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315 anti cancer approved drugs  (TargetMol)


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    TargetMol 315 anti cancer approved drugs
    315 Anti Cancer Approved Drugs, supplied by TargetMol, used in various techniques. Bioz Stars score: 93/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/315 anti cancer approved drugs/product/TargetMol
    Average 93 stars, based on 14 article reviews
    315 anti cancer approved drugs - by Bioz Stars, 2026-04
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    TargetMol 315 anti cancer approved drugs
    315 Anti Cancer Approved Drugs, supplied by TargetMol, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    TargetMol anti cancer approved drug library
    ( A ) Upper graph: Vemurafinib treatment of Mel-DCC CLs. Cells were incubated with doses ranging from 0.025 µM to 5 µM Vemurafenib for 5 days. Cell viability is shown for BRAF wt Mel-DCC-07 (red, n = 4), BRAF V600K-mutated Mel-DCC-13 (gray, n = 4), and BRAF V600E-mutated Mel-DCC-02 (black, n = 5). Lower graph: Binimetinib treatment of Mel-DCC CLs. Cells were incubated with Binimetinib at doses ranging from 0.001 µM to 1 µM for 5 days. Cell viability is shown for NRAS Q61R-mutated Mel-DCC-04 (red, n = 4), NRAS T58I-mutated Mel-DCC-07 (gray, n = 6), and NRAS Q61K-mutated Mel-DCC-01 (black, n = 4). Each dot represents the mean value ± SD of biological replicates. ( B ) Generation of a Vemurafenib-resistant BRAF-mutated melanoma cell line (Mel-DCC-11-R). Resistance was generated through stepwise exposure to increasing concentrations of Vemurafenib over the indicated timeframe. Sensitivity of Mel-DCC-11 (black, n = 3) vs. Mel-DCC-11-R (red, n = 5) to Vemurafenib is shown. Each dot represents the mean value ± SD of biological replicates. ( C ) Outcome of experimental drug testing with <t>315</t> <t>anti-cancer</t> drugs on BRAF V600E-mutated Mel-DCC-11 and Vemurafenib-resistant Mel-DCC-11-R, alone or in combination with 8 µM Vemurafenib (Mel-DCC-11-R + V). The number of drugs that reduce cell viability to less than 80% is indicated. ( D ) Heatmap showing the drug-induced reduction of the viability in the Vemurafenib-restistant CL, screened in the presence (Mel-DCC-11-R + V) or absence (Mel-DCC-11-R) of Vemurafenib, alongside the parental Vemurafenib-sensitive Mel-DCC-11, screened without Vemurafenib. The mean viability of two biological replicates is shown. .
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    TargetMol targetmol anti cancer drugs library
    ( A ) Upper graph: Vemurafinib treatment of Mel-DCC CLs. Cells were incubated with doses ranging from 0.025 µM to 5 µM Vemurafenib for 5 days. Cell viability is shown for BRAF wt Mel-DCC-07 (red, n = 4), BRAF V600K-mutated Mel-DCC-13 (gray, n = 4), and BRAF V600E-mutated Mel-DCC-02 (black, n = 5). Lower graph: Binimetinib treatment of Mel-DCC CLs. Cells were incubated with Binimetinib at doses ranging from 0.001 µM to 1 µM for 5 days. Cell viability is shown for NRAS Q61R-mutated Mel-DCC-04 (red, n = 4), NRAS T58I-mutated Mel-DCC-07 (gray, n = 6), and NRAS Q61K-mutated Mel-DCC-01 (black, n = 4). Each dot represents the mean value ± SD of biological replicates. ( B ) Generation of a Vemurafenib-resistant BRAF-mutated melanoma cell line (Mel-DCC-11-R). Resistance was generated through stepwise exposure to increasing concentrations of Vemurafenib over the indicated timeframe. Sensitivity of Mel-DCC-11 (black, n = 3) vs. Mel-DCC-11-R (red, n = 5) to Vemurafenib is shown. Each dot represents the mean value ± SD of biological replicates. ( C ) Outcome of experimental drug testing with <t>315</t> <t>anti-cancer</t> drugs on BRAF V600E-mutated Mel-DCC-11 and Vemurafenib-resistant Mel-DCC-11-R, alone or in combination with 8 µM Vemurafenib (Mel-DCC-11-R + V). The number of drugs that reduce cell viability to less than 80% is indicated. ( D ) Heatmap showing the drug-induced reduction of the viability in the Vemurafenib-restistant CL, screened in the presence (Mel-DCC-11-R + V) or absence (Mel-DCC-11-R) of Vemurafenib, alongside the parental Vemurafenib-sensitive Mel-DCC-11, screened without Vemurafenib. The mean viability of two biological replicates is shown. .
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    TargetMol targetmol anticancer set
    ( A ) Upper graph: Vemurafinib treatment of Mel-DCC CLs. Cells were incubated with doses ranging from 0.025 µM to 5 µM Vemurafenib for 5 days. Cell viability is shown for BRAF wt Mel-DCC-07 (red, n = 4), BRAF V600K-mutated Mel-DCC-13 (gray, n = 4), and BRAF V600E-mutated Mel-DCC-02 (black, n = 5). Lower graph: Binimetinib treatment of Mel-DCC CLs. Cells were incubated with Binimetinib at doses ranging from 0.001 µM to 1 µM for 5 days. Cell viability is shown for NRAS Q61R-mutated Mel-DCC-04 (red, n = 4), NRAS T58I-mutated Mel-DCC-07 (gray, n = 6), and NRAS Q61K-mutated Mel-DCC-01 (black, n = 4). Each dot represents the mean value ± SD of biological replicates. ( B ) Generation of a Vemurafenib-resistant BRAF-mutated melanoma cell line (Mel-DCC-11-R). Resistance was generated through stepwise exposure to increasing concentrations of Vemurafenib over the indicated timeframe. Sensitivity of Mel-DCC-11 (black, n = 3) vs. Mel-DCC-11-R (red, n = 5) to Vemurafenib is shown. Each dot represents the mean value ± SD of biological replicates. ( C ) Outcome of experimental drug testing with <t>315</t> <t>anti-cancer</t> drugs on BRAF V600E-mutated Mel-DCC-11 and Vemurafenib-resistant Mel-DCC-11-R, alone or in combination with 8 µM Vemurafenib (Mel-DCC-11-R + V). The number of drugs that reduce cell viability to less than 80% is indicated. ( D ) Heatmap showing the drug-induced reduction of the viability in the Vemurafenib-restistant CL, screened in the presence (Mel-DCC-11-R + V) or absence (Mel-DCC-11-R) of Vemurafenib, alongside the parental Vemurafenib-sensitive Mel-DCC-11, screened without Vemurafenib. The mean viability of two biological replicates is shown. .
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    Selleck Chemicals anti cancer drugs
    ( A ) Upper graph: Vemurafinib treatment of Mel-DCC CLs. Cells were incubated with doses ranging from 0.025 µM to 5 µM Vemurafenib for 5 days. Cell viability is shown for BRAF wt Mel-DCC-07 (red, n = 4), BRAF V600K-mutated Mel-DCC-13 (gray, n = 4), and BRAF V600E-mutated Mel-DCC-02 (black, n = 5). Lower graph: Binimetinib treatment of Mel-DCC CLs. Cells were incubated with Binimetinib at doses ranging from 0.001 µM to 1 µM for 5 days. Cell viability is shown for NRAS Q61R-mutated Mel-DCC-04 (red, n = 4), NRAS T58I-mutated Mel-DCC-07 (gray, n = 6), and NRAS Q61K-mutated Mel-DCC-01 (black, n = 4). Each dot represents the mean value ± SD of biological replicates. ( B ) Generation of a Vemurafenib-resistant BRAF-mutated melanoma cell line (Mel-DCC-11-R). Resistance was generated through stepwise exposure to increasing concentrations of Vemurafenib over the indicated timeframe. Sensitivity of Mel-DCC-11 (black, n = 3) vs. Mel-DCC-11-R (red, n = 5) to Vemurafenib is shown. Each dot represents the mean value ± SD of biological replicates. ( C ) Outcome of experimental drug testing with <t>315</t> <t>anti-cancer</t> drugs on BRAF V600E-mutated Mel-DCC-11 and Vemurafenib-resistant Mel-DCC-11-R, alone or in combination with 8 µM Vemurafenib (Mel-DCC-11-R + V). The number of drugs that reduce cell viability to less than 80% is indicated. ( D ) Heatmap showing the drug-induced reduction of the viability in the Vemurafenib-restistant CL, screened in the presence (Mel-DCC-11-R + V) or absence (Mel-DCC-11-R) of Vemurafenib, alongside the parental Vemurafenib-sensitive Mel-DCC-11, screened without Vemurafenib. The mean viability of two biological replicates is shown. .
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    Selleck Chemicals tumor drug library
    ( A ) Upper graph: Vemurafinib treatment of Mel-DCC CLs. Cells were incubated with doses ranging from 0.025 µM to 5 µM Vemurafenib for 5 days. Cell viability is shown for BRAF wt Mel-DCC-07 (red, n = 4), BRAF V600K-mutated Mel-DCC-13 (gray, n = 4), and BRAF V600E-mutated Mel-DCC-02 (black, n = 5). Lower graph: Binimetinib treatment of Mel-DCC CLs. Cells were incubated with Binimetinib at doses ranging from 0.001 µM to 1 µM for 5 days. Cell viability is shown for NRAS Q61R-mutated Mel-DCC-04 (red, n = 4), NRAS T58I-mutated Mel-DCC-07 (gray, n = 6), and NRAS Q61K-mutated Mel-DCC-01 (black, n = 4). Each dot represents the mean value ± SD of biological replicates. ( B ) Generation of a Vemurafenib-resistant BRAF-mutated melanoma cell line (Mel-DCC-11-R). Resistance was generated through stepwise exposure to increasing concentrations of Vemurafenib over the indicated timeframe. Sensitivity of Mel-DCC-11 (black, n = 3) vs. Mel-DCC-11-R (red, n = 5) to Vemurafenib is shown. Each dot represents the mean value ± SD of biological replicates. ( C ) Outcome of experimental drug testing with <t>315</t> <t>anti-cancer</t> drugs on BRAF V600E-mutated Mel-DCC-11 and Vemurafenib-resistant Mel-DCC-11-R, alone or in combination with 8 µM Vemurafenib (Mel-DCC-11-R + V). The number of drugs that reduce cell viability to less than 80% is indicated. ( D ) Heatmap showing the drug-induced reduction of the viability in the Vemurafenib-restistant CL, screened in the presence (Mel-DCC-11-R + V) or absence (Mel-DCC-11-R) of Vemurafenib, alongside the parental Vemurafenib-sensitive Mel-DCC-11, screened without Vemurafenib. The mean viability of two biological replicates is shown. .
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    ( A ) Upper graph: Vemurafinib treatment of Mel-DCC CLs. Cells were incubated with doses ranging from 0.025 µM to 5 µM Vemurafenib for 5 days. Cell viability is shown for BRAF wt Mel-DCC-07 (red, n = 4), BRAF V600K-mutated Mel-DCC-13 (gray, n = 4), and BRAF V600E-mutated Mel-DCC-02 (black, n = 5). Lower graph: Binimetinib treatment of Mel-DCC CLs. Cells were incubated with Binimetinib at doses ranging from 0.001 µM to 1 µM for 5 days. Cell viability is shown for NRAS Q61R-mutated Mel-DCC-04 (red, n = 4), NRAS T58I-mutated Mel-DCC-07 (gray, n = 6), and NRAS Q61K-mutated Mel-DCC-01 (black, n = 4). Each dot represents the mean value ± SD of biological replicates. ( B ) Generation of a Vemurafenib-resistant BRAF-mutated melanoma cell line (Mel-DCC-11-R). Resistance was generated through stepwise exposure to increasing concentrations of Vemurafenib over the indicated timeframe. Sensitivity of Mel-DCC-11 (black, n = 3) vs. Mel-DCC-11-R (red, n = 5) to Vemurafenib is shown. Each dot represents the mean value ± SD of biological replicates. ( C ) Outcome of experimental drug testing with <t>315</t> <t>anti-cancer</t> drugs on BRAF V600E-mutated Mel-DCC-11 and Vemurafenib-resistant Mel-DCC-11-R, alone or in combination with 8 µM Vemurafenib (Mel-DCC-11-R + V). The number of drugs that reduce cell viability to less than 80% is indicated. ( D ) Heatmap showing the drug-induced reduction of the viability in the Vemurafenib-restistant CL, screened in the presence (Mel-DCC-11-R + V) or absence (Mel-DCC-11-R) of Vemurafenib, alongside the parental Vemurafenib-sensitive Mel-DCC-11, screened without Vemurafenib. The mean viability of two biological replicates is shown. .
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    TargetMol targetmol l2110
    ( A ) Upper graph: Vemurafinib treatment of Mel-DCC CLs. Cells were incubated with doses ranging from 0.025 µM to 5 µM Vemurafenib for 5 days. Cell viability is shown for BRAF wt Mel-DCC-07 (red, n = 4), BRAF V600K-mutated Mel-DCC-13 (gray, n = 4), and BRAF V600E-mutated Mel-DCC-02 (black, n = 5). Lower graph: Binimetinib treatment of Mel-DCC CLs. Cells were incubated with Binimetinib at doses ranging from 0.001 µM to 1 µM for 5 days. Cell viability is shown for NRAS Q61R-mutated Mel-DCC-04 (red, n = 4), NRAS T58I-mutated Mel-DCC-07 (gray, n = 6), and NRAS Q61K-mutated Mel-DCC-01 (black, n = 4). Each dot represents the mean value ± SD of biological replicates. ( B ) Generation of a Vemurafenib-resistant BRAF-mutated melanoma cell line (Mel-DCC-11-R). Resistance was generated through stepwise exposure to increasing concentrations of Vemurafenib over the indicated timeframe. Sensitivity of Mel-DCC-11 (black, n = 3) vs. Mel-DCC-11-R (red, n = 5) to Vemurafenib is shown. Each dot represents the mean value ± SD of biological replicates. ( C ) Outcome of experimental drug testing with <t>315</t> <t>anti-cancer</t> drugs on BRAF V600E-mutated Mel-DCC-11 and Vemurafenib-resistant Mel-DCC-11-R, alone or in combination with 8 µM Vemurafenib (Mel-DCC-11-R + V). The number of drugs that reduce cell viability to less than 80% is indicated. ( D ) Heatmap showing the drug-induced reduction of the viability in the Vemurafenib-restistant CL, screened in the presence (Mel-DCC-11-R + V) or absence (Mel-DCC-11-R) of Vemurafenib, alongside the parental Vemurafenib-sensitive Mel-DCC-11, screened without Vemurafenib. The mean viability of two biological replicates is shown. .
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    ( A ) Upper graph: Vemurafinib treatment of Mel-DCC CLs. Cells were incubated with doses ranging from 0.025 µM to 5 µM Vemurafenib for 5 days. Cell viability is shown for BRAF wt Mel-DCC-07 (red, n = 4), BRAF V600K-mutated Mel-DCC-13 (gray, n = 4), and BRAF V600E-mutated Mel-DCC-02 (black, n = 5). Lower graph: Binimetinib treatment of Mel-DCC CLs. Cells were incubated with Binimetinib at doses ranging from 0.001 µM to 1 µM for 5 days. Cell viability is shown for NRAS Q61R-mutated Mel-DCC-04 (red, n = 4), NRAS T58I-mutated Mel-DCC-07 (gray, n = 6), and NRAS Q61K-mutated Mel-DCC-01 (black, n = 4). Each dot represents the mean value ± SD of biological replicates. ( B ) Generation of a Vemurafenib-resistant BRAF-mutated melanoma cell line (Mel-DCC-11-R). Resistance was generated through stepwise exposure to increasing concentrations of Vemurafenib over the indicated timeframe. Sensitivity of Mel-DCC-11 (black, n = 3) vs. Mel-DCC-11-R (red, n = 5) to Vemurafenib is shown. Each dot represents the mean value ± SD of biological replicates. ( C ) Outcome of experimental drug testing with 315 anti-cancer drugs on BRAF V600E-mutated Mel-DCC-11 and Vemurafenib-resistant Mel-DCC-11-R, alone or in combination with 8 µM Vemurafenib (Mel-DCC-11-R + V). The number of drugs that reduce cell viability to less than 80% is indicated. ( D ) Heatmap showing the drug-induced reduction of the viability in the Vemurafenib-restistant CL, screened in the presence (Mel-DCC-11-R + V) or absence (Mel-DCC-11-R) of Vemurafenib, alongside the parental Vemurafenib-sensitive Mel-DCC-11, screened without Vemurafenib. The mean viability of two biological replicates is shown. .

    Journal: EMBO Molecular Medicine

    Article Title: Micrometastasis-derived models enable drug testing for early-stage, high-risk melanoma patients

    doi: 10.1038/s44321-025-00339-8

    Figure Lengend Snippet: ( A ) Upper graph: Vemurafinib treatment of Mel-DCC CLs. Cells were incubated with doses ranging from 0.025 µM to 5 µM Vemurafenib for 5 days. Cell viability is shown for BRAF wt Mel-DCC-07 (red, n = 4), BRAF V600K-mutated Mel-DCC-13 (gray, n = 4), and BRAF V600E-mutated Mel-DCC-02 (black, n = 5). Lower graph: Binimetinib treatment of Mel-DCC CLs. Cells were incubated with Binimetinib at doses ranging from 0.001 µM to 1 µM for 5 days. Cell viability is shown for NRAS Q61R-mutated Mel-DCC-04 (red, n = 4), NRAS T58I-mutated Mel-DCC-07 (gray, n = 6), and NRAS Q61K-mutated Mel-DCC-01 (black, n = 4). Each dot represents the mean value ± SD of biological replicates. ( B ) Generation of a Vemurafenib-resistant BRAF-mutated melanoma cell line (Mel-DCC-11-R). Resistance was generated through stepwise exposure to increasing concentrations of Vemurafenib over the indicated timeframe. Sensitivity of Mel-DCC-11 (black, n = 3) vs. Mel-DCC-11-R (red, n = 5) to Vemurafenib is shown. Each dot represents the mean value ± SD of biological replicates. ( C ) Outcome of experimental drug testing with 315 anti-cancer drugs on BRAF V600E-mutated Mel-DCC-11 and Vemurafenib-resistant Mel-DCC-11-R, alone or in combination with 8 µM Vemurafenib (Mel-DCC-11-R + V). The number of drugs that reduce cell viability to less than 80% is indicated. ( D ) Heatmap showing the drug-induced reduction of the viability in the Vemurafenib-restistant CL, screened in the presence (Mel-DCC-11-R + V) or absence (Mel-DCC-11-R) of Vemurafenib, alongside the parental Vemurafenib-sensitive Mel-DCC-11, screened without Vemurafenib. The mean viability of two biological replicates is shown. .

    Article Snippet: Anti-Cancer Approved Drug Library (315 compounds) , TargetMol , Cat# L2110.

    Techniques: Incubation, Generated