
    1 mM 2.3314 mL 11.6572 mL 23.3144 mL
    5 mM 0.4663 mL 2.3314 mL 4.6629 mL
    10 mM 0.2331 mL 1.1657 mL 2.3314 mL
    Please refer to the solubility information to select the appropriate solvent.
    Kinase Assay

    The ability of AZD5363 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 contain 1 to 3 nM AKT1, AKT2, or AKT3 enzymes; 1.5 μM peptide substrate; ATP at Km for each AKT isoform; 10 mM MgCl2, 4 mM dithiothreitol (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. To determine the kinase selectivity profile, AZD5363 is also tested against PKA, ROCK1, ROCK2, and P70S6K. PKA, ROCK1, and ROCK2 activity are determined by Caliper Off-Chip Incubation Mobility Shift Assay[1]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Cell Assay

    AZD5363 is prepared in DMSO (10 mM) and stored under nitrogen. The final concentration of DMSO is less than 0.5%[1].

    Cell proliferation assay is determined by 2 methods, MTS and Sytox Green. Briefly, cells are seeded in 96-well plates (at a density to allow for logarithmic growth during the 72-hour assay) and incubated overnight at 37°C, 5% CO2. Cells are then exposed to concentrations of AZD5363 ranging from 30 to 0.003 μM for 72 hours. For the MTS endpoint, cell proliferation is measured by the CellTiter AQueous Non-Radioactive Cell Proliferation Assay reagent. Absorbance is measured with a Tecan Ultra instrument. 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 (GI50) values are determined using absorbance readings (MTS) or live cell counts[1]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration

    AZD5363 is solubilized in a 10% DMSO 25% w/v Kleptose HPB[1].

    Specific, pathogen-free, female nude mice (nu/nu: Alpk) and male SCID mice (SCID/CB17; 786-0 xenograft studies) are used. When mean tumor sizes reach approximately 0.2 cm3, the mice are 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 (Roquette) 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 is 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 are recorded twice weekly for the duration of the study. Mice are sacrificed by CO2 euthanasia. The tumor volume is 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 is assessed by comparison of the differences in tumor volume between control and treated groups. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Molecular Weight




    CAS No.



    O=C(C1(N)CCN(C2=C3C(NC=C3)=NC=N2)CC1)N[[email protected]](C4=CC=C(Cl)C=C4)CCO

    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month

    Room temperature in continental US; may vary elsewhere

    Solvent & Solubility

    DMSO: ≥ 10 mg/mL

    * "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

    Purity: 99.71%

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