T3-CLK

T3-CLK is a pan inhibitor of CDC-like kinases (Clks; IC₅₀s = 0.67, 15, and 110 nM for Clk1, Clk2, and Clk3, respectively).¹ It is selective for Clk1-3 over dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) and DYRK1B (IC₅₀s = 260 and 230 nM, respectively), as well as 62 kinases in a panel at 1,000 nM and four kinases in the same panel at 1,110 nM. T3-CLK modulates Clk-responsive alternative splicing events and reduces exon recognition, as well as increases levels of conjoined gene transcripts, in HCT116 colorectal cancer cells and 184-hTERT mammary epithelial cells. It reduces the expression of VEGFR2 in human umbilical vein endothelial cells (HUVECs) when used at concentrations ranging from 300 to 1,000 nM.² T3-CLK also inhibits VEGF-induced-sprouting in HUVEC spheroids when used at concentrations of 300 and 1,000 nM and inhibits HUVEC migration at 500, 800, and 1,000 nM.

WARNING This product is not for human or veterinary use.

1. Funnell, T., Tasaki, S., Oloumi, A., et al. CLK-dependent exon recognition and conjoined gene formation revealed with a novel small molecule inhibitor. Nat. Commun. 8(1), 7 (2017).

2. Zech, T.J., Wolf, A., Hector, M., et al. 2-Desaza-annomontine (C₈₁) impedes angiogenesis through reduced VEGFR2 expression derived from inhibition of CDC2-like kinases. Angiogenesis 27(2), 245-272 (2024).