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pdgfr inhibitor  (MedChemExpress)


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    MedChemExpress pdgfr inhibitor
    <t>PDGFR</t> inhibitors suppress EnzaR PCa cell growth and xenograft tumor progression. a PDGFC secretion levels were measured by ELISA in LNCaP and LNCaP-EnzaR (left) as well as in LNCaP-EnzaR-shNC and shPDGFC (right). b The expression of PDGFRα and PDGFRβ were analyzed in Antonarakis ES dataset. c–g EnzaR cells treatment with DMSO, ENZA, imatinib/CP-673451, or a combination of enzalutamide and imatinib/CP-673451, respectively. Cell viability was measured by CCK-8 ( c , d ), colony-formation assays ( e ), and EdU assays (scale bar = 50 μm) ( f , g ). h , i Tumor growth curves from DMSO, ENZA, CP-673451, and CP-673451 combined with ENZA treatment group were measured. At the endpoint, Tumor size and tumor weight were recorded. j IHC assayed the proliferation index Ki67 in xenograft (scale bar = 20 μm). p values are shown for each comparison (* P < 0.05; ** P < 0.01; ns, not significant)
    Pdgfr Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 32 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pdgfr+inhibitor/CP-673451/pmc12460851-88-6-10
    Average 95 stars, based on 32 article reviews
    pdgfr inhibitor - by Bioz Stars, 2026-08
    95/100 stars

    Images

    1) Product Images from "PDGFC facilitates enzalutamide resistance in prostate cancer through activation of the Rap1-MAPK pathway"

    Article Title: PDGFC facilitates enzalutamide resistance in prostate cancer through activation of the Rap1-MAPK pathway

    Journal: Journal of Cancer Research and Clinical Oncology

    doi: 10.1007/s00432-025-06276-w

    PDGFR inhibitors suppress EnzaR PCa cell growth and xenograft tumor progression. a PDGFC secretion levels were measured by ELISA in LNCaP and LNCaP-EnzaR (left) as well as in LNCaP-EnzaR-shNC and shPDGFC (right). b The expression of PDGFRα and PDGFRβ were analyzed in Antonarakis ES dataset. c–g EnzaR cells treatment with DMSO, ENZA, imatinib/CP-673451, or a combination of enzalutamide and imatinib/CP-673451, respectively. Cell viability was measured by CCK-8 ( c , d ), colony-formation assays ( e ), and EdU assays (scale bar = 50 μm) ( f , g ). h , i Tumor growth curves from DMSO, ENZA, CP-673451, and CP-673451 combined with ENZA treatment group were measured. At the endpoint, Tumor size and tumor weight were recorded. j IHC assayed the proliferation index Ki67 in xenograft (scale bar = 20 μm). p values are shown for each comparison (* P < 0.05; ** P < 0.01; ns, not significant)
    Figure Legend Snippet: PDGFR inhibitors suppress EnzaR PCa cell growth and xenograft tumor progression. a PDGFC secretion levels were measured by ELISA in LNCaP and LNCaP-EnzaR (left) as well as in LNCaP-EnzaR-shNC and shPDGFC (right). b The expression of PDGFRα and PDGFRβ were analyzed in Antonarakis ES dataset. c–g EnzaR cells treatment with DMSO, ENZA, imatinib/CP-673451, or a combination of enzalutamide and imatinib/CP-673451, respectively. Cell viability was measured by CCK-8 ( c , d ), colony-formation assays ( e ), and EdU assays (scale bar = 50 μm) ( f , g ). h , i Tumor growth curves from DMSO, ENZA, CP-673451, and CP-673451 combined with ENZA treatment group were measured. At the endpoint, Tumor size and tumor weight were recorded. j IHC assayed the proliferation index Ki67 in xenograft (scale bar = 20 μm). p values are shown for each comparison (* P < 0.05; ** P < 0.01; ns, not significant)

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing, CCK-8 Assay, Comparison



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    <t>PDGFR</t> inhibitors suppress EnzaR PCa cell growth and xenograft tumor progression. a PDGFC secretion levels were measured by ELISA in LNCaP and LNCaP-EnzaR (left) as well as in LNCaP-EnzaR-shNC and shPDGFC (right). b The expression of PDGFRα and PDGFRβ were analyzed in Antonarakis ES dataset. c–g EnzaR cells treatment with DMSO, ENZA, imatinib/CP-673451, or a combination of enzalutamide and imatinib/CP-673451, respectively. Cell viability was measured by CCK-8 ( c , d ), colony-formation assays ( e ), and EdU assays (scale bar = 50 μm) ( f , g ). h , i Tumor growth curves from DMSO, ENZA, CP-673451, and CP-673451 combined with ENZA treatment group were measured. At the endpoint, Tumor size and tumor weight were recorded. j IHC assayed the proliferation index Ki67 in xenograft (scale bar = 20 μm). p values are shown for each comparison (* P < 0.05; ** P < 0.01; ns, not significant)
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    Image Search Results


    PDGFR inhibitors suppress EnzaR PCa cell growth and xenograft tumor progression. a PDGFC secretion levels were measured by ELISA in LNCaP and LNCaP-EnzaR (left) as well as in LNCaP-EnzaR-shNC and shPDGFC (right). b The expression of PDGFRα and PDGFRβ were analyzed in Antonarakis ES dataset. c–g EnzaR cells treatment with DMSO, ENZA, imatinib/CP-673451, or a combination of enzalutamide and imatinib/CP-673451, respectively. Cell viability was measured by CCK-8 ( c , d ), colony-formation assays ( e ), and EdU assays (scale bar = 50 μm) ( f , g ). h , i Tumor growth curves from DMSO, ENZA, CP-673451, and CP-673451 combined with ENZA treatment group were measured. At the endpoint, Tumor size and tumor weight were recorded. j IHC assayed the proliferation index Ki67 in xenograft (scale bar = 20 μm). p values are shown for each comparison (* P < 0.05; ** P < 0.01; ns, not significant)

    Journal: Journal of Cancer Research and Clinical Oncology

    Article Title: PDGFC facilitates enzalutamide resistance in prostate cancer through activation of the Rap1-MAPK pathway

    doi: 10.1007/s00432-025-06276-w

    Figure Lengend Snippet: PDGFR inhibitors suppress EnzaR PCa cell growth and xenograft tumor progression. a PDGFC secretion levels were measured by ELISA in LNCaP and LNCaP-EnzaR (left) as well as in LNCaP-EnzaR-shNC and shPDGFC (right). b The expression of PDGFRα and PDGFRβ were analyzed in Antonarakis ES dataset. c–g EnzaR cells treatment with DMSO, ENZA, imatinib/CP-673451, or a combination of enzalutamide and imatinib/CP-673451, respectively. Cell viability was measured by CCK-8 ( c , d ), colony-formation assays ( e ), and EdU assays (scale bar = 50 μm) ( f , g ). h , i Tumor growth curves from DMSO, ENZA, CP-673451, and CP-673451 combined with ENZA treatment group were measured. At the endpoint, Tumor size and tumor weight were recorded. j IHC assayed the proliferation index Ki67 in xenograft (scale bar = 20 μm). p values are shown for each comparison (* P < 0.05; ** P < 0.01; ns, not significant)

    Article Snippet: To evaluate the therapeutic effect of PDGFR inhibitor (CP-673451, HY-12050, MCE, China) treatment on EnzaR tumors, after castration surgery, the mice were randomly divided into four groups and treated as follows: Group 1, vehicle control; Group 2, enzalutamide (30 mg/kg, orally); Group 3, CP-673451 (40 mg/kg, orally); Group 4, enzalutamide (30 mg/kg, orally) and CP-673451 (40 mg/kg, orally).

    Techniques: Enzyme-linked Immunosorbent Assay, Expressing, CCK-8 Assay, Comparison