Fasudil (HA-1077) HCl
Molecular Weight(MW): 327.83
Fasudil(HA-1077), a potent and selective inhibitor of Rho kinase, displays less potent inhibiton over PKA, PKG, PKC and MLCK with Ki of 1.6, 1.6, 3.3, and 36 μM in cell-free assays, respectively.
Cited by 36 Publications
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|Description||Fasudil(HA-1077), a potent and selective inhibitor of Rho kinase, displays less potent inhibiton over PKA, PKG, PKC and MLCK with Ki of 1.6, 1.6, 3.3, and 36 μM in cell-free assays, respectively.|
Fasudil is a class of calcium antagonists. Fasudil produces a competitive inhibition of the Ca2+-induced contraction of the depolarized rabbit aorta. Fasudil is able to inhibit contractile responses to KCl, phenylephnne (PHE) and prostaglandin (PG) F2a.  Fasudil also exhibits vasodilator actions by inhibition of 5-hydroxytryptamine, noradrenaline, histamine, angiotensin, and dopamine induced spiral strips contraction.  Fasudil induces disorganization of actin stress fiber and cell migration inhibition.  Fasudil inhibits hepatic stellate cells spreading, the formation of stress fibers, and expression of α-SMA with concomitant suppression of cell growth, but does not induce apoptosis. Fasudil suppresses the LPA-induced phosphorylation of ERK1/2, JNK and p38 MAPK. 
|In vivo||Intra-coronary injection of Fasudil to dogs (30 μg i.a.) produces an approximate 50% increase in CBF. Fasudil (0.01, 0.03, 0.1 and 0.3 mg/kg, bolus, i.v.) dose-dependently decreases MBP and increases HR, VBF, CBF, RBF, and FBF. A total dose of 1.0 ng/mL Fasudil increases cardiac output. The infusion of Fasudil i.v. produces a significant fall in MBP, left ventricular systolic pressure and total peripheral resistance with an increase in HR and cardiac output, but without significant changes in right atrial pressure, dP/dt or left ventricular minute work in dogs.  Fasudil administration displays protectable effects on cardiovascular disease and reduces the activation of JNK and attenuates mitochondrial-nuclear translocation of AIF under ischemic injury.  The oral administration of Fasudil (a dosage of 100 mg/kg/day) significantly reduces incidence and mean maximum clinical score of EAE in SJL/J mice immunized with PLP p139-151. Treatment of mice with Fasudil suppresses the proliferative response of splenocytes to the antigen. Oral administration of Fasudil decreases inflammation, demyelination, axonal loss and APP positivein spinal cord of Fasudil-treated mice. |
-  Ono-Saito N, et al. Pharmacol Ther, 1999, 82(2-3), 123-131.
-  Asano T, et al. J Pharmacol Exp Ther, 1987, 241(3), 1033-1040.
-  Asano T, et al. Br J Pharmacol, 1989, 98(4), 1091-1100.
|In vitro||Water||65 mg/mL (198.27 mM)|
|DMSO||5 mg/mL (15.25 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
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