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Amgen c-met inhibitor compound-a
C Met Inhibitor Compound A, supplied by Amgen, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/c-met+inhibitor+compound-a/c+met+inhibitors/pm32318883-127-33-26
Average 90 stars, based on 1 article reviews
c-met inhibitor compound-a - by Bioz Stars, 2026-10
90/100 stars

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Related Articles

Activation Assay:

Article Title: Targeting the HGF/c-MET pathway in advanced pancreatic cancer: a key element of treatment that limits primary tumour growth and eliminates metastasis
Article Snippet: It has been shown to be well tolerated by the mice (1, 2). iv) Ci group: c-MET inhibitor, Compound-A, is a small molecule inhibitor that prevents the activation of c-MET (HGF receptor) manufactured by Amgen Inc.

Article Title: Dasatinib Treatment Increases Sensitivity to c-Met Inhibition in Triple-Negative Breast Cancer Cells.
Article Snippet: Acknowledgments: We would like to acknowledge Amgen, who kindly gave us access to the c-Met inhibitor Compound-A used in our studies.

Article Title: Targeting c-Met in triple negative breast cancer: preclinical studies using the c-Met inhibitor, Cpd A.
Article Snippet: Introduction Triple negative breast cancer (TNBC) represents a heterogeneous subtype of breast cancer that carries a poorer prognosis.. There remains a need to identify novel drivers of TNBC, which may represent targets to treat the disease. c-Met overexpression is linked with decreased survival and is associated with the basal subtype of breast cancer.. Cpd A, a kinase inhibitor selective/specific for Met kinase has demonstrated preclinical anti-cancer efficacy in TNBC.

Modification:

Article Title: Targeting the HGF/c-MET pathway in advanced pancreatic cancer: a key element of treatment that limits primary tumour growth and eliminates metastasis
Article Snippet: It has been shown to be well tolerated by the mice (1, 2). iv) Ci group: c-MET inhibitor, Compound-A, is a small molecule inhibitor that prevents the activation of c-MET (HGF receptor) manufactured by Amgen Inc.

Article Title: Dasatinib Treatment Increases Sensitivity to c-Met Inhibition in Triple-Negative Breast Cancer Cells.
Article Snippet: Acknowledgments: We would like to acknowledge Amgen, who kindly gave us access to the c-Met inhibitor Compound-A used in our studies.

Article Title: Targeting c-Met in triple negative breast cancer: preclinical studies using the c-Met inhibitor, Cpd A.
Article Snippet: Introduction Triple negative breast cancer (TNBC) represents a heterogeneous subtype of breast cancer that carries a poorer prognosis.. There remains a need to identify novel drivers of TNBC, which may represent targets to treat the disease. c-Met overexpression is linked with decreased survival and is associated with the basal subtype of breast cancer.. Cpd A, a kinase inhibitor selective/specific for Met kinase has demonstrated preclinical anti-cancer efficacy in TNBC.

Cell Culture:

Article Title: Targeting the HGF/c-MET pathway in advanced pancreatic cancer: a key element of treatment that limits primary tumour growth and eliminates metastasis
Article Snippet: It has been shown to be well tolerated by the mice (1, 2). iv) Ci group: c-MET inhibitor, Compound-A, is a small molecule inhibitor that prevents the activation of c-MET (HGF receptor) manufactured by Amgen Inc.

Article Title: Dasatinib Treatment Increases Sensitivity to c-Met Inhibition in Triple-Negative Breast Cancer Cells.
Article Snippet: Acknowledgments: We would like to acknowledge Amgen, who kindly gave us access to the c-Met inhibitor Compound-A used in our studies.

Article Title: Targeting c-Met in triple negative breast cancer: preclinical studies using the c-Met inhibitor, Cpd A.
Article Snippet: Introduction Triple negative breast cancer (TNBC) represents a heterogeneous subtype of breast cancer that carries a poorer prognosis.. There remains a need to identify novel drivers of TNBC, which may represent targets to treat the disease. c-Met overexpression is linked with decreased survival and is associated with the basal subtype of breast cancer.. Cpd A, a kinase inhibitor selective/specific for Met kinase has demonstrated preclinical anti-cancer efficacy in TNBC.



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(A, B) The proliferation rates of thyroid cancer cell lines and MDA-MB-435 (control melanoma cell line) cultured with increasing concentrations of either <t>Tivantinib</t> (A) or Crizotinib (B) as measured by MTT assay (Material and Methods). Results represent the mean ± SD of MTT experiment results performed in triplicates.
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(A, B) The proliferation rates of thyroid cancer cell lines and MDA-MB-435 (control melanoma cell line) cultured with increasing concentrations of either Tivantinib (A) or Crizotinib (B) as measured by MTT assay (Material and Methods). Results represent the mean ± SD of MTT experiment results performed in triplicates.

Journal: Molecular cancer therapeutics

Article Title: Off Target Effects of c-MET Inhibitors on Thyroid Cancer Cells

doi: 10.1158/1535-7163.MCT-13-0187

Figure Lengend Snippet: (A, B) The proliferation rates of thyroid cancer cell lines and MDA-MB-435 (control melanoma cell line) cultured with increasing concentrations of either Tivantinib (A) or Crizotinib (B) as measured by MTT assay (Material and Methods). Results represent the mean ± SD of MTT experiment results performed in triplicates.

Article Snippet: Compound c-MET inhibitors Tivantinib [ActiveBiochem (Maplewood, NJ)], Crizotinib and SU11274 [Selleck Chemical (Houston, TX)] were suspended in DMSO and stored until use in small aliquots at −20°C.

Techniques: Control, Cell Culture, MTT Assay

(A) Cell cycle analysis of SW1737, T2, TL3 thyroid cancer cell lines after treatment with increasing concentrations of Tivantinib and Crizotinib (0.1, 1.0, 10 μM, 24 hours). (B) Graphic display of G2/M data shown on Panel A. (C) Apoptosis measurement (% Annexin V positive cells) after these cells were treated with either Tivantinib or Crizotinib (0.1, 1.0, 10 μM, 24 hours). Results expressed as Mean ± SD. *: P < 0.05; **: P < 0.01.

Journal: Molecular cancer therapeutics

Article Title: Off Target Effects of c-MET Inhibitors on Thyroid Cancer Cells

doi: 10.1158/1535-7163.MCT-13-0187

Figure Lengend Snippet: (A) Cell cycle analysis of SW1737, T2, TL3 thyroid cancer cell lines after treatment with increasing concentrations of Tivantinib and Crizotinib (0.1, 1.0, 10 μM, 24 hours). (B) Graphic display of G2/M data shown on Panel A. (C) Apoptosis measurement (% Annexin V positive cells) after these cells were treated with either Tivantinib or Crizotinib (0.1, 1.0, 10 μM, 24 hours). Results expressed as Mean ± SD. *: P < 0.05; **: P < 0.01.

Article Snippet: Compound c-MET inhibitors Tivantinib [ActiveBiochem (Maplewood, NJ)], Crizotinib and SU11274 [Selleck Chemical (Houston, TX)] were suspended in DMSO and stored until use in small aliquots at −20°C.

Techniques: Cell Cycle Assay

Cells were pre-starved in culture medium containing 0.5% FBS (24 hour) ± either Crizotinib or Tivantinib (0.1, 1.0, 10 μM) or SU11274 (10 μM), and stimulated with 20 ng/ml recombinant human HGF for 10 minutes before lysates were made for western blotting. A series of c-MET downstream signaling pathway proteins and phosphor-proteins were detected using western blotting. β-actin was used as a loading balance control.

Journal: Molecular cancer therapeutics

Article Title: Off Target Effects of c-MET Inhibitors on Thyroid Cancer Cells

doi: 10.1158/1535-7163.MCT-13-0187

Figure Lengend Snippet: Cells were pre-starved in culture medium containing 0.5% FBS (24 hour) ± either Crizotinib or Tivantinib (0.1, 1.0, 10 μM) or SU11274 (10 μM), and stimulated with 20 ng/ml recombinant human HGF for 10 minutes before lysates were made for western blotting. A series of c-MET downstream signaling pathway proteins and phosphor-proteins were detected using western blotting. β-actin was used as a loading balance control.

Article Snippet: Compound c-MET inhibitors Tivantinib [ActiveBiochem (Maplewood, NJ)], Crizotinib and SU11274 [Selleck Chemical (Houston, TX)] were suspended in DMSO and stored until use in small aliquots at −20°C.

Techniques: Recombinant, Western Blot, Control

 Tivantinib  and Crizotinib inhibition (IC50) of p-MET and cell growth of cancer cells.

Journal: Molecular cancer therapeutics

Article Title: Off Target Effects of c-MET Inhibitors on Thyroid Cancer Cells

doi: 10.1158/1535-7163.MCT-13-0187

Figure Lengend Snippet: Tivantinib and Crizotinib inhibition (IC50) of p-MET and cell growth of cancer cells.

Article Snippet: Compound c-MET inhibitors Tivantinib [ActiveBiochem (Maplewood, NJ)], Crizotinib and SU11274 [Selleck Chemical (Houston, TX)] were suspended in DMSO and stored until use in small aliquots at −20°C.

Techniques: Inhibition