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targetmol anti cancer  (TargetMol)


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    Structured Review

    TargetMol targetmol anti cancer
    Screening libraries and concentrations used
    Targetmol Anti Cancer, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti-cancer+approved+drug+library/Anti-Cancer+Approved+Drug+Library/pmc13207355-29-0-0
    Average 94 stars, based on 15 article reviews
    targetmol anti cancer - by Bioz Stars, 2026-10
    94/100 stars

    Images

    1) Product Images from "A comprehensive pharmacological survey across heterogeneous patient-derived glioblastoma stem cell models"

    Article Title: A comprehensive pharmacological survey across heterogeneous patient-derived glioblastoma stem cell models

    Journal: iScience

    doi: 10.1016/j.isci.2026.115839

    Screening libraries and concentrations used
    Figure Legend Snippet: Screening libraries and concentrations used

    Techniques Used: Screening


    Figure Legend Snippet:

    Techniques Used: Cell-Signaling, Recombinant, Drug discovery, Extraction, Image Analysis and Quantification, Biomarker Discovery, Stem Cell, Software, Analysis, High Content Screening, Cell Cycle Assay

    Related Articles

    other:

    Article Title: Micrometastasis-derived models enable drug testing for early-stage, high-risk melanoma patients.
    Article Snippet: # S7007 Pembrolizumab (anti-PD-1) Selleckchem Cat# A2005 Nivolumab (anti-PD-1) Selleckchem Cat# A2002 Ipilimumab (anti-CTLA-4) Selleckchem Cat# A2001 Anti-Cancer Approved Drug Library (315 compounds) TargetMol Cat# L2110 CellTiter-Blue® Cell Viability Assay Promega Cat# G8081 ATPlite 1step Luminescence Assay System PerkinElmer Cat# 6016739 Zombie NIR™ Fixable Viability Kit BioLegend Cat# 423105 Flu



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    ( A ) Schematic overview of drug screening comparing non-malignant melanocytes (NHEM-hTERT) and the BRAF V600E-mutated Mel-DCC-11 cell line. The number of drugs that reduced cell viability by more than 50% is indicated, with comparisons selected based on viability values shown in ( B ). ( B ) Viability values of NHEM-hTERT plotted against the viability values of Mel-DCC-11 for all tested 315 compounds at 1 µM. Each dot represents the mean value of two biological replicates. The dotted lines separate the toxic (+/+), Mel-DCC-11-specific (−/+), and Mel-DCC-unspecific (+/−) drugs, which reduce the viability to less than 50% in each group. ( C ) Heatmap of viability values for top-scoring drugs affecting NHEM-hTERT and Mel-DTC-11 (upper panel, n = 12 drugs) or selectively inhibiting Mel-DCC-11 viability by more than 50% (lower panel, n = 19 drugs). The mean viability values of two biological replicates are shown.  .
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    ( A ) Schematic overview of drug screening comparing non-malignant melanocytes (NHEM-hTERT) and the BRAF V600E-mutated Mel-DCC-11 cell line. The number of drugs that reduced cell viability by more than 50% is indicated, with comparisons selected based on viability values shown in ( B ). ( B ) Viability values of NHEM-hTERT plotted against the viability values of Mel-DCC-11 for all tested 315 compounds at 1 µM. Each dot represents the mean value of two biological replicates. The dotted lines separate the toxic (+/+), Mel-DCC-11-specific (−/+), and Mel-DCC-unspecific (+/−) drugs, which reduce the viability to less than 50% in each group. ( C ) Heatmap of viability values for top-scoring drugs affecting NHEM-hTERT and Mel-DTC-11 (upper panel, n = 12 drugs) or selectively inhibiting Mel-DCC-11 viability by more than 50% (lower panel, n = 19 drugs). The mean viability values of two biological replicates are shown.  .
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    ( A ) Schematic overview of drug screening comparing non-malignant melanocytes (NHEM-hTERT) and the BRAF V600E-mutated Mel-DCC-11 cell line. The number of drugs that reduced cell viability by more than 50% is indicated, with comparisons selected based on viability values shown in ( B ). ( B ) Viability values of NHEM-hTERT plotted against the viability values of Mel-DCC-11 for all tested 315 compounds at 1 µM. Each dot represents the mean value of two biological replicates. The dotted lines separate the toxic (+/+), Mel-DCC-11-specific (−/+), and Mel-DCC-unspecific (+/−) drugs, which reduce the viability to less than 50% in each group. ( C ) Heatmap of viability values for top-scoring drugs affecting NHEM-hTERT and Mel-DTC-11 (upper panel, n = 12 drugs) or selectively inhibiting Mel-DCC-11 viability by more than 50% (lower panel, n = 19 drugs). The mean viability values of two biological replicates are shown.  .
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    ( A ) Schematic overview of drug screening comparing non-malignant melanocytes (NHEM-hTERT) and the BRAF V600E-mutated Mel-DCC-11 cell line. The number of drugs that reduced cell viability by more than 50% is indicated, with comparisons selected based on viability values shown in ( B ). ( B ) Viability values of NHEM-hTERT plotted against the viability values of Mel-DCC-11 for all tested 315 compounds at 1 µM. Each dot represents the mean value of two biological replicates. The dotted lines separate the toxic (+/+), Mel-DCC-11-specific (−/+), and Mel-DCC-unspecific (+/−) drugs, which reduce the viability to less than 50% in each group. ( C ) Heatmap of viability values for top-scoring drugs affecting NHEM-hTERT and Mel-DTC-11 (upper panel, n = 12 drugs) or selectively inhibiting Mel-DCC-11 viability by more than 50% (lower panel, n = 19 drugs). The mean viability values of two biological replicates are shown.  .
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    ( A ) Schematic overview of drug screening comparing non-malignant melanocytes (NHEM-hTERT) and the BRAF V600E-mutated Mel-DCC-11 cell line. The number of drugs that reduced cell viability by more than 50% is indicated, with comparisons selected based on viability values shown in ( B ). ( B ) Viability values of NHEM-hTERT plotted against the viability values of Mel-DCC-11 for all tested 315 compounds at 1 µM. Each dot represents the mean value of two biological replicates. The dotted lines separate the toxic (+/+), Mel-DCC-11-specific (−/+), and Mel-DCC-unspecific (+/−) drugs, which reduce the viability to less than 50% in each group. ( C ) Heatmap of viability values for top-scoring drugs affecting NHEM-hTERT and Mel-DTC-11 (upper panel, n = 12 drugs) or selectively inhibiting Mel-DCC-11 viability by more than 50% (lower panel, n = 19 drugs). The mean viability values of two biological replicates are shown.  .
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    Image Search Results


    Screening libraries and concentrations used

    Journal: iScience

    Article Title: A comprehensive pharmacological survey across heterogeneous patient-derived glioblastoma stem cell models

    doi: 10.1016/j.isci.2026.115839

    Figure Lengend Snippet: Screening libraries and concentrations used

    Article Snippet: TargetMol Anti-cancer (2018) , TargetMol , Cat# L2110.

    Techniques: Screening

    Journal: iScience

    Article Title: A comprehensive pharmacological survey across heterogeneous patient-derived glioblastoma stem cell models

    doi: 10.1016/j.isci.2026.115839

    Figure Lengend Snippet:

    Article Snippet: TargetMol Anti-cancer (2018) , TargetMol , Cat# L2110.

    Techniques: Cell-Signaling, Recombinant, Drug discovery, Extraction, Image Analysis and Quantification, Biomarker Discovery, Stem Cell, Software, Analysis, High Content Screening, Cell Cycle Assay

    ( A ) Schematic overview of drug screening comparing non-malignant melanocytes (NHEM-hTERT) and the BRAF V600E-mutated Mel-DCC-11 cell line. The number of drugs that reduced cell viability by more than 50% is indicated, with comparisons selected based on viability values shown in ( B ). ( B ) Viability values of NHEM-hTERT plotted against the viability values of Mel-DCC-11 for all tested 315 compounds at 1 µM. Each dot represents the mean value of two biological replicates. The dotted lines separate the toxic (+/+), Mel-DCC-11-specific (−/+), and Mel-DCC-unspecific (+/−) drugs, which reduce the viability to less than 50% in each group. ( C ) Heatmap of viability values for top-scoring drugs affecting NHEM-hTERT and Mel-DTC-11 (upper panel, n = 12 drugs) or selectively inhibiting Mel-DCC-11 viability by more than 50% (lower panel, n = 19 drugs). The mean viability values of two biological replicates are 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 ) Schematic overview of drug screening comparing non-malignant melanocytes (NHEM-hTERT) and the BRAF V600E-mutated Mel-DCC-11 cell line. The number of drugs that reduced cell viability by more than 50% is indicated, with comparisons selected based on viability values shown in ( B ). ( B ) Viability values of NHEM-hTERT plotted against the viability values of Mel-DCC-11 for all tested 315 compounds at 1 µM. Each dot represents the mean value of two biological replicates. The dotted lines separate the toxic (+/+), Mel-DCC-11-specific (−/+), and Mel-DCC-unspecific (+/−) drugs, which reduce the viability to less than 50% in each group. ( C ) Heatmap of viability values for top-scoring drugs affecting NHEM-hTERT and Mel-DTC-11 (upper panel, n = 12 drugs) or selectively inhibiting Mel-DCC-11 viability by more than 50% (lower panel, n = 19 drugs). The mean viability values of two biological replicates are shown. .

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

    Techniques: Drug discovery

    ( 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, Sensitivity, Cell Viability Assay, Drug discovery

    Reagents and tools table

    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: Reagents and tools table

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

    Techniques: Recombinant, Sequencing, Diagnostic Assay, Membrane, Tissue, DNA Labeling, Microarray, Drug discovery, Cell Viability Assay, Luminescence Assay, Staining, Software, Extraction, Analysis