1. PI3K/Akt/mTOR
  2. mTOR
  3. WYE-132

WYE-132 (Synonyms: WYE-125132)

Cat. No.: HY-10044 Purity: 98.61%
Handling Instructions

WYE-132 (WYE-125132) is a highly potent, ATP-competitive, and specific mTOR kinase inhibitor (IC50: 0.19±0.07 nM; >5,000-fold selective versus PI3Ks). WYE-132 (WYE-125132) inhibits mTORC1 and mTORC2.

For research use only. We do not sell to patients.

WYE-132 Chemical Structure

WYE-132 Chemical Structure

CAS No. : 1144068-46-1

Size Price Stock Quantity
10 mM * 1 mL in DMSO USD 165 In-stock
Estimated Time of Arrival: December 31
2 mg USD 108 In-stock
Estimated Time of Arrival: December 31
5 mg USD 144 In-stock
Estimated Time of Arrival: December 31
10 mg USD 252 In-stock
Estimated Time of Arrival: December 31
50 mg USD 864 In-stock
Estimated Time of Arrival: December 31
100 mg USD 1440 In-stock
Estimated Time of Arrival: December 31
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Customer Review

Based on 5 publication(s) in Google Scholar

Top Publications Citing Use of Products

    WYE-132 purchased from MCE. Usage Cited in: Patent. US20160089377A1.

    Treatment with WYE125132 rescues cellular, synaptic and molecular abnormalities in Cntnap2 mutants. Bar graphs (top) indicate that the dramatic increase in phosphorylation of S6 (Phospho-S6: S6) in the cortex of Cntnap2−/− and Cntnap2+/− mice is completely reversed with by treatment with WYE125132. In Bar graphs, each pair reflects untreated (left) and treated (right) values. Representative immunoblots are shown (bottom).

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    WYE-132 (WYE-125132) is a highly potent, ATP-competitive, and specific mTOR kinase inhibitor (IC50: 0.19±0.07 nM; >5,000-fold selective versus PI3Ks). WYE-132 (WYE-125132) inhibits mTORC1 and mTORC2.

    IC50 & Target


    0.19 nM (IC50)






    1.179 μM (IC50)


    2.38 μM (IC50)


    1.25 μM (IC50)

    In Vitro

    WYE-132 (WYE-125132) potently inhibits recombinant mTOR via an ATP-competitive mechanism. WYE-132 is a potent antiproliferative agent against a panel of cancer cell lines with IC50 values generally in the nanomolar range. In the typical 3-day dose-response studies, WYE-132 exhibits a more profound antiproliferative activity than CCI-779 in MDA361 and other cells, as shown by the sharper inhibition at doses up to 10 μM. Fluorescence-activated cell sorting (FACS) analysis of inhibitor-treated (1 μM, 24 hours) MDA468, PC3MM2, U87MG, A549, and HCT116 cells indicates that WYE-132 elicits a more profound increase in G1-phase and a reduction in S-phase cells than CCI-779. The WYE-132-induced cell death is evident at 10 and 30 nM (6.2% and 13%, respectively) and is dose dependent, reaching 47% at 1 μM and 59% at 3 μM[1].

    In Vivo

    A single i.v. administration of 50 mg/kg WYE-132 (WYE-125132) into tumor-bearing mice leads to suppression of P-S6K(T389) and P-AKT(S473) for at least 8 hours in PC3MM2, MDA361, HCT116, and HT29 tumors, whereas the steady-state level of P-AKT(T308) is not significantly reduced, indicating that the antitumor efficacy of WYE-132 under such dosing regimens reflects the suppression of mTOR rather than PI3K. Oral administration of WYE-132 causes dose-dependent tumor growth delay in the PI3K/mTOR- and HER2-hyperactive MDA361 tumors with significant antitumor activity at 5 mg/kg, which correlates with a suppression P-S6 and P-AKT(S473) but not P-AKT(T308). An optimal dose of 50 mg/kg WYE-132 induces a substantial regression of large MDA361 tumors. WYE-132 also causes a potent and substantial tumor growth delay in the PTEN-null U87MG glioma[1].

    Molecular Weight




    CAS No.





    Room temperature in continental US; may vary elsewhere.

    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 62 mg/mL (119.32 mM)

    *"≥" means soluble, but saturation unknown.

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 1.9246 mL 9.6228 mL 19.2456 mL
    5 mM 0.3849 mL 1.9246 mL 3.8491 mL
    10 mM 0.1925 mL 0.9623 mL 1.9246 mL
    *Please refer to the solubility information to select the appropriate solvent.
    Cell Assay

    Cell lines of MDA-MB-361, MDA-MB-231, MDA-MB-468, BT549, LNCap, A549, H1975, H157, H460, U87MG, A498, 786-O, HCT116, MG63, Rat1, HEK293, HeLa and PC3MM2 are used. MDA361 cells are treated for 3 d with CCI-779 and WYE-132 (0.1 nM, 1 nM, 10 nM,100 nM, 1000 nM 10μM and 100μM). Cell growth assays and IC50 determination are performed. For immunoblotting, cultured cells are treated as indicated. Total cell lysates are prepared using NuPAGE lithium dodecyl sulfate sample buffer and immunoblotted with various antibodies[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration

    For mTOR biomarker studies, various tumors (400 mm3) grown s.c. in female nude mice are dosed by a single i.v. or oral injection with vehicle or WYE-125132 formulated in 5% ethanol, 2% Tween 80, and 5% polyethylene glycol-400. Tumor lysates are prepared and immunoblotted. For efficacy studies, nude mice bearing U87MG, MDA361, H1975, A549, A498, or 786-O tumors are staged and randomized into treatment groups (n=10). Mice are dosed orally with vehicle or WYE-125132 following qd x5 cycle regimen (5 d on, 2 d off) for up to four cycles. Temsirolimus/CCI-779 is formulated as WYE-132 and dosed i.v. once weekly. Bevacizumab is formulated in PBS and dosed i.p. via its clinical regimen (200 μg/mouse; once weekly). Tumor growth is monitored and analyzed.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.


    Purity: 98.61%

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