WARNING: This product is for research use only, not for human or veterinary use.
MedKoo CAT#: 408086
Description: T3-CLK is a pan-CLK inhibitor, T3-CLK as well as the negative control T3-CLK-N have been developed in collaboration with Takeda 3 (5). T3-CLK is a potent inhibitor of CLK1, CLK2 and CLK3 with IC50 of 0.67/15/110 nM, respectively. T3-CLK is >30 fold selective against the closest off targets DYRK1A and DYRK1B with an IC50 of 260 nM and 230 nM, respectively in cellular assays. T3-CLK is non-toxic in cells and inhibits the phosphorylation of SRSF in HeLa cells in a time and dose dependent manner. (https://www.thesgc.org/chemical-probes/T3-CLK)
MedKoo Cat#: 408086
Chemical Formula: C28H30N6O2
Exact Mass: 482.243
Molecular Weight: 482.588
Elemental Analysis: C, 69.69; H, 6.27; N, 17.41; O, 6.63
Related CAS #: 2109805-56-1
Synonym: T3, CLK Inhibitor T3; T3-CLK; CLK-IN-T3; MDK-5561; MDK 5561; MDK5561.
IUPAC/Chemical Name: 4-(2-Methyl-1-(4-methylpiperazin-1-yl)-1-oxopropan-2-yl)-N-(6-(pyridin-4-yl)imidazo[1,2-a]pyridin-2-yl)benzamide
InChi Key: IEFFSHLHNYVSEF-UHFFFAOYSA-N
InChi Code: InChI=1S/C28H30N6O2/c1-28(2,27(36)33-16-14-32(3)15-17-33)23-7-4-21(5-8-23)26(35)31-24-19-34-18-22(6-9-25(34)30-24)20-10-12-29-13-11-20/h4-13,18-19H,14-17H2,1-3H3,(H,31,35)
SMILES Code: O=C(NC1=CN2C=C(C3=CC=NC=C3)C=CC2=N1)C4=CC=C(C(C)(C)C(N5CCN(C)CC5)=O)C=C4
The Cdc2-like kinases (CLK) are evolutionary highly conserved dual specificity protein kinases. The CLK family consists of four members, namely CLK1, 2, 3, and 4 (1). CLKs have a highly conserved domain structure at the C-terminus, containing a signature amino acid motif EHLAMMERILG, why they are often referred to as ‘LAMMER kinases’ (2). CLKs auto-phosphorylate on serine/threonine and tyrosine residues and phosphorylate exogenous substrates on serine/threonine residues (3). They play an important role in the regulation of RNA splicing through phosphorylation of members of the serine and arginine-rich family of splicing factors (SRSF). Phosphorylation of SRSF on numerous serine residues is a prerequisite for entry of SRSF into the nucleus and for the assembly of the spliceosome (4). Being part of the splicing machinery, CLKs are often associated with the development of many pathologies, including cancer and neurodegenerative disorders. However, to date CLK-dependent RNA processing events remains poorly defined