1. Protein Tyrosine Kinase/RTK
  2. Bcr-Abl
  3. Ponatinib

Ponatinib (Synonyms: AP24534)

Cat. No.: HY-12047 Purity: 99.13%
Handling Instructions

Ponatinib (AP24534) is an orally active multi-targeted kinase inhibitor with IC50s of 0.37 nM, 1.1 nM, 1.5 nM, 2.2 nM, and 5.4 nM for Abl, PDGFRα, VEGFR2, FGFR1, and Src, respectively.

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Ponatinib Chemical Structure

Ponatinib Chemical Structure

CAS No. : 943319-70-8

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Customer Review

Based on 13 publication(s) in Google Scholar

Top Publications Citing Use of Products

    Ponatinib purchased from MCE. Usage Cited in: Exp Hematol. 2014 May;42(5):369-379.e3.

    (B,D) Phosphorylation levels of F/P (or its mutant), STAT5, or ERK in lysates of CMPs expressing Hes1 with F/P, F/P-D842V, or F/P-T674I, which have been treated with indicated doses of (B) Imatinib or (D) Ponatinib for 15 min. Data are representative of three independent experiments.

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    • Biological Activity

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    • Customer Review


    Ponatinib (AP24534) is an orally active multi-targeted kinase inhibitor with IC50s of 0.37 nM, 1.1 nM, 1.5 nM, 2.2 nM, and 5.4 nM for Abl, PDGFRα, VEGFR2, FGFR1, and Src, respectively[1].

    IC50 & Target[1]


    1.5 nM (IC50)


    1.1 nM (IC50)


    2.2 nM (IC50)


    12.5 nM (IC50)

    In Vitro

    Ponatinib (AP24534) potently inhibits native ABL (IC50: 0.37 nM), ABLT315I (IC50: 2.0 nM), and other clinically important ABL kinase domain mutants (IC50: 0.30-0.44 nM). Ponatinib also inhibits SRC (IC50: 5.4 nM) and members of the VEGFR, FGFR, and PDGFR families of receptor tyrosine kinases. Ponatinib potently inhibits proliferation of Ba/F3 cells expressing native BCR-ABL (IC50: 0.5 nM). All BCR-ABL mutants tested remained sensitive to Ponatinib (IC50: 0.5-36 nM) including BCR-ABLT315I (IC50: 11 nM)[1].
    Ponatinib inhibits the in vitro kinase activity of FLT3, KIT, FGFR1, and PDGFRα with IC50 values of 13, 13, 2, and 1 nM, respectively. Ponatinib inhibits phosphorylation of all 4 RTKs in a dose-dependent manner, with IC50 values between 0.3 to 20 nM. Consistent with these activated receptors being important in driving leukemogenesis Ponatinib also potently inhibits the viability of all 4 cell lines with IC50 values of 0.5 to 17 nM. In contrast, the IC50 for inhibition of RS4;11 cells which express native (unmutated) FLT3, is more than 100 nM[2].

    In Vivo

    In a survival model in which mice are instead injected with Ba/F3 BCR-ABLT315I cells, administration of Dasatinib at doses as high as 300 mg/kg has no effect on survival time. By contrast, treatment with Ponatinib (AP24534) prolongs survival in a dose-dependent manner. Ponatinib dosed orally for 19 days at 5, 15, and 25 mg/kg prolongs median survival to 19.5, 26, and 30 days, respectively compare to 16 days for vehicle-treated mice (p<0.01 for all three dose levels). The anti-tumor activity of Ponatinib (AP24534) is further assessed in a xenograft model in which Ba/F3 BCR-ABLT315I cells are injected subcutaneously into mice. Tumor growth is inhibited by Ponatinib in a dose-dependent manner compare to vehicle-treated mice, with significant suppression of tumor growth upon daily oral dosing at 10 and 30 mg/kg (%T/C = 68% and 20%, respectively; p<0.01 for both dose levels). Daily oral dosing of 50 mg/kg Ponatinib causes significant tumor regression (%T/C = 0.9%, p<0.01), with a 96% reduction in mean tumor volume at the final measurement compared to the start of treatment. Ponatinib is well tolerated at all efficacious dose levels for the duration of the study; maximal decreases in body weight are <5%, <5%, and <12% for the 10, 30, and 50 mg/kg dose groups, respectively, with no signs of overt toxicity[1].
    Ponatinib (1-25 mg/kg) is administered orally, once daily for 28 days, to mice bearing MV4-11 xenografts. Ponatinib potently inhibits tumor growth in a dose-dependent manner. Administration of 1 mg/kg, the lowest dose tested, leads to significant inhibition of tumor growth (TGI=46%, P<0.01) and doses of 2.5 mg/kg or greater results in tumor regression[2].

    Clinical Trial
    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 : ≥ 50 mg/mL (93.89 mM)

    *"≥" means soluble, but saturation unknown.

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 1.8777 mL 9.3886 mL 18.7772 mL
    5 mM 0.3755 mL 1.8777 mL 3.7554 mL
    10 mM 0.1878 mL 0.9389 mL 1.8777 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: ≥ 10 mg/mL (18.78 mM); Clear solution

    • 2.

      Add each solvent one by one:  10% DMSO    90% corn oil

      Solubility: ≥ 10 mg/mL (18.78 mM); Clear solution

    *All of the co-solvents are provided by MCE.
    Cell Assay

    Ba/F3 cell lines are distributed in 96-well plates (4×103 cells/well) and incubated with escalating concentrations of Ponatinib for 72 hr. The inhibitor ranges used are: 0-625 nM for cells expressing BCR-ABL and 0-10,000 nM for BCR-ABL negative cells. Proliferation is measured using a methanethiosulfonate (MTS)-based viability assay. IC50 values are reported as the mean of three independent experiments performed in quadruplicate. For cell proliferation experiments with CML or normal primary cells, mononuclear cells are plated in 96-well plates (5×104 cells/well) over graded concentrations of Ponatinib (0-1000 nM) in RPMI supplemented with 10% FBS, L-glutamine, penicillin/streptomycin, and 100 μM β-mercaptoethanol. Following a 72 hr incubation, cell viability is assessed by subjecting cells to an MTS assay[1].

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

    Animal Administration

    For Ba/F3 survival model, Ba/F3 cells expressing native BCR-ABL or BCR-ABLT315I are injected into the tail vein of female SCID mice (100 μL of a 1×107 cells/mL suspension in serum-free medium). Beginning 72 hr later mice are treated once daily by oral gavage with vehicle (25 mM citrate buffer, pH 2.75), Ponatinib, or Dasatinib for up to 19 consecutive days. Moribund animals are sacrificed as per IACUC guidelines. On necropsy, mice have marked splenomegaly due to tumor cell infiltration. Survival data are analyzed using Kaplan-Meier method, and statistical significance is evaluated with a Log-rank test comparing the survival time of each treatment group with the vehicle group. For Ba/F3 Tumor Model, Ba/F3 BCR-ABLT315I cells are implanted subcutaneously into the right flank of female nude mice (100 μL of a 1×107 cells/mL cell suspension in serum-free medium). Mice are randomized to treatment groups when the average tumor volume reaches approximately 500 mm3. Mice are treated once daily by oral gavage with vehicle (25 mM citrate buffer, pH 2.75) or Ponatinib for up to 19 consecutive days. Tumor volume (mm3) is calculated. To determine tumor growth inhibition when the treatment period is finished, mean tumor volume for treatment group/mean tumor volume for control group (%T/C) is calculated at the final measurement.

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


    Purity: 99.13%

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    PonatinibAP24534AP 24534AP-24534Bcr-AblPDGFRVEGFRFGFRSrcAutophagyPlatelet-derived growth factor receptorVascular endothelial growth factor receptorFibroblast growth factor receptororallyactivemulti-targetedkinaseAblPDGFRαVEGFR2FGFR1Inhibitorinhibitorinhibit

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