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osimertinib  (MedChemExpress)


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    MedChemExpress osimertinib
    HEK-EGFR-19del-T790M-C797S stable cells were treated with the indicated doses of ( A ) third-generation EGFR TKI <t>(osimertinib),</t> ( B ) P2Y2 inhibitor (kaempferol), and ( C ) FAK inhibitor (PF-562271) and analyzed for cell proliferation using the CyQUANT assay for 4 days. The heatmap graph illustrates the percentile scores of EGFR-19del-T790M-C797S cell proliferation using combination therapies: ( D ) kaempferol with osimertinib, ( E ) PF-562271 with osimertinib, and ( F ) kaempferol with PF-562271, presented as average fluorescence intensities. ( G ) Schematic model of the stability of EGFR-WT and mutants. The left panel depicts ATP levels and EGFR degradation in normal cells, the middle panel represents EGFR-mutant tumor cells, and the right panel outlines strategies to target EGFR stability (represented in red). Ab, antibody. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( H ) Schematic representation of the stability of EGFR mutants resulting from the increased extracellular ATP levels, activating P2Y2 in complex with integrins and stabilizing EGFR. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( I ) Proposed model for comprehensive targeting of diverse EGFR mutants in NSCLC using a P2Y2 inhibitor, NTPDase, FAK inhibitor, or a combination with TKIs to overcome TKI resistance. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . Statistical analysis was performed using an ANOVA. ** P ≤ 0.01, *** P ≤ 0.001, and **** P ≤ 0.0001.
    Osimertinib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 178 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 97 stars, based on 178 article reviews
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    Images

    1) Product Images from "A genome-wide genetic screen reveals the P2Y2-integrin axis as a stabilizer of EGFR mutants in non–small cell lung cancer (NSCLC)"

    Article Title: A genome-wide genetic screen reveals the P2Y2-integrin axis as a stabilizer of EGFR mutants in non–small cell lung cancer (NSCLC)

    Journal: Science Advances

    doi: 10.1126/sciadv.adv3980

    HEK-EGFR-19del-T790M-C797S stable cells were treated with the indicated doses of ( A ) third-generation EGFR TKI (osimertinib), ( B ) P2Y2 inhibitor (kaempferol), and ( C ) FAK inhibitor (PF-562271) and analyzed for cell proliferation using the CyQUANT assay for 4 days. The heatmap graph illustrates the percentile scores of EGFR-19del-T790M-C797S cell proliferation using combination therapies: ( D ) kaempferol with osimertinib, ( E ) PF-562271 with osimertinib, and ( F ) kaempferol with PF-562271, presented as average fluorescence intensities. ( G ) Schematic model of the stability of EGFR-WT and mutants. The left panel depicts ATP levels and EGFR degradation in normal cells, the middle panel represents EGFR-mutant tumor cells, and the right panel outlines strategies to target EGFR stability (represented in red). Ab, antibody. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( H ) Schematic representation of the stability of EGFR mutants resulting from the increased extracellular ATP levels, activating P2Y2 in complex with integrins and stabilizing EGFR. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( I ) Proposed model for comprehensive targeting of diverse EGFR mutants in NSCLC using a P2Y2 inhibitor, NTPDase, FAK inhibitor, or a combination with TKIs to overcome TKI resistance. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . Statistical analysis was performed using an ANOVA. ** P ≤ 0.01, *** P ≤ 0.001, and **** P ≤ 0.0001.
    Figure Legend Snippet: HEK-EGFR-19del-T790M-C797S stable cells were treated with the indicated doses of ( A ) third-generation EGFR TKI (osimertinib), ( B ) P2Y2 inhibitor (kaempferol), and ( C ) FAK inhibitor (PF-562271) and analyzed for cell proliferation using the CyQUANT assay for 4 days. The heatmap graph illustrates the percentile scores of EGFR-19del-T790M-C797S cell proliferation using combination therapies: ( D ) kaempferol with osimertinib, ( E ) PF-562271 with osimertinib, and ( F ) kaempferol with PF-562271, presented as average fluorescence intensities. ( G ) Schematic model of the stability of EGFR-WT and mutants. The left panel depicts ATP levels and EGFR degradation in normal cells, the middle panel represents EGFR-mutant tumor cells, and the right panel outlines strategies to target EGFR stability (represented in red). Ab, antibody. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( H ) Schematic representation of the stability of EGFR mutants resulting from the increased extracellular ATP levels, activating P2Y2 in complex with integrins and stabilizing EGFR. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( I ) Proposed model for comprehensive targeting of diverse EGFR mutants in NSCLC using a P2Y2 inhibitor, NTPDase, FAK inhibitor, or a combination with TKIs to overcome TKI resistance. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . Statistical analysis was performed using an ANOVA. ** P ≤ 0.01, *** P ≤ 0.001, and **** P ≤ 0.0001.

    Techniques Used: CyQUANT Assay, Fluorescence, Mutagenesis



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    HEK-EGFR-19del-T790M-C797S stable cells were treated with the indicated doses of ( A ) third-generation EGFR TKI <t>(osimertinib),</t> ( B ) P2Y2 inhibitor (kaempferol), and ( C ) FAK inhibitor (PF-562271) and analyzed for cell proliferation using the CyQUANT assay for 4 days. The heatmap graph illustrates the percentile scores of EGFR-19del-T790M-C797S cell proliferation using combination therapies: ( D ) kaempferol with osimertinib, ( E ) PF-562271 with osimertinib, and ( F ) kaempferol with PF-562271, presented as average fluorescence intensities. ( G ) Schematic model of the stability of EGFR-WT and mutants. The left panel depicts ATP levels and EGFR degradation in normal cells, the middle panel represents EGFR-mutant tumor cells, and the right panel outlines strategies to target EGFR stability (represented in red). Ab, antibody. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( H ) Schematic representation of the stability of EGFR mutants resulting from the increased extracellular ATP levels, activating P2Y2 in complex with integrins and stabilizing EGFR. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( I ) Proposed model for comprehensive targeting of diverse EGFR mutants in NSCLC using a P2Y2 inhibitor, NTPDase, FAK inhibitor, or a combination with TKIs to overcome TKI resistance. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . Statistical analysis was performed using an ANOVA. ** P ≤ 0.01, *** P ≤ 0.001, and **** P ≤ 0.0001.
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    HEK-EGFR-19del-T790M-C797S stable cells were treated with the indicated doses of ( A ) third-generation EGFR TKI (osimertinib), ( B ) P2Y2 inhibitor (kaempferol), and ( C ) FAK inhibitor (PF-562271) and analyzed for cell proliferation using the CyQUANT assay for 4 days. The heatmap graph illustrates the percentile scores of EGFR-19del-T790M-C797S cell proliferation using combination therapies: ( D ) kaempferol with osimertinib, ( E ) PF-562271 with osimertinib, and ( F ) kaempferol with PF-562271, presented as average fluorescence intensities. ( G ) Schematic model of the stability of EGFR-WT and mutants. The left panel depicts ATP levels and EGFR degradation in normal cells, the middle panel represents EGFR-mutant tumor cells, and the right panel outlines strategies to target EGFR stability (represented in red). Ab, antibody. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( H ) Schematic representation of the stability of EGFR mutants resulting from the increased extracellular ATP levels, activating P2Y2 in complex with integrins and stabilizing EGFR. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( I ) Proposed model for comprehensive targeting of diverse EGFR mutants in NSCLC using a P2Y2 inhibitor, NTPDase, FAK inhibitor, or a combination with TKIs to overcome TKI resistance. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . Statistical analysis was performed using an ANOVA. ** P ≤ 0.01, *** P ≤ 0.001, and **** P ≤ 0.0001.

    Journal: Science Advances

    Article Title: A genome-wide genetic screen reveals the P2Y2-integrin axis as a stabilizer of EGFR mutants in non–small cell lung cancer (NSCLC)

    doi: 10.1126/sciadv.adv3980

    Figure Lengend Snippet: HEK-EGFR-19del-T790M-C797S stable cells were treated with the indicated doses of ( A ) third-generation EGFR TKI (osimertinib), ( B ) P2Y2 inhibitor (kaempferol), and ( C ) FAK inhibitor (PF-562271) and analyzed for cell proliferation using the CyQUANT assay for 4 days. The heatmap graph illustrates the percentile scores of EGFR-19del-T790M-C797S cell proliferation using combination therapies: ( D ) kaempferol with osimertinib, ( E ) PF-562271 with osimertinib, and ( F ) kaempferol with PF-562271, presented as average fluorescence intensities. ( G ) Schematic model of the stability of EGFR-WT and mutants. The left panel depicts ATP levels and EGFR degradation in normal cells, the middle panel represents EGFR-mutant tumor cells, and the right panel outlines strategies to target EGFR stability (represented in red). Ab, antibody. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( H ) Schematic representation of the stability of EGFR mutants resulting from the increased extracellular ATP levels, activating P2Y2 in complex with integrins and stabilizing EGFR. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . ( I ) Proposed model for comprehensive targeting of diverse EGFR mutants in NSCLC using a P2Y2 inhibitor, NTPDase, FAK inhibitor, or a combination with TKIs to overcome TKI resistance. Created in BioRender. G. T. K. Boopathy (2025); https://biorender.com/yklytxg . Statistical analysis was performed using an ANOVA. ** P ≤ 0.01, *** P ≤ 0.001, and **** P ≤ 0.0001.

    Article Snippet: The following antibodies were used for immunoblotting and/or IP: pY1068-EGFR (Thermo Fisher Scientific, cat. no. 44-788G); Mouse anti-EGF Receptor [13/EGFR (RUO) BD Biosciences, cat. no. 555996]; anti-GFP (Abcam; ab290); anti-Lamp1 [Cell Signaling Technology (CST), cat. no. 9091]; anti–phospho-AKT (CST, no. 4060); anti-AKT (CST, no. 9272); anti–phospho-ERK1/2 (CST, cat. no. 9102); anti-ERK1/2 (CST, cat. no. 4370); anti–phospho-FAK (Tyr 397 ) (CST, cat. no. 3283); anti-FAK (CST, cat. no. 3285); anti–Integrin Beta1 (Developmental Studies Hybridoma Bank; clone AIIB2); anti-FLAG M2 clone for Western blotting (Sigma-Aldrich, cat. no. F3165); EZview Red ANTI-FLAG M2 Affinity Gel for IP (Sigma-Aldrich, cat. no. F2426); ChromoTek GFP-Trap magnetic agarose (Proteintech, cat. no. gtma); anti–β-Actin-HRP [Santa Cruz Biotechnology (SCBT), sc-47778 HRP]; anti-rabbit IgG-HRP (SCBT, sc-2357) and m-IgGκ BP-HRP (SCBT, sc-516102); recombinant human EGF (Sino Biological, cat. no. 10605-HNAE); ATP (Sigma-Aldrich, cat. no. A1852); apyrase (Sigma-Aldrich, cat. no. A6535); RGDS peptide (Sigma-Aldrich, cat. no. A9041); PF-562271 (Selleck Chemicals, cat. no. S2890); AR-C 118925XX (Tocris Bioscience, cat. no. 4890); osimertinib (MedChemExpress, cat. no. HY-15772); kaempferol (MedChemExpress, cat. no. HY-14590).

    Techniques: CyQUANT Assay, Fluorescence, Mutagenesis