1. Protein Tyrosine Kinase/RTK
    Apoptosis
  2. c-Met/HGFR
    Apoptosis
  3. Capmatinib dihydrochloride

Capmatinib dihydrochloride (Synonyms: INC280 dihydrochloride; INCB28060 dihydrochloride)

Cat. No.: HY-13404A
Handling Instructions

Capmatinib (INC280; INCB28060) dihydrochloride is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib dihydrochloride can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib dihydrochloride potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib dihydrochloride is largely metabolized by CYP3A4 and aldehyde oxidase.

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

Capmatinib dihydrochloride Chemical Structure

Capmatinib dihydrochloride Chemical Structure

CAS No. : 1197376-85-4

Size Stock
100 mg   Get quote  
250 mg   Get quote  
500 mg   Get quote  

* Please select Quantity before adding items.

Other In-stock Forms of Capmatinib dihydrochloride:

Other Forms of Capmatinib dihydrochloride:

Top Publications Citing Use of Products

    Capmatinib dihydrochloride purchased from MCE. Usage Cited in: Department Cancer Biology. Wayne State University. 2014 Jan.

    The c-Met Inhibitor INC280 Reveals HGF Activation of c-Met Leads to β4 Activation. (A) Dose-dependent assay to determine the concentration of INC280 required to prevent HGF-induced c-Met phosphorylation. Cells are pre-treated for two hours with INC280 at the indicated concentrations and then stimulated with 50 ng/mL HGF for 30 minutes. Phosphorylated (upper panel) and total c-Met (lower panel) are analyzed by Western blot. Densitometry represents the ratio of phosphorylated to total c-Met as a p
    • Biological Activity

    • Purity & Documentation

    • References

    • Customer Review

    Description

    Capmatinib (INC280; INCB28060) dihydrochloride is a potent, orally active, selective, and ATP competitive c-Met kinase inhibitor (IC50=0.13 nM). Capmatinib dihydrochloride can inhibit phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5. Capmatinib dihydrochloride potently inhibits c-MET-dependent tumor cell proliferation and migration and effectively induces apoptosis. Antitumor activity. Capmatinib dihydrochloride is largely metabolized by CYP3A4 and aldehyde oxidase[1][2][3].

    IC50 & Target

    IC50: 0.13 nM (c-MET)[1]

    In Vitro

    Capmatinib (INCB28060) inhibits c-MET phosphorylation with an IC50 value of approximately 1 nM and a concentration of approximately 4 nM inhibits c-MET more than 90%, which is reversible and the effect is significantly reduced in several hours after the compound is removed and completely disappeared by 48 hours[1].
    Capmatinib (INCB28060) (0-10000 nM; 72 h) inhibits the proliferation of SNU-5, S114, H441 and U-87MG[1].
    Capmatinib (INCB28060) (0.06-62.25 nM; 2h) effectively inhibits phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5[1].
    Capmatinib (INCB28060) (0.24-63 nM; over night) prevents HGF-stimulated H441 cell migration[1].
    Capmatinib (INCB28060) (0.5-50 nM; 20 min) suppresses phosphorylation of both EGFR and HER-3 rapidly[1].
    Capmatinib (INCB28060) (0-333 nM; 24 h) induces apoptosis in SNU-5 cells[1].

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

    Cell Viability Assay[1]

    Cell Line: SNU-5, S114, H441 and U-87MG
    Concentration: 0-10000 nM
    Incubation Time: 72 h
    Result: Inhibited the cell viability of SNU-5 and S114, as well as the colony formation of H441 and U-87MG, with IC50 values of 1.2 nM, 12.4 nM, ~0.5 nM and 2 nM, respectively.

    Cell Migration Assay [1]

    Cell Line: H441 (stimulated with 50 ng/mL recombinant human HGF for 24h)
    Concentration: 0.24, 1, 4, 16 and 63 nM
    Incubation Time: Over night
    Result: Prevented HGF-stimulated H441 cell migration, with IC50 of approximately 2 nM, and less cell migration at 16 nM.

    Western Blot Analysis[1]

    Cell Line: SNU-5
    Concentration: 0.06, 0.24, 0.98, 3.91, 15.63 and 62.25 nM
    Incubation Time: 2 h
    Result: Effectively inhibited phosphorylation of c-MET as well as c-MET pathway downstream effectors such as ERK1/2, AKT, FAK, GAB1, and STAT3/5.

    Western Blot Analysis[1]

    Cell Line: H1993 cells
    Concentration: 0.5, 5 and 50 nM
    Incubation Time: 20 min
    Result: Suppressed phosphorylation of both EGFR and HER-3 rapidly and as effectively as the compound inhibited c-MET phosphorylation in H1993 cells.

    Apoptosis Analysis[1]

    Cell Line: SNU-5 cells
    Concentration: 0.017, 0.15, 1.37, 12.33, 111 and 333 nM
    Incubation Time: 24 h
    Result: Effectively induced DNA fragmentation.
    In Vivo

    Capmatinib (INCB28060) (1-30 mg/kg; PO, twice daily, for 2 weeks) exhibits dose-dependent inhibition of tumor growth, and shows well tolerance at all doses during the treatment periods, with no evidence of overt toxicity or weight loss in U-87MG tumor mice model[1].
    Capmatinib (INCB28060) (0.03-10 mg/kg; PO, single dosage) causes inhibition of c-MET phosphorylation in S114 tumor mice model[1].

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

    Animal Model: Female Balb/c nu/nu mice (inoculated subcutaneously with 5×106 U-87MG glioblastoma cells)[1]
    Dosage: 1, 3, 10 and 30 mg/kg
    Administration: PO, twice daily, for 2 weeks
    Result: Exhibited dose-dependent inhibition of tumor growth with 35% and 76% at 1 and 3 mg/kg once daily; resulted in partial regressions in 6 of 10 U-87MG tumor-bearing mice at 10 mg/kg once daily; and showed well tolerance at all doses during the treatment periods, with no evidence of overt toxicity or weight loss.
    Animal Model: Female Balb/c nu/nu mice (inoculated subcutaneously with 4×106 S114 tumor cells)[1]
    Dosage: 0.03, 0.1, 0.3, 1, 3 and 10 mg/kg
    Administration: PO, single dosage
    Result: Caused approximately 50% and 90% inhibition of c-MET phosphorylation at 0.03 and 0.3 mg/kg after administration of 30 min, and inhibition of phospho-c-MET exceeded 90% after 7 hours.
    Molecular Weight

    485.34

    Formula

    C23H19Cl2FN6O

    CAS No.
    SMILES

    O=C(NC)C1=CC=C(C2=NN3C(N=C2)=NC=C3CC4=CC=C5N=CC=CC5=C4)C=C1F.Cl.Cl

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

    Please store the product under the recommended conditions in the Certificate of Analysis.

    Purity & Documentation
    References
    • No file chosen (Maximum size is: 1024 Kb)
    • If you have published this work, please enter the PubMed ID.
    • Your name will appear on the site.
    • Molarity Calculator

    • Dilution Calculator

    The molarity calculator equation

    Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

    Mass   Concentration   Volume   Molecular Weight *
    = × ×

    The dilution calculator equation

    Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

    This equation is commonly abbreviated as: C1V1 = C2V2

    Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
    × = ×
    C1   V1   C2   V2

    Your Recently Viewed Products:

    Inquiry Online

    Your information is safe with us. * Required Fields.

    Product Name

     

    Salutation

    Applicant Name *

     

    Email address *

    Phone number *

     

    Organization name *

    Department *

     

    Requested quantity *

    Country or Region *

         

    Remarks

    Bulk Inquiry

    Inquiry Information

    Product Name:
    Capmatinib dihydrochloride
    Cat. No.:
    HY-13404A
    Quantity:
    MCE Japan Authorized Agent: