Molecular Weight(MW): 326.37
RKI-1447 is a potent inhibitor of ROCK1 and ROCK2, with IC50 of 14.5 nM and 6.2 nM, respectively, has anti-invasive and antitumor activities.
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(d) ROCK inhibition blocks CC-RCC migration in a transwell assay. RCC10 or 786-O cells were treated with Y-27632, RKI 1447 or DMSO vehicle (as indicated) for 6 h. The assay was performed in duplicate and the experiment was repeated three times. Statistical analysis in (b-d) was performed using a paired t-test comparing each normalized dose to the negative control (*P<0.05, **P<0.01 and ***P<0.001); s.e.m.'s are shown.
Oncogene, 2016, 1-10.. RKI-1447 purchased from Selleck.
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|Description||RKI-1447 is a potent inhibitor of ROCK1 and ROCK2, with IC50 of 14.5 nM and 6.2 nM, respectively, has anti-invasive and antitumor activities.|
RKI-1447 is a cell-permeable pyridylthiazolyl-urea that acts as a potent, ATP site-targeting Rho Kinase inhibitor, displaying much reduced potency against PKA, PKN1/PRK1, p70S6K/RPS6kB1, AKT1, MRCKa/CDC42BPA (85.5%, 80.5%, 61.9%, 56.0%, and 50.4% inhibition, respectively, by 1 µM RKI-1447) or 15 other kinases. Crystal structures of the RKI-1447/ROCK1 complex reveals that RKI-1447 is a Type I kinase inhibitor that binds the ATP binding site through interactions with the hinge region and the DFG motif. RKI-1447 suppresses phosphorylation of the ROCK substrates MLC-2 and MYPT-1 in human cancer cells, but had no effect on the phosphorylation levels of the AKT, MEK, and S6 kinase at concentrations as high as 10 μM. RKI-1447 is also highly selective at inhibiting ROCK-mediated cytoskeleton re-organization (actin stress fiber formation) following LPA stimulation, but does not affect PAK-meditated lamellipodia and filopodia formation following PDGF and Bradykinin stimulation. RKI-1447 inhibits migration, invasion and anchorage-independent tumor growth of breast cancer cells. 
|In vivo||RKI-1447 is highly effective at inhibiting the outgrowth of mammary tumors in a transgenic mouse model. Tumors from mice treated with the RKI-1447 increases in size with an average percent change in tumor volume of only 8.8%. Thus, RKI-1447 inhibited mammary tumor growth by 87%, and on average the mammary tumors from Compared with those tumors from mice treated with the vehicle control, RKI-1447 treated mice are 7.7-fold smaller. RKI-1447 treatments does not result in mouse weight loss. |
Z-Lyte FRET kinase assay:Kinase inhibition is measured using the Invitrogen Z-Lyte® FRET kinase assay with Ser/Thr 13 peptide substrate based on the myosin light chain sequence KKRPQRRYSNVF. Compounds are tested on three separate days with 8 point dilutions performed in duplicate to determine average IC50 values. The assay conditions are optimized to 15 μL of kinase reaction volume with 5 ng of enzyme in 50 mM HEPES (pH 7.5), 10 mM MgCl2, 1 mM EGTA, and 0.01% Brij-35. The reaction is incubated for 1 h at room temperature in the presence of 1.5 μM of peptide substrate with 12.5 μM of ATP (for ROCK1) or 2 μM of substrate with 50 μM of ATP (for ROCK2). The reaction is then stopped and the ratio of phosphorylated to unphosphorylated peptides is determined by selective cleavage of only the unphosphorylated peptide as described by the manufacturer. This is followed by excitation of coumarin at 400 nm resulting in emission at 445 nm and energy transfer to fluorescein and final emission at 520 nm. The substrate contains both coumarin and fluorescein and only uncleaved phosphorylated substrate will undergo FRET. The ratio of the signals at 445 nm and 520 nm is measured using a Wallac EnVision Plate Reader, model 2102 plate-reader.
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|In vitro||DMSO||65 mg/mL (199.16 mM)|
|In vivo||15% Captisol||30 mg/mL|
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