HydroxyfasudilRho-kinase inhibitor and vasodilator CAS# 105628-72-6 |
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Quality Control & MSDS
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| Cas No. | 105628-72-6 | SDF | Download SDF |
| PubChem ID | 3064778 | Appearance | Powder |
| Formula | C14H17N3O3S | M.Wt | 307.37 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | HA-1100 | ||
| Solubility | DMSO : ≥ 31 mg/mL (100.86 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 5-(1,4-diazepan-1-ylsulfonyl)-2H-isoquinolin-1-one | ||
| SMILES | C1CNCCN(C1)S(=O)(=O)C2=CC=CC3=C2C=CNC3=O | ||
| Standard InChIKey | ZAVGJDAFCZAWSZ-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C14H17N3O3S/c18-14-12-3-1-4-13(11(12)5-7-16-14)21(19,20)17-9-2-6-15-8-10-17/h1,3-5,7,15H,2,6,8-10H2,(H,16,18) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Hydroxyfasudil is a ROCK inhibitor, with IC50s of 0.73 and 0.72 μM for ROCK1 and ROCK2, respectively.In Vitro:Hydroxyfasudil is a ROCK inhibitor, with IC50s of 0.73 and 0.72 μM for ROCK1 and ROCK2, respectively. Hydroxyfasudil also less potently inhibits PKA, with an IC50 of 37 μM, 50-fold higher than those of the ROCKs. Hydroxyfasudil increases eNOS mRNA levels, with an EC50 value of 0.8 ± 0.3 μM. Hydroxyfasudil (0-100 μM) concentration-dependently increases eNOS activity and stimulates NO production in human aortic endothelial cells (HAEC). Hydroxyfasudil (10 μM) increases the half-life of eNOS mRNA from 13 to 16 hours, but does not affect eNOS promoter activity at concentrations from 0.1 to 100 μM[1].In Vivo:Hydroxyfasudil (10 mg/kg, i.p.) significantly increases both the average and maximal voided volumes in SD rats. Hydroxyfasudil also significantly decreases the maximal detrusor pressure[2]. Hydroxyfasudil (3 mg/kg, i.p) inhibits hypercontractility induced by norepinephrine in spontaneously hypertensive rats (SHRs). Furthermore, Hydroxyfasudil (3, 10 mg/kg, i.p) significantly ameliorates decreased penile cGMP contents in rats[3]. References: | |||||
Hydroxyfasudil Dilution Calculator
Hydroxyfasudil Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.2534 mL | 16.267 mL | 32.5341 mL | 65.0682 mL | 81.3352 mL |
| 5 mM | 0.6507 mL | 3.2534 mL | 6.5068 mL | 13.0136 mL | 16.267 mL |
| 10 mM | 0.3253 mL | 1.6267 mL | 3.2534 mL | 6.5068 mL | 8.1335 mL |
| 50 mM | 0.0651 mL | 0.3253 mL | 0.6507 mL | 1.3014 mL | 1.6267 mL |
| 100 mM | 0.0325 mL | 0.1627 mL | 0.3253 mL | 0.6507 mL | 0.8134 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Description: IC50 Value: 0.12 uM (ROCK1); 0.17 uM (ROCK2) [1] Hydroxyfasudil, metabolite of Fasudil, is a potent Rho-kinase inhibitor and vasodilator. in vitro: Fasudil (1-10 μM) and hydroxyfasudil (0.3-10 μM) significantly prevented endothelin-induced cardiomyocyte hypertrophy [2]. Hydroxyfasudil significantly attenuated serotonin (IC)-induced vasoconstriction of SA (-7 +/- 1% vs. 2 +/- 1%, p < 0.01). Coronary I/R significantly impaired coronary vasodilation to acetylcholine after I/R (SA, p < 0.05; and A, p < 0.01 vs. before I/R) and L-NMMA further reduced the vasodilation, whereas hydroxyfasudil completely preserved the responses. in vivo: Treatment with hydroxyfasudil significantly improved bladder intercontraction intervals. Rats treated with hydroxyfasudil also showed a significant reduction of histopathological features associated with cystitis [3]. Twelve-week-old male SHRs were treated with hydroxyfasudil (3 or 10 mg/kg, i.p.) once a day for 6 weeks. Treatment with hydroxyfasudil significantly improved the decreased penile cGMP concentrations, the increased Rho kinase activities, the increased norepinephrine-induced contractions, and the decreased acetylcholine-induced relaxation in a dose-dependent manner [4]. Toxicity: The proportion of patients with good clinical outcome was 74.5% (41/55) in the fasudil group and 61.7% (37/60) in the nimodipine group. There were no serious adverse events reported in the fasudil group [5]. Clinical trial: N/A
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Aldehyde oxidase-dependent species difference in hepatic metabolism of fasudil to hydroxyfasudil.[Pubmed:28166443]
Xenobiotica. 2018 Feb;48(2):170-177.
1. An investigation on the metabolic mechanism of fasudil to Hydroxyfasudil was conducted in vitro using liver subcellular fractions of different species. Hydroxyfasudil was generated in large amounts by rat liver S9 and to a similar extent by human liver S9 but was not detected in dog liver S9 incubations. 2. Studies with various molybdenum hydroxylase inhibitors demonstrated that aldehyde oxidase (AO), but not xanthine oxidase (XO), selectively catalyzed fasudil to Hydroxyfasudil in both rat and human liver cytosol. In addition, the oxygen atom incorporated into Hydroxyfasudil was derived from water rather than atmospheric oxygen, which further corroborated AO involvement. 3. Enzyme kinetics experiments revealed that fasudil had a higher affinity to human hepatic AO than to rat hepatic AO. Besides, significantly different in vivo pharmacokinetic parameters observed between male and female rats indicated that the AO activity in rats was gender-dependent. 4. The present study provided first evidences that AO causes differences in fasudil metabolism between species.
Impact of Rho-Kinase Inhibitor Hydroxyfasudil in Protamine Sulphate Induced Cystitis Rat Bladder.[Pubmed:26663691]
Low Urin Tract Symptoms. 2015 May;7(2):108-14.
OBJECTIVES: The objective of the present study was to evaluate anti-inflammatory effects of Hydroxyfasudil in a protamine sulfate (PS) induced cystitis rat model. Additionally, we investigated prevention of bladder overactivity (BO), and tissue damage in these experiments. METHODS: Animals were divided into four groups. In Groups 1 and 2, chemical induced cystitis model was created by administrating intravesical PS with PE50 catheter by the transurethral route. In Group 1, Rho-kinase inhibitor Hydroxyfasudil was administered intaperitoneally, and in Group 2, subjects were administered a corresponding volume of saline in the same way. In Group 3, vehicle was administered intravesically and Hydroxyfasudil was administrated intraperitoneally. Group 4 was a control Group, and the vehicle was administered intravesically and intraperitoneally. Micturition frequencies were recorded. Biochemical analyses were performed for oxidative stress, and pathological evaluations were investigated. In vitro contractions of bladder tissue strips were measured in tissue-bath. RESULTS: There were significantly lower Lipid peroxidase levels and higher levels of Glutathione in Group 1 than Group 2 (P = 0.016, P = 0.001, respectively). There was generally more inflammation in Group 2 than the other groups as determined by microscopy. There were significantly higher frequencies of micturition, lower volume, and mean voided maximum urine output after PS administration in Groups 1 and 2. In vitro contraction responses of bladder strips to potassium chloride and acetylcholine were statistically higher in Group 2 than Groups 1 and 3. CONCLUSIONS: Significant reduction of inflammation by affecting the anti-oxidant defense systems was provided by Hydroxyfasudil. Decreased in vitro responses to contractions of bladder smooth muscle strips were obtained. Hydroxyfasudil may be a potential new therapeutic option for inflammation and BO, in rat bladder.
Protective effect of hydroxyfasudil, a Rho kinase inhibitor, on ventral prostatic hyperplasia in the spontaneously hypertensive rat.[Pubmed:26286428]
Prostate. 2015 Nov;75(15):1774-82.
BACKGROUND: Rho kinase (ROCK) pathway is associated with various cellular functions, such as smooth muscle contraction, inflammatory response, and cell proliferation. The spontaneously hypertensive rat (SHR) is commonly used genetically hypertensive rat model which develops hyperplastic morphological abnormalities in the ventral prostate. We investigated whether administration of Hydroxyfasudil, a ROCK inhibitor, could reduce the levels of growth factors, inflammatory markers, and morphological abnormalities in the ventral prostate of the SHR. METHODS: Twelve-week-old SHRs were treated with Hydroxyfasudil (1 mg/kg/day, i.p.) or vehicle once daily for another 6 weeks. Wistar Kyoto (WKY) rats treated with vehicle were used as normotensive controls. At 18 weeks of age, blood pressure and heart rate were measured by the tail cuff method. Then the rats were sacrificed, and the ventral prostates were removed. The levels of ROCK activity, growth factors (TGF-beta1 and bFGF), a smooth muscle differentiation marker (alpha-SMA) and an inflammatory cytokine (IL-6) in the ventral prostate were measured by ELISA and western blot. A histological evaluation in each group was also performed. RESULTS: There were significant increases in blood pressure, prostate weight, prostate body weight ratio, and tissue levels of ROCK activity, TGF-beta1, bFGF, alpha-SMA, and IL-6 in the SHR compared to the WKY rat. Histological examination of the ventral prostate showed morphological abnormalities such as a higher degree of proliferation in the glandular epithelial and stromal area in the SHR compared to the WKY rat. Treatment with Hydroxyfasudil reduced the elevated ROCK activity, TGF-beta1, bFGF, alpha-SMA, and IL-6 found in the ventral prostate of the SHR. Moreover, treatment with Hydroxyfasudil decreased the morphological abnormalies in the SHR ventral prostate. CONCLUSIONS: Treatment with Hydroxyfasudil decreased the growth factors, an inflammatory cytokine, and morphological abnormalies in the SHR ventral prostate. These results suggest that chronic treatment with Hydroxyfasudil may inhibit the progression of prostatic hyperplasia in the SHR.
N-[(11)C]-methyl-hydroxyfasudil is a potential biomarker of cardiac hypertrophy.[Pubmed:25451216]
Nucl Med Biol. 2015 Feb;42(2):192-7.
INTRODUCTION: Pathologic cardiac hypertrophy is one of the leading causes of sudden death from cardiac disease and involves a complex network of bio-signaling mechanisms. To date, the clinical detection and pathologic progression of hypertrophy remains elusive. Here we tested whether imaging Rho kinase activity would serve an accurate proxy for detecting hypertrophy. Specifically, we examine the use of the N-[(11)C]-methylated derivative of Hydroxyfasudil, a Rho kinase inhibitor, as a biomarker for accurate identification of cardiomyocyte hypertrophy. METHODS: Both transformed and primary neonatal cardiomyocytes were treated with isoproterenol to induce beta-adrenergic receptor stimulation and hypertrophy. Phenotypic hypertrophy was verified using cytochemical evaluation of cell and nuclear size. Western blot and activity assays were used to detect ERK 1/2 mTOR and Rho kinase activation. N-[(11)C]-methyl-Hydroxyfasudil binding was verified using in vitro binding assays with isoproterenol stimulated cells. RESULTS: Isoproterenol induced a rapid and distinct activation of ERK 1/2, mTOR and Rho kinase with negligible cytotoxicity. Subsequent expansion in cell and nuclear size that is typically associated with hypertrophy was also observed. Enhanced retention of N-[(11)C]-methyl-Hydroxyfasudil observed after ISO-induced Rho kinase activation in hypertrophic cells was prevented by pre-treatment with unlabeled Hydroxyfasudil. CONCLUSIONS: N-[(11)C]-methyl-Hydroxyfasudil is able to measure increased Rho kinase activity via specific binding in hypertrophied cardiomyocytes and demonstrates the potential for molecular imaging of altered Rho kinase activity in diseases such as cardiac hypertrophy.
