Fasudil dihydrochloride, also known as HA-1077 and AT877, is a nonspecific inhibitor of RhoA/ROCK. Fasudil dihydrochloride exhibits inhibitory effects on protein kinases including ROCK1 (Ki = 0.33 μM), ROCK2 (IC50 = 0.158 μM), PKA (IC50 = 4.58 μM), PKC (IC50 = 12.30 μM), and PKG (IC50 = 1.650 μM), while also acting as a potent Ca2+ channel blocker and vasodilator, providing a multifunctional pharmacological tool for vascular, cardiovascular, and cellular signaling research.

PKA:4.58 μM, PKG:1.65 μM, ROCK2:0.158 μM, ROCK1 (p160ROCK):0.33 μM (Ki), PKC:12.3 μM

Fasudil dihydrochloride (100 μM) can inhibit cell spreading, stress fiber formation, and α-SMA expression in rat hepatic stellate cells (HSCs) and human HSC-derived TWNT-4 cells, while also significantly suppressing the proliferation of these two cell types [4].
Fasudil dihydrochloride (50–100 μM) can inhibit lysophosphatidic acid (LPA)-induced phosphorylation levels of ERK1/2, JNK, and p38 in rat hepatic stellate cells and human HSC-derived TWNT-4 cells [4].
Fasudil dihydrochloride (25–100 μM, 24 h) can suppress the transcription of collagen and tissue inhibitor of metalloproteinases (TIMP), and simultaneously promote the transcription of matrix metalloproteinase-1 (MMP-1) in human HSC-derived TWNT-4 cells [4].

Fasudil dihydrochloride (10 mg/kg, i.v., administered 1 hour before surgery) exhibits protective effects on the cardiovascular system under ischemic injury conditions, reduces the activation level of JNK, and attenuates the mitochondrial-nuclear translocation of AIF [5].
Fasudil dihydrochloride (50 mg/kg/day, i.p.) can suppress acute and recurrent EAE induced by proteolipid protein PLP p139-151, inhibit lymphocyte proliferation, downregulate the expression of IL-17, and significantly reduce the IFN-γ/IL-4 ratio [6].
Fasudil dihydrochloride (100 mg/kg/day, p.o.) significantly decreases the incidence and pathological scores of EAE in SJL/J mice, while alleviating inflammatory responses, demyelination, axonal loss in spinal cord tissues, and reducing the accumulation of APP-positive signals in the spinal cord [6].