GPS167

GPS167 potently and selectively inhibits recombinant human CLK1, CLK2 and CLK4 with IC₅₀ values of 0.0896 μM, 0.0820 μM and 0.1230 μM, and shows weak or negligible activity against most other tested human kinases. In non-radioactive proximity assays, GPS167 yields an IC₅₀ of 0.5069 μM for CLK1 and displays poor inhibitory potency toward DYRK1A and DYRK1B; and its inhibitory effect on SRSF10 phosphorylation is preferential than its inhibitory effect on SRSF1 phosphorylation^[1][2].
GPS167 (1-30 μM; 6 h) increases Thr212-Tau phosphorylation in SH-SY5Y cells expressing human 4R-Tau^[1].
GPS167 (48 h) is non-cytotoxic to HT22 murine hippocampal neuronal cells, with an IC₅₀ for viability >100 μM^[1].
GPS167 (0.05-100 μM; 48 h) modulates BCLAF1 alternative splicing in HCT116 cells, reducing BCLAF1-L variant levels with an EC₅₀ of ~2 μM^[2].
GPS167 (10-20 μM; 24 h cell incubation, 10 min pull-down incubation) promotes dephosphorylation of specific serine residues on SRSF10 and increases the interaction between SRSF10 and CLK1 in HCT116 cells^[2].
GPS167 (10 μM; 0-80 h) induces potent cytotoxicity in human colorectal cancer cell lines (HCT116, COLO205, SW620) but has minimal effects on Caco-2 cells and normal colonocyte cell lines (CRL-1831, CRL-1790)^[2].
GPS167 induces apoptosis in human colorectal cancer HCT116, COLO205 and SW620 cells accompanied by elevated cleaved PARP and cleaved caspase-3, whereas no apoptotic effect is observed in Caco-2 and normal colon epithelial CRL-1831 cells. It inhibits cancer cell migration as evidenced by decreased scratch wound closure rate^[2].
GPS167 (10-20 μM; up to 120 h viability, up to 84 h cytotoxicity, 72 h PARP cleavage) impairs viability, induces cytotoxicity and apoptosis, and disrupts structure in human and mouse colorectal cancer organoids, but has minimal effects on normal colorectal organoids^[2].
GPS167 (10-20 μM; 24 h viability and caspase activity, up to 72 h cytotoxicity) elicits p53-dependent growth inhibition, cytotoxicity, and apoptosis in HCT116 colorectal cancer cells, with increased p53 expression and DNA damage observed in p53-proficient cells^[2].
GPS167 (8 days) in NALM-6 cells, depletion of genes involved in mitotic cell cycle checkpoint/chromosome segregation increases sensitivity to GPS167, while depletion of mitotic spindle assembly-related genes reduces GPS167 sensitivity^[3].
GPS167 disrupts the expression and alternative splicing of EMT-relevant genes, including FLNB and CD44, in HCT116 colorectal cancer cells^[3].
GPS167 (1 μM; 4 days) in MCF10A breast epithelial cells, upregulates the epithelial marker ECAD (both with and without TGF-β treatment) and inhibits TGF-β-induced EMT morphological changes, without altering mesenchymal marker expression^[3].
GPS167 (20 μM; up to 72 h) in HCT116 colorectal cancer cells, depletion of the dsRNA sensor DHX33 significantly reduces cytotoxicity over 72 hours^[3].
GPS167 inhibits proliferation and induces p53-dependent apoptosis in multiple cancer cell lines (including colorectal, melanoma, leukemia, breast, ovarian, and renal) and colorectal organoids, while sparing normal colonocyte cells and organoids^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.