Product Data?SheetFasudil HydrochlorideInhibitors?Agonists?Cat. No.:CAS No.:分?式:分?量:作?靶点:作?通路:HY-10341105628-07-7C??H??ClN?O?S327.83ROCK; Calcium Channel; Autophagy; PKA; PKC; HIVCell Cycle/DNA Damage; Cytoskeleton; Stem Cell/Wnt; TGF-beta/Smad; Membrane Transporter/Ion Channel; Neuronal Signaling; Autophagy; Protein Tyrosine Kinase/RTK; Epigenetics; Anti-infectionScreening Libraries储存?式:PowderIn solvent-20°C4°C-80°C-20°C3 years2 years6 months1 month溶解性数据体外实验H2O : 55 mg/mL (167.77 mM; Need ultrasonic)DMSO : ≥ 31 mg/mL (94.56 mM)* \Mass1 mg5 mg10 mgSolventConcentration制备储备液1 mM5 mM10 mM3.0504 mL0.6101 mL0.3050 mL15.2518 mL3.0504 mL1.5252 mL30.5036 mL6.1007 mL3.0504 mL请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；?旦配成溶液，请分装保存，避免反复冻融造成的产品失效。储备液的保存?式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个?内使?，-20°C 储存时，请在 1 个?内使?。体内实验请根据您的实验动物和给药?式选择适当的溶解?案。以下溶解?案都请先按照 In Vitro ?式配制澄清的储备液，再依次添加助溶剂： 为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的?作液，建议您现?现配，当天使?； 以下溶剂前显?的百分?是指该溶剂在您配制终溶液中的体积占?；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的?式助溶1. 请依序添加每种溶剂：?10% DMSO ?? 40% PEG300 ?? 5% Tween-80 ?? 45% salineSolubility: ≥ 2.08 mg/mL (6.34 mM); Clear solutionPage 1 of 2 www.MedChemExpress.cn
此?案可获得 ≥ 2.08 mg/mL (6.34 mM，饱和度未知) 的澄清溶液。 以 1 mL ?作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加? 50 μL Tween-80，混合均匀；然后继续加? 450 μL ?理盐?定容? 1 mL。2. 请依序添加每种溶剂：?10% DMSO ?? 90% (20% SBE-β-CD in saline)Solubility: ≥ 2.08 mg/mL (6.34 mM); Clear solution此?案可获得 ≥ 2.08 mg/mL (6.34 mM，饱和度未知) 的澄清溶液。 以 1 mL ?作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD ?理盐??溶液中，混合均匀。3. 请依序添加每种溶剂：?10% DMSO ?? 90% corn oilSolubility: ≥ 2.08 mg/mL (6.34 mM); Clear solution此?案可获得 ≥ 2.08 mg/mL (6.34 mM，饱和度未知) 的澄清溶液，此?案不适?于实验周期在半个?以上的实验。 以 1 mL ?作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL ??油中，混合均匀。BIOLOGICAL ACTIVITY?物活性Fasudil Hydrochloride (HA-1077 Hydrochloride; AT877 Hydrochloride) 是?种?特异性 ROCK 抑制剂，对蛋?激酶也有抑制作?，ROCK1 的 Ki 值为 0.33 μM，ROCK2 和 PKA，PKC，PKG 的 IC50 值分别 0.158 μM 和 4.58 μM，12.30 μM，1.650 μM。Fasudil Hydrochloride 也是?种有效的 Ca2+ 通道拮抗剂和?管扩张剂。IC?? & Targetp160ROCK0.33 μM (Ki)PKG1.65 μM (IC50)体外研究Fasudil Hydrochloride (100 μM) inhibits cell spreading, the formation of stress fibers, and expression of α-SMA with concomitant suppression of cell growth in rat HSCs and human HSC-derived TWNT-4 cells[4]. Fasudil Hydrochloride (50-100 μM; 24 hours) inhibits the LPA-induced phosphorylation of ERK1/2, JNK, and p38 detected by western blotting in rat HSCs and human HSC-derived TWNT-4 cells[4]. Fasudil Hydrochloride (25-100 μM; 24 hours) suppresses transcription of collagen and TIMP, stimulates transcription of MMP-1 in human HSC-derived TWNT-4 cells[4]. Western Blot Analysis[4]Cell Line:Concentration:Incubation Time:Result:Rat HSCs and human HSC-derived TWNT-4 cells50 μM; 100 μM24 hoursSuppressed the LPA-induced phosphorylation of ERK1/2, JNK and p38 MAPK by 60%, 70%,and 90%, respectively.RT-PCR[4]Cell Line:Concentration:Incubation Time:Rat HSCs and human HSC-derived TWNT-4 cells25 μM; 50 μM; 100 μM 24 hours24 hoursROCK20.158 μM (IC50)PKA4.58 μM (IC50)PKC12.30 μM (IC50)Page 2 of 3 www.MedChemExpress.cn
Result:Reduced the expression of type I collagen, a-SMA, and TIMP-1.体内研究Fasudil (30 μg) increases CBF by 50% via intra-coronary injection to dogs. Fasudil (0.01, 0.03, 0.1 and 0.3 mg/kg, bolus, i.v.) decreases MBP and increases HR, VBF, CBF, RBF, and FBF. Fasudil (1.0 ng/mL) increases cardiac output. Fasudil via 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 obvious effect on right atrial pressure, dP/dt or left ventricular minute work in dogs[3]. Fasudil exhibits protectable effects on cardiovascular disease and reduces the activation of JNK and attenuates mitochondrial-nuclear translocation of AIF under ischemic injury[6]. Fasudil (100 mg/kg/day, p.o.) significantly reduces incidence and mean maximum clinical score of EAE in SJL/J mice immunized with PLP p139-151. Fasudil inhibits the proliferative response of splenocytes to the antigen in mice. Fasudil decreases inflammation, demyelination, axonal loss and APP positivein spinal cord of Fasudil-treated mice via p.o. administration[7].客户使?本产品发表的科研?献????Sci Transl Med. 2018 Jul 18;10(450). pii: eaaq1093.????Sci Rep. 2018 Feb 6;8(1):2477.????Adipocyte. 2019 Dec;8(1):114-124.????Translational Neuroscience. 2020 May.????Biomed Rep. 2015 May;3(3):361-364.See more customer validations on www.MedChemExpress.cnREFERENCES[1].?Chen M, et al. Fasudil and its analogs: a new powerful weapon in the long war against central nervous system disorders? Expert Opin Investig Drugs. 2013 Apr;22(4):537-50.[2].?Huang XN, et al. The effects of fasudil on the permeability of the rat blood-brain barrier and blood-spinal cordbarrier following experimental autoimmune encephalomyelitis. J Neuroimmunol. 2011 Oct 28;239(1-2):61-7.[3].?Uehata M, et al. Calcium sensitization of smooth muscle mediated by a Rho-associated protein kinase in hypertension. Nature. 1997 Oct 30;389(6654):990-4.[4].?Fukushima M, et al. Fasudil hydrochloride hydrate, a Rho-kinase (ROCK) inhibitor, suppresses collagen production and enhances collagenase activity in hepatic stellate cells. Liver Int. 2005 Aug;25(4):829-38.[5].?Corbin KD, et al. Choline metabolism provides novel insights into nonalcoholic fatty liver disease and its progression. Curr Opin Gastroenterol. 2012 Mar;28(2):159-65.[6].?Zhang J, et al. Inhibition of the activity of Rho-kinase reduces cardiomyocyte apoptosis in heart ischemia/reperfusion via suppressing JNK-mediated AIF translocation. Clin Chim Acta. 2009 Mar;401(1-2):76-80.[7].?Sun X, et al. The selective Rho-kinase inhibitor Fasudil is protective and therapeutic in experimental autoimmune encephalomyelitis. J Neuroimmunol. 2006 Nov;180(1-2):126-34. Epub 2006 Sep 22.McePdfHeightPage 3 of 4 www.MedChemExpress.cn
Caution: Product has not been fully validated for medical applications. For research use only.
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Master of Small Molecules — 您?边的抑制剂?师
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