Fasudil

SKU: orb1745275

Description

Fasudil (HA-1077) is a cell-permeable, potent inhibitor targeting ROCK1, PKA, PKC, and MLCK kinases. It is widely used in cardiovascular and neurological research, demonstrating efficacy in both in vitro assays and in vivo models of vasospasm and neurodegeneration.

Research Area

Cell Biology, Epigenetics & Chromatin, Metabolism Research, Pharmacology & Drug Discovery, Signal Transduction, Stem Cell & Developmental Biology

Key Properties

• CAS Number: 103745-39-7
• MW: 291.37
• Purity: 99.84% (May vary between batches)
• Formula: C₁₄H₁₇N₃O₂S
• SMILES: O=S(=O)(N1CCCNCC1)c1cccc2cnccc12
• Target: Serine/threonin kinase|||ROCK|||PKC|||Calcium Channel|||PKA|||Autophagy
• Solubility: DMSO:61.875 mg/mL (212.36 mM)

Bioactivity

• Target IC50:
  ROCK1:0.33 μM(Ki)|ROCK2:0.158 μM|MLCK:55 μM(Ki)|PKC:9.3 μM(Ki)|PKA:1.0 μM(Ki)|PKG:1.65 μM
• In Vivo:
  Fasudil (30 μg) produces an approximate 50% increase in CBF via intra-coronary injection to dogs. 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.
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• In Vitro:
  Fasudil (Hydrochloride) has vasodilatory action and occupies the adenine pocket of the ATP-binding site of the enzyme. 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.
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Storage & Handling

• Storage: -20°C
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Ca2+ channel antagonist, Ca2+ channels, Calcium Channel, Ca channels, Autophagy, AT 877, AT877, AT-877, a-SMA, collagen, CalciumChannel, lysophoaphatidic acid, LPA, MLCK, orally active, inhibit, JNK, ERK1/2, Fasudil, HA 1077, HA1077, HA-1077, Inhibitor, human HSC, p38, Serine kinase, threoninkinase, threonin kinase, Serinekinase, PKC, PKA, PKG, rat HSCs, TIMP-1, Protein kinase A, protein kinases, Protein kinase C, ROCK, ROCK2, ROK, Rho-kinase, Rho-associated protein kinase, Rho-associated kinase, TWNT-4 cells, vasodilator

Compound Identifiers

PubChem CID

3547