- The best-characterized LIMK inhibitor
LIM domain kinases (LIMKs) are serine/threonine and tyrosine kinases which phosphorylate and inactivate the ADF/cofilin family of proteins through serine 3 phosphorylation (Yang et al., 1998). LIMK regulates actin dynamics through phosphorylating cofilin, and this phosphorylation inhibits cofilin-mediated depolymerization of the actin filaments. Both LIMKs (LIMK1 and LIMK2) contain two N-terminal LIM domains, a PDZ domain, and a C-terminal protein kinase domain. LIMKs are regulated by small GTPases of the Rho family, Rho-dependent kinase (ROCK), and the p21-activated kinases PAK1/PAK4. LIMKs are involved in many cellular processes associated with actin dynamics and actin cytoskeletal rearrangement, such as cell migration, chemotaxis, cell development, neuronal differentiation, cell-cell interaction, tissue repair, wound healing, cancer metastasis, and viral infection (Foletta et al., 2004; Manetti, 2012; Yoshioka et al., 2003). LIMK is highly expressed in many metastatic cancer cells, and has been identified as a possible therapeutic target (Endo et al., 2007; Nishimura et al., 2006). In addition, LIMK has been shown to be involved in the infection and pathogenesis of multiple viruses such as HIV, influenza A, pseudorabies virus, EBOV, RVFV, VEEV, and HSV-1 (Liu et al., 2014; Vorster et al., 2011). LIMK inhibitors have also been shown to possess broad-spectrum anti-viral activities.
The LIMK inhibitor R10015 is the best biochemically and biologically characterized LIMK inhibitor (Yi et al., 2017). R10015 has been profiled against a panel of 62 kinases (Table 1). It directly inhibits the kinase activity of LIMK by binding to the ATP-binding pocket of LIMK. The in vitro IC50 value for inhibiting recombinant LIMK1 protein was approximately 38 nM (Fig. 1). R10015 blocks the phosphorylation of cofilin at serine 3 in human T cells (Fig. 2). R10015 also inhibits T cell chemotaxis and chemokine-induced actin polymerization (Fig. 3).
R10015
R10015 highlights:
- Molecular weight (M.W.) = 525.9
- LIM Kinase inhibition IC50 = 38±5 nM
- Dissolves in DMSO (Dimethyl sulfoxide)
- Best biochemically characterized LIMK inhibitor (profiled against 62 kinases for specificity in vitro)
- Best biologically characterized LIMK inhibitor (tested for specificity in vivo in T cells)
- Profiled against multiple viruses
Table 1. Profiling R10015 against 62 kinases (DMSO control, 100% activity)
Kinase | % Activity | Kinase | % Activity |
ABL1 | 89.2 | LIMK1 | 6.4 |
AKT2 | 73.1 | LRRK2 (G2019S) | 6.7 |
ALK | 95.5 | MEK1 | 75.6 |
AMPK(A1/B1/G1) | 76.6 | MLCK/MYLK | 83.3 |
Aurora A | 60.3 | MRCKa/CDC42BPA | 96.5 |
BRAF | 91.9 | mTOR/FRAP1 | 100.0 |
BTK | 90.2 | NEK1 | 67.2 |
CAMK2b | 90.8 | P38a/MAPK14 | 98.6 |
CDK2/cyclin A | 82.7 | p70S6K/RPS6KB1 | 10.0 |
CDK5/p35 | 85.5 | PAK2 | 98.2 |
CK1d | 85.0 | PDGFRb | 78.6 |
CK2a | 94.2 | PIM2 | 97.6 |
c-Kit | 81.3 | PKA | 24.0 |
c-MET | 82.1 | PKCa | 47.5 |
c-Src | 92.4 | PKN1/PRK1 | 58.6 |
DAPK1 | 87.8 | PLK2 | 103.2 |
EGFR | 93.2 | RET | 46.5 |
EPHA3 | 91.1 | ROCK1 | 42.3 |
ERK2/MAPK1 | 87.2 | ROCK2 | 29.5 |
FAK/PTK2 | 81.5 | RSK1 | 47.2 |
FGFR1 | 86.5 | SGK1 | 61.0 |
FLT3 | 32.2 | SLK/STK2 | 108.0 |
GSK3b | 67.8 | STK16 | 48.6 |
IGF1R | 90.0 | STK33 | 56.5 |
IKKa/CHUK | 90.5 | TAK1 | 82.4 |
IKKb/IKBKB | 85.1 | TAOK1 | 54.0 |
IKKe/IKBKE | 84.1 | TBK1 | 82.0 |
JAK3 | 61.1 | TESK1 | 90.2 |
JNK1 | 95.2 | TLK1 | 98.5 |
JNK3 | 85.7 | WEE1 | 97.2 |
KDR/VEGFR2 | 87.2 | ZIPK/DAPK3 | 98.5 |
- The % data were the average of two determinations.
- R10015 used was 1 µM.
- The ATP concentration used was 10 µM.
- Staurosporine was used as the control for assay validation.
Catalog No. | Products | Price1 | ||
LIMK-10 | LIMK inhibitor R10015 (10 mg) | $158 | ||
LIMK-50 | LIMK inhibitor R10015 (50 mg) | $658 | ||
IPS-PCOF | Intracellular p-cofilin staining kit | $350 | ||
IPS-250 | Intracellular protein staining kit (250 ml) | $190 | ||
IPS-500 | Intracellular protein staining kit (500 ml) | $350 | ||
1Academic and government price. Others please inquire. | ||||
Technical Support Email: info@virongy.com | ||||
References