small molecule inhibitors  (TargetMol)

Journal: bioRxiv

Article Title: Functional and sensitivity profiling of the KIT Mutation Landscape in Melanoma

doi: 10.64898/2026.02.18.706482

Figure Lengend Snippet: KIT mutations shows differential responses towards common KIT inhibitors in vitro. (A) Western Blot analysis revealed changes in cell growth and proliferation pathways upon expression of KIT mutants in MeWO melanoma cells. (B) Upper panel: Monitoring relative growth of melanoma cell spheroids expressing KIT mutants using high-content microscopy. Lower panel: Representative image depicting spheroid size after 8 days of growth in 3D environment. (C) Western Blot demonstrating the expression of KIT in Ba/F3 cells. (D) Assessment of relative growth of Ba/F3 cells expressing different KIT mutants following withdrawal of IL-3 from the culture medium, measured using cell-titre glo assay. (E) Heatmap shows the relative IC50 of Ba/F3 cell with KIT mutants against KIT inhibitors. (F) Violin plot illustrating the IC50 values of MeWo cells expressing KIT mutants when treated with various KIT inhibitors. Results were obtained from three independent experiments. The horizontal line represents the mean, and statistical analysis was performed using one-way ANOVA.

Article Snippet: Small molecule inhibitors (Imatinib, Sunitinib, Nilotinib, Nintedanib, and Ripretinib) were purchased from MedChemExpress, dissolved in DMSO to a 10 mM stock, and stored at −80°C.

Techniques: In Vitro, Western Blot, Expressing, Microscopy, Glo Assay

Journal: bioRxiv

Article Title: Functional and sensitivity profiling of the KIT Mutation Landscape in Melanoma

doi: 10.64898/2026.02.18.706482

Figure Lengend Snippet: In vivo anti-tumor efficacy of KIT inhibitors against MeWo cells expressing KIT WT/mutants in a mouse xenograft model. (A-C) Response of MeWO-KIT-WT, MeWo-KIT p.L576P, and MeWo-KIT-p.N822K mouse xenograft models to Imatinib, Sunitinib, Nilotinib, and Nintedanib, respectively (n = 3 independent experiments). (D-F) Response of MeWO-KIT-WT, MeWo-KIT p.L576P, and MeWo-KIT-p.N822K mouse xenograft models to Ripretinib (n = 3 independent experiments). Fraction of tumor growth represents the change in tumor volume normalized to day 0 of treatment.

Article Snippet: Small molecule inhibitors (Imatinib, Sunitinib, Nilotinib, Nintedanib, and Ripretinib) were purchased from MedChemExpress, dissolved in DMSO to a 10 mM stock, and stored at −80°C.

Techniques: In Vivo, Expressing

Journal: bioRxiv

Article Title: A human immune system mouse model for preclinical evaluation of therapies in pemphigoid disease

doi: 10.64898/2026.01.15.699625

Figure Lengend Snippet: ( A ) Flow cytometric analysis of cytosolic ROS production in human peripheral blood cells after stimulation with COL7 c -IgG immune complexes (IC) upon pre-treatment with 1µM BX-795 or vehicle control. n=4 independent experiments using cells from different donors were performed. ( B ) Quantification of secreted human cytokines in the supernatants of COL7 c -IC stimulated human cells, comparing presence or absence of PDK1 kinase inhibitor BX-795, measured using the LEGENDplex TM Human Inflammation Panel 1. ( C ) Induction of dermal-epidermal separation in cryosections of human skin was performed upon treatment of neutrophils with 1µM BX-795 compared to untreated control cells. Line symbols the dermal-epidermal junction, asterisks separation. Scale bar 500 µm. Statistical analyses employed the Shapiro-Wilk normality test. Depending on Gaussian distribution either paired t-test or Wilcoxon test was used. * p < 0.05; ** p < 0.01.

Article Snippet: For evaluating the kinase PDK1 as a therapeutic target, HIS mice were treated orally with the small-molecule inhibitor BX-795 (Selleckchem) at 30 mg/kg daily.

Techniques: Control

Journal: bioRxiv

Article Title: A human immune system mouse model for preclinical evaluation of therapies in pemphigoid disease

doi: 10.64898/2026.01.15.699625

Figure Lengend Snippet: ( A ) Schematic representation of the experimental approach for inducing an EBA-like phenotype in human immune system mice, combined with p.o. administration of 30 mg/kg BX-795 or vehicle as control. ( B ) Assessment of skin disease severity shown as % ABSA over time (left) and as AUC (right). ( C ) Histological analysis of skin sections using PAS staining for tissue structure and infiltrate evaluation (arrow) and quantification of epidermal thickness (in µm, right). Veh. Ctrl., vehicle control. ( D ) Human immune cell composition in digested skin samples (left, per gram skin and 100000 live cells), including expression of activation markers CD86 and CD18 (middle), and intracellular ROS production (right). C., classical. ΔMFI, median fluorescence intensity after subtraction of fluorescence minus one. ( E ) Quantification of human cytokines in plasma on day 6 using the LEGENDplex TM Human Inflammation Panel 1. Symbols indicate individual mice and bars indicate means. Statistical analyses were performed using Shapiro-Wilk normality test. Depending on Gaussian distribution, samples were analyzed using unpaired t-test or Mann-Whitney test, respectively. *p < 0.05; **p < 0.01; ***p < 0.001; ****p <0.0001.

Article Snippet: For evaluating the kinase PDK1 as a therapeutic target, HIS mice were treated orally with the small-molecule inhibitor BX-795 (Selleckchem) at 30 mg/kg daily.

Techniques: Control, Staining, Expressing, Activation Assay, Fluorescence, Clinical Proteomics, MANN-WHITNEY