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TargetMol
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TargetMol
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Image Search Results
Journal: BMC Biology
Article Title: Identification of Epinastine as CD96/PVR inhibitor for cancer immunotherapy
doi: 10.1186/s12915-025-02132-y
Figure Lengend Snippet: Virtual screening of small molecules from the FDA-approved drug library. A Crystal structure of CD96 in complex with PVR (PDB Code: 6ARQ), with the binding interface highlighted in blue. B Detailed depiction of amino acids involved in the CD96/PVR interaction, with residues shown in stick representation. C Relationship between molecular weight and S-value for selected small molecules. Red indicates molecules with molecular weights between 250 and 700 and S-values of -5 or less. D-F Results of further screening of small molecules interacting with the CD96/PVR binding interface. G Distribution of S-values for the final 15 selected small molecules
Article Snippet: 1729 small molecules were obtained from
Techniques: Drug discovery, Binding Assay, Molecular Weight
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:
Techniques: Incubation, Generated