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 8 Publications
4 Customer Reviews
The ROCK inhibitors fasudil and Y27632 prevented SCP2 cell bone metastasis in nude mice (n = 10 per group). Shown are BLI images of bone metastases, IHC analyses of SMAD3 C-tail phosphorylation and PTHLH, osteoclast TRAP staining, and BLI quantitation.
J Clin Invest 2014 124(4), 1646-59. Fasudil (HA-1077) HCl purchased from Selleck.
Tamoxifen was administered to adult Psmc1fl/wt and Psmc1fl/fl Pdgf-Cre-ER mice, followed by treatment with fasudil control (4 and 48 hours after tamoxifen). Representative images of Dylight 488-positive megakaryocytes present in crude bone marrow isolated from Psmc1fl/wt and Psmc1fl/flPdgf-Cre-ER mice immediately after euthanasia. Bone marrow for these studies was isolated from a subset of the mice in A (n=2 per treatment group). Scale bars: 100 um.
J Clin Invest 2014 124(9), 3757-66. Fasudil (HA-1077) HCl purchased from Selleck.
Effects of GLP-1, fasudil, and H89 on high-glucose (HG)-induced oxidative stress in CMECs. Representative diagram showing dihydroethidine (DHE) staining of CMECs (red, DHE; blue, DAPI; scale bar, 25 um).
Diabetes 2013 62(5), 1697-708. Fasudil (HA-1077) HCl purchased from Selleck.
Purity & Quality Control
Choose Selective ROCK Inhibitors
|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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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03391219||Recruiting||Retinal Vein Occlusion||Shahid Beheshti University of Medical Sciences||January 2018||Phase 2|Phase 3|
|NCT03404843||Completed||Cardiovascular Diseases||Colorado State University||July 14 2017||Phase 2|
|NCT01935518||Unknown status||Amyotrophic Lateral Sclerosis||Peking University Third Hospital||September 2013||Phase 2|
|NCT01823081||Completed||Diabetic Macular Edema||Shahid Beheshti University of Medical Sciences||January 2013||Phase 3|
|NCT00670202||Terminated||Carotid Stenosis||Brigham and Women''s Hospital|Doris Duke Charitable Foundation||March 13 2008||Phase 2|
|NCT00498615||Completed||Raynaud|Scleroderma||Johns Hopkins University||April 2007||Phase 3|
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