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small molecule inhibitors  (TargetMol)


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    TargetMol small molecule inhibitors
    Small Molecule Inhibitors, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 16 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti-cancer+drug+library/Anti-Cancer+Drug+Library/pm41902212-64-0-21
    Average 94 stars, based on 16 article reviews
    small molecule inhibitors - by Bioz Stars, 2026-10
    94/100 stars

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    Article Title: Zosuquidar Promotes Antitumor Immunity by Inducing Autophagic Degradation of PD-L1.
    Article Snippet: om BD Biosciences (State of New Jersey, USA). Reagents: The library of anti-cancer drugs which contains 320 chemical compounds dissolved at 10 × 10−3 m in dimethyl sulfoxide (DMSO) was purchased from TargetMol (Shanghai, China). Amlodipine (T1385), zosuqudiar trihydrochloride (T6018), chloroquine (T8689), and MG132 (T2154) were purchased from TargetMol (Shanghai, China). NH4Cl (326372), sulforhodam



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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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    ( 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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    ( 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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    ( 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