Fasudil (HA-1077) HCl

Catalog No.S1573

Fasudil (HA-1077) HCl Chemical Structure

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.

Size Price Stock Quantity  
In DMSO USD 88 In stock
USD 97 In stock
USD 170 In stock
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3 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

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Biological Activity

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.
ROCK2 [1]
(Cell-free assay)
PKA [1]
(Cell-free assay)
PKG [1]
(Cell-free assay)
PKC [1]
(Cell-free assay)
330 nM(Ki) 1.6 μM(Ki) 1.6 μM(Ki) 3.3 μM(Ki)
In vitro

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. [2] Fasudil also exhibits vasodilator actions by inhibition of 5-hydroxytryptamine, noradrenaline, histamine, angiotensin, and dopamine induced spiral strips contraction. [3] Fasudil induces disorganization of actin stress fiber and cell migration inhibition. [4] 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. [5]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Sf9 cells NIG2O4hHfW6ldHnvckBie3OjeR?= MVm5NEBucW6| MnvzTY5pcWKrdHnvckBw\iCqdX3hckBz\WOxbXLpcoFvfCCQLYTldo1qdmGuIHjpd{11[WepZXSgVm9EUzFiKEOtOVQ{MSCneIDy[ZN{\WRiaX6gZoFkfWyxdnnyeZMhcW6oZXP0[YQhW2Z7IHPlcIx{KHW|aX7nJGJqd3Srbj3BbJguSUuUUlzTV2xTSS2FT17INkB{fWK|dILheIUh[W6mIGvnZY1u[S1|M2DdRXRRKGGodHXyJFkxKG2rboOgZpkhe2OrboTpcIxifGmxbjDwdo95cW2rdImgZZN{[XluIFnDOVA:OC5|IN88UU4> NFLrR4EyPzBzOE[5Ny=>
insect cells M{Tyc2Z2dmO2aX;uJIF{e2G7 MluyNVAhdWmwcx?= NILFbG9KdmirYnn0bY9vKG:oIHj1cYFvKGyndXvvZ5l1cWNiUl;DT|Eh\XiycnXzd4VlKGmwIHnud4VkfCClZXzsd{B2e2mwZzDLT3JPWlSOU2[gZZMhe3Wkc4TyZZRmKGGodHXyJFExKG2rboOgZpkheHm{dY\heIUhc2mwYYPlM4xi[3SjdHWg[IVpgWS{b3flcoF{\SClb4XwcIVlKGG|c3H5MEBMcT1yLkWzJO69VS5? NUnKW3J4OjZyM{m1O|A>
Sf9 cells NYPwSplDTnWwY4Tpc44h[XO|YYm= NV;TTVA5UW6qaXLpeIlwdiCxZjDyZZQhWk:FS{Kg[ZhxemW|c3XkJIlvKFOoOTDj[YxteyxiSVO1NF0yNjlizszNMi=> MXKxNFk6QDN3MR?=
HEK293 cells NFjlc3FHfW6ldHnvckBie3OjeR?= MnWxTY5pcWKrdHnvckBw\iCKaYOteIFo\2WmIHj1cYFvKFCUS{Kg[ZhxemW|c3XkJIlvKEiHS{K5N{Bk\WyuczygTWM2OD12IN88UU4> NWHnSZl4OTB7OUizOVE>
Sf9 cells MU\GeY5kfGmxbjDhd5NigQ>? M2nmZWlvcGmkaYTpc44hd2ZiSHnzMZRi\2enZDDoeY1idiCPU1uxJIV5eHKnc4Pl[EBqdiCVZkmgZ4VtdHNuIFnDOVA:PSEQvF2u MXSxNFk6QDN3MR?=
U937 cells MnLwSpVv[3Srb36gZZN{[Xl? NGnvNmlKdmirYnn0bY9vKG:oIF3DVFEucW6mdXPl[EBkcGWvb4ThfIl{KGmwIGW5N|ch[2WubIOgc5ZmemW6cILld5NqdmdiQ1PSNkwhUUN3ME2zOUDPxE1w MoflNVcxQDRyOEe=

... Click to View More Cell Line Experimental Data

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. [3] Fasudil administration displays protectable effects on cardiovascular disease and reduces the activation of JNK and attenuates mitochondrial-nuclear translocation of AIF under ischemic injury. [6] 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. [7]


Solubility (25°C)

In vitro Water 65 mg/mL (198.27 mM)
DMSO 5 mg/mL (15.25 mM)
Ethanol Insoluble
In vivo Add solvents individually and in order:
30 mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 327.83


CAS No. 105628-07-7
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01935518 Unknown status Amyotrophic Lateral Sclerosis Peking University Third Hospital September 2013 Phase 2
NCT01823081 Unknown status Diabetic Macular Edema Shahid Beheshti University of Medical Sciences January 2013 Phase 3
NCT00670202 Unknown status Carotid Stenosis Brigham and Womens Hospital|Doris Duke Charitable Foundation April 2008 Phase 2
NCT00498615 Completed Raynaud|Scleroderma Johns Hopkins University April 2007 Phase 3
NCT00120718 Completed Atherosclerosis|Hypercholesterolemia Brigham and Womens Hospital June 2002 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID