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rmc 6236  (MedChemExpress)


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    Structured Review

    MedChemExpress rmc 6236
    (A) Proliferation assays of MTAP-deficient HCC4006 cells treated with AMG 193 for six days in combination with 1 μM osimertinib. (B) Time-course of HCC4006 cell proliferation assessed by live-cell imaging following treatment with AMG 193, osimertinib or their combination. (C) Loewe synergy scores of MTAP-deficient, oncogene-driven NSCLC cell lines were calculated from cell proliferation assays performed cells treated with the combination of TKI (osimertinib – EGFR, lorlatinib – <t>ALK,</t> <t>RMC-6236</t> – KRAS) and AMG 193 for 5 or 10 days. (D) AMG 193 sensitivity (AUC of cell proliferation dose-response assays) in cell lines derived from targeted therapy–naïve versus previously treated tumors. (E) Cell proliferation of matched parental and resistant cell line pairs (HCC4006/HCC4006-GR, H3122/H3122-LR, and LU99A/LU99A-RR) following treatment with AMG 193 for six days. (F) Time course of HCC4006 cell proliferation assessed by live-cell imaging upon treatment with 1 μM osimertinib followed by switch to or addition of 100 nM AMG 193. (G) HCC4006 cells were treated with osimertinib for 14 days to establish DTP cells, the treated with the indicated drugs. Cell proliferation was assessed by live-cell imaging. (H) Colony formation assays demonstrating enhanced efficacy of AMG 193 and TKI combination in both parental and DTP conditions. DTP populations were generated by treatment with osimertinib (HCC4006) or lorlatinib (H3122) for 14 days prior to the experiment.
    Rmc 6236, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rmc 6236/product/MedChemExpress
    Average 94 stars, based on 10 article reviews
    rmc 6236 - by Bioz Stars, 2026-02
    94/100 stars

    Images

    1) Product Images from "Prevalence and Actionability of MTAP Loss in Oncogene-Driven Lung Cancer"

    Article Title: Prevalence and Actionability of MTAP Loss in Oncogene-Driven Lung Cancer

    Journal: bioRxiv

    doi: 10.64898/2026.01.21.700721

    (A) Proliferation assays of MTAP-deficient HCC4006 cells treated with AMG 193 for six days in combination with 1 μM osimertinib. (B) Time-course of HCC4006 cell proliferation assessed by live-cell imaging following treatment with AMG 193, osimertinib or their combination. (C) Loewe synergy scores of MTAP-deficient, oncogene-driven NSCLC cell lines were calculated from cell proliferation assays performed cells treated with the combination of TKI (osimertinib – EGFR, lorlatinib – ALK, RMC-6236 – KRAS) and AMG 193 for 5 or 10 days. (D) AMG 193 sensitivity (AUC of cell proliferation dose-response assays) in cell lines derived from targeted therapy–naïve versus previously treated tumors. (E) Cell proliferation of matched parental and resistant cell line pairs (HCC4006/HCC4006-GR, H3122/H3122-LR, and LU99A/LU99A-RR) following treatment with AMG 193 for six days. (F) Time course of HCC4006 cell proliferation assessed by live-cell imaging upon treatment with 1 μM osimertinib followed by switch to or addition of 100 nM AMG 193. (G) HCC4006 cells were treated with osimertinib for 14 days to establish DTP cells, the treated with the indicated drugs. Cell proliferation was assessed by live-cell imaging. (H) Colony formation assays demonstrating enhanced efficacy of AMG 193 and TKI combination in both parental and DTP conditions. DTP populations were generated by treatment with osimertinib (HCC4006) or lorlatinib (H3122) for 14 days prior to the experiment.
    Figure Legend Snippet: (A) Proliferation assays of MTAP-deficient HCC4006 cells treated with AMG 193 for six days in combination with 1 μM osimertinib. (B) Time-course of HCC4006 cell proliferation assessed by live-cell imaging following treatment with AMG 193, osimertinib or their combination. (C) Loewe synergy scores of MTAP-deficient, oncogene-driven NSCLC cell lines were calculated from cell proliferation assays performed cells treated with the combination of TKI (osimertinib – EGFR, lorlatinib – ALK, RMC-6236 – KRAS) and AMG 193 for 5 or 10 days. (D) AMG 193 sensitivity (AUC of cell proliferation dose-response assays) in cell lines derived from targeted therapy–naïve versus previously treated tumors. (E) Cell proliferation of matched parental and resistant cell line pairs (HCC4006/HCC4006-GR, H3122/H3122-LR, and LU99A/LU99A-RR) following treatment with AMG 193 for six days. (F) Time course of HCC4006 cell proliferation assessed by live-cell imaging upon treatment with 1 μM osimertinib followed by switch to or addition of 100 nM AMG 193. (G) HCC4006 cells were treated with osimertinib for 14 days to establish DTP cells, the treated with the indicated drugs. Cell proliferation was assessed by live-cell imaging. (H) Colony formation assays demonstrating enhanced efficacy of AMG 193 and TKI combination in both parental and DTP conditions. DTP populations were generated by treatment with osimertinib (HCC4006) or lorlatinib (H3122) for 14 days prior to the experiment.

    Techniques Used: Live Cell Imaging, Derivative Assay, Generated

    (A) Proliferation assays of MTAP-deficient MGH707-1, SKLU1 and MGH1089-1 cells treated with AMG 193 for six days in combination with 1 μM osimertinib or 300 nM RMC-6236. (B–C) 2×2 dose–response matrices and Loewe synergy scores for AMG 193 combined with targeted therapies after 5 (B) or 10 (C) days of treatment. Most combinations showed additive effects, with some variability in synergy at individual dose levels observed across models. (D–E) Growth inhibition index values for AMG 193 combined with targeted therapies after 5 (D) or 10 (E) days of treatment. 0 = no proliferation effect (value of untreated cells at end of experiment), 100 = cytostasis (no change from day 0), 200 = cytotoxicity (no viability signal at end of experiment).
    Figure Legend Snippet: (A) Proliferation assays of MTAP-deficient MGH707-1, SKLU1 and MGH1089-1 cells treated with AMG 193 for six days in combination with 1 μM osimertinib or 300 nM RMC-6236. (B–C) 2×2 dose–response matrices and Loewe synergy scores for AMG 193 combined with targeted therapies after 5 (B) or 10 (C) days of treatment. Most combinations showed additive effects, with some variability in synergy at individual dose levels observed across models. (D–E) Growth inhibition index values for AMG 193 combined with targeted therapies after 5 (D) or 10 (E) days of treatment. 0 = no proliferation effect (value of untreated cells at end of experiment), 100 = cytostasis (no change from day 0), 200 = cytotoxicity (no viability signal at end of experiment).

    Techniques Used: Inhibition



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    rmc 6236  (MedChemExpress)
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    MedChemExpress rmc 6236
    (A) Proliferation assays of MTAP-deficient HCC4006 cells treated with AMG 193 for six days in combination with 1 μM osimertinib. (B) Time-course of HCC4006 cell proliferation assessed by live-cell imaging following treatment with AMG 193, osimertinib or their combination. (C) Loewe synergy scores of MTAP-deficient, oncogene-driven NSCLC cell lines were calculated from cell proliferation assays performed cells treated with the combination of TKI (osimertinib – EGFR, lorlatinib – <t>ALK,</t> <t>RMC-6236</t> – KRAS) and AMG 193 for 5 or 10 days. (D) AMG 193 sensitivity (AUC of cell proliferation dose-response assays) in cell lines derived from targeted therapy–naïve versus previously treated tumors. (E) Cell proliferation of matched parental and resistant cell line pairs (HCC4006/HCC4006-GR, H3122/H3122-LR, and LU99A/LU99A-RR) following treatment with AMG 193 for six days. (F) Time course of HCC4006 cell proliferation assessed by live-cell imaging upon treatment with 1 μM osimertinib followed by switch to or addition of 100 nM AMG 193. (G) HCC4006 cells were treated with osimertinib for 14 days to establish DTP cells, the treated with the indicated drugs. Cell proliferation was assessed by live-cell imaging. (H) Colony formation assays demonstrating enhanced efficacy of AMG 193 and TKI combination in both parental and DTP conditions. DTP populations were generated by treatment with osimertinib (HCC4006) or lorlatinib (H3122) for 14 days prior to the experiment.
    Rmc 6236, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rmc 6236/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    rmc 6236 - by Bioz Stars, 2026-02
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    pan rasi rmc 6236 inhibitor  (MedChemExpress)
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    (A) Proliferation assays of MTAP-deficient HCC4006 cells treated with AMG 193 for six days in combination with 1 μM osimertinib. (B) Time-course of HCC4006 cell proliferation assessed by live-cell imaging following treatment with AMG 193, osimertinib or their combination. (C) Loewe synergy scores of MTAP-deficient, oncogene-driven NSCLC cell lines were calculated from cell proliferation assays performed cells treated with the combination of TKI (osimertinib – EGFR, lorlatinib – <t>ALK,</t> <t>RMC-6236</t> – KRAS) and AMG 193 for 5 or 10 days. (D) AMG 193 sensitivity (AUC of cell proliferation dose-response assays) in cell lines derived from targeted therapy–naïve versus previously treated tumors. (E) Cell proliferation of matched parental and resistant cell line pairs (HCC4006/HCC4006-GR, H3122/H3122-LR, and LU99A/LU99A-RR) following treatment with AMG 193 for six days. (F) Time course of HCC4006 cell proliferation assessed by live-cell imaging upon treatment with 1 μM osimertinib followed by switch to or addition of 100 nM AMG 193. (G) HCC4006 cells were treated with osimertinib for 14 days to establish DTP cells, the treated with the indicated drugs. Cell proliferation was assessed by live-cell imaging. (H) Colony formation assays demonstrating enhanced efficacy of AMG 193 and TKI combination in both parental and DTP conditions. DTP populations were generated by treatment with osimertinib (HCC4006) or lorlatinib (H3122) for 14 days prior to the experiment.
    Pan Rasi Rmc 6236 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pan rasi rmc 6236 inhibitor/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    pan rasi rmc 6236 inhibitor - by Bioz Stars, 2026-02
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    (A) Proliferation assays of MTAP-deficient HCC4006 cells treated with AMG 193 for six days in combination with 1 μM osimertinib. (B) Time-course of HCC4006 cell proliferation assessed by live-cell imaging following treatment with AMG 193, osimertinib or their combination. (C) Loewe synergy scores of MTAP-deficient, oncogene-driven NSCLC cell lines were calculated from cell proliferation assays performed cells treated with the combination of TKI (osimertinib – EGFR, lorlatinib – ALK, RMC-6236 – KRAS) and AMG 193 for 5 or 10 days. (D) AMG 193 sensitivity (AUC of cell proliferation dose-response assays) in cell lines derived from targeted therapy–naïve versus previously treated tumors. (E) Cell proliferation of matched parental and resistant cell line pairs (HCC4006/HCC4006-GR, H3122/H3122-LR, and LU99A/LU99A-RR) following treatment with AMG 193 for six days. (F) Time course of HCC4006 cell proliferation assessed by live-cell imaging upon treatment with 1 μM osimertinib followed by switch to or addition of 100 nM AMG 193. (G) HCC4006 cells were treated with osimertinib for 14 days to establish DTP cells, the treated with the indicated drugs. Cell proliferation was assessed by live-cell imaging. (H) Colony formation assays demonstrating enhanced efficacy of AMG 193 and TKI combination in both parental and DTP conditions. DTP populations were generated by treatment with osimertinib (HCC4006) or lorlatinib (H3122) for 14 days prior to the experiment.

    Journal: bioRxiv

    Article Title: Prevalence and Actionability of MTAP Loss in Oncogene-Driven Lung Cancer

    doi: 10.64898/2026.01.21.700721

    Figure Lengend Snippet: (A) Proliferation assays of MTAP-deficient HCC4006 cells treated with AMG 193 for six days in combination with 1 μM osimertinib. (B) Time-course of HCC4006 cell proliferation assessed by live-cell imaging following treatment with AMG 193, osimertinib or their combination. (C) Loewe synergy scores of MTAP-deficient, oncogene-driven NSCLC cell lines were calculated from cell proliferation assays performed cells treated with the combination of TKI (osimertinib – EGFR, lorlatinib – ALK, RMC-6236 – KRAS) and AMG 193 for 5 or 10 days. (D) AMG 193 sensitivity (AUC of cell proliferation dose-response assays) in cell lines derived from targeted therapy–naïve versus previously treated tumors. (E) Cell proliferation of matched parental and resistant cell line pairs (HCC4006/HCC4006-GR, H3122/H3122-LR, and LU99A/LU99A-RR) following treatment with AMG 193 for six days. (F) Time course of HCC4006 cell proliferation assessed by live-cell imaging upon treatment with 1 μM osimertinib followed by switch to or addition of 100 nM AMG 193. (G) HCC4006 cells were treated with osimertinib for 14 days to establish DTP cells, the treated with the indicated drugs. Cell proliferation was assessed by live-cell imaging. (H) Colony formation assays demonstrating enhanced efficacy of AMG 193 and TKI combination in both parental and DTP conditions. DTP populations were generated by treatment with osimertinib (HCC4006) or lorlatinib (H3122) for 14 days prior to the experiment.

    Article Snippet: For cell culture, the following tyrosine kinase inhibitors (TKIs) were used: gefitinib (first-generation EGFR inhibitor; Selleck Chemicals, Houston, TX, USA), osimertinib (third-generation EGFR inhibitor; Selleck Chemicals, Houston, TX, USA), RMC-6236 (pan-KRAS inhibitor; MedChemExpress, Monmouth Junction, NJ, USA), alectinib (second-generation ALK inhibitor; Selleck Chemicals, Houston, TX, USA), crizotinib (first-generation ALK inhibitor; Selleck Chemicals, Houston, TX, USA), and lorlatinib (third-generation ALK inhibitor; MedChemExpress, Monmouth Junction, NJ, USA).

    Techniques: Live Cell Imaging, Derivative Assay, Generated

    (A) Proliferation assays of MTAP-deficient MGH707-1, SKLU1 and MGH1089-1 cells treated with AMG 193 for six days in combination with 1 μM osimertinib or 300 nM RMC-6236. (B–C) 2×2 dose–response matrices and Loewe synergy scores for AMG 193 combined with targeted therapies after 5 (B) or 10 (C) days of treatment. Most combinations showed additive effects, with some variability in synergy at individual dose levels observed across models. (D–E) Growth inhibition index values for AMG 193 combined with targeted therapies after 5 (D) or 10 (E) days of treatment. 0 = no proliferation effect (value of untreated cells at end of experiment), 100 = cytostasis (no change from day 0), 200 = cytotoxicity (no viability signal at end of experiment).

    Journal: bioRxiv

    Article Title: Prevalence and Actionability of MTAP Loss in Oncogene-Driven Lung Cancer

    doi: 10.64898/2026.01.21.700721

    Figure Lengend Snippet: (A) Proliferation assays of MTAP-deficient MGH707-1, SKLU1 and MGH1089-1 cells treated with AMG 193 for six days in combination with 1 μM osimertinib or 300 nM RMC-6236. (B–C) 2×2 dose–response matrices and Loewe synergy scores for AMG 193 combined with targeted therapies after 5 (B) or 10 (C) days of treatment. Most combinations showed additive effects, with some variability in synergy at individual dose levels observed across models. (D–E) Growth inhibition index values for AMG 193 combined with targeted therapies after 5 (D) or 10 (E) days of treatment. 0 = no proliferation effect (value of untreated cells at end of experiment), 100 = cytostasis (no change from day 0), 200 = cytotoxicity (no viability signal at end of experiment).

    Article Snippet: For cell culture, the following tyrosine kinase inhibitors (TKIs) were used: gefitinib (first-generation EGFR inhibitor; Selleck Chemicals, Houston, TX, USA), osimertinib (third-generation EGFR inhibitor; Selleck Chemicals, Houston, TX, USA), RMC-6236 (pan-KRAS inhibitor; MedChemExpress, Monmouth Junction, NJ, USA), alectinib (second-generation ALK inhibitor; Selleck Chemicals, Houston, TX, USA), crizotinib (first-generation ALK inhibitor; Selleck Chemicals, Houston, TX, USA), and lorlatinib (third-generation ALK inhibitor; MedChemExpress, Monmouth Junction, NJ, USA).

    Techniques: Inhibition