Nafamostat hydrochlorideCAS# 80251-32-7 |
- SU14813
Catalog No.:BCC1971
CAS No.:627908-92-3
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| Cas No. | 80251-32-7 | SDF | Download SDF |
| PubChem ID | 13050562 | Appearance | Powder |
| Formula | C19H19Cl2N5O2 | M.Wt | 420.29 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | Soluble in DMSO | ||
| Chemical Name | (6-carbamimidoylnaphthalen-2-yl) 4-(diaminomethylideneamino)benzoate;dihydrochloride | ||
| SMILES | C1=CC(=CC=C1C(=O)OC2=CC3=C(C=C2)C=C(C=C3)C(=N)N)N=C(N)N.Cl.Cl | ||
| Standard InChIKey | GKGJACPQHBIISL-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C19H17N5O2.2ClH/c20-17(21)14-2-1-13-10-16(8-5-12(13)9-14)26-18(25)11-3-6-15(7-4-11)24-19(22)23;;/h1-10H,(H3,20,21)(H4,22,23,24);2*1H | ||
| 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 | Nafamostat hydrochloride, a synthetic serine protease inhibitor, is an anticoagulant.
Target: Serine Protease
Tranilast (FUT-175) is an antiallergic drug for bronchial asthma. It has been used for the treatment of allergic disorders such as asthma, allergic rhinitis and atopic dermatitis. It has also been investigated for use as an antiproliferative drug on drug-eluting stents.
A 20-40 mg/h dose of FUT-175 prolonged coagulation time sufficiently in the instrumental blood of the extracorporeal circuit but not in the systemic blood. Its anticoagulant activity decreased immediately after hemodialysis. Therefore, we could manage all patients without any bleeding trouble during hemodialysis with FUT-175 as an anticoagulant. Although there were side effects of FUT-175, such as nausea, vomiting, itching and eruption, they were not serious, and FUT-175 could be administered without interruption. FUT-175 seems to be useful as an anticoagulant during hemodialysis for patients susceptible to bleeding. References: | |||||
Nafamostat hydrochloride Dilution Calculator
Nafamostat hydrochloride Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.3793 mL | 11.8965 mL | 23.7931 mL | 47.5862 mL | 59.4827 mL |
| 5 mM | 0.4759 mL | 2.3793 mL | 4.7586 mL | 9.5172 mL | 11.8965 mL |
| 10 mM | 0.2379 mL | 1.1897 mL | 2.3793 mL | 4.7586 mL | 5.9483 mL |
| 50 mM | 0.0476 mL | 0.2379 mL | 0.4759 mL | 0.9517 mL | 1.1897 mL |
| 100 mM | 0.0238 mL | 0.119 mL | 0.2379 mL | 0.4759 mL | 0.5948 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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Nafamostat hydrochloride, a synthetic serine protease inhibitor, is an anticoagulant.
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Successful treatment of levodopa-induced neuroleptic malignant syndrome (NMS) and disseminated intravascular coagulation (DIC) in a patient with Parkinson's disease.[Pubmed:1295627]
Intern Med. 1992 Nov;31(11):1298-302.
After 9 years of treatment for Parkinson's disease, a 68-year-old woman developed the complications of neuroleptic malignant syndrome (NMS) and disseminated intravascular coagulation (DIC) while she was still receiving levodopa, bromocriptine and amantadine hydrochloride. The patient displayed a high fever (40 degrees C), impaired consciousness, marked systemic muscle rigidity, tremor and bloody stools. The diagnosis of NMS and DIC was made on the basis of the symptoms and the results of blood serological tests. The antiparkinsonian drugs that had been administered until her admission to our hospital were continued unchanged, while the NMS was treated with dantrolene sodium and the DIC, with nafamostat mesilate. Both of the above-mentioned therapies were effective. The present case is rare in that the patient developed NMS and DIC during treatment and not after the discontinuation of the antiparkinsonian drugs.
[Malignant syndrome associated with disseminated intravascular coagulation and a high level of amylase in serum, followed by diabetic coma in an elderly patient with Parkinson's disease during L-dopa therapy].[Pubmed:9584493]
Nihon Ronen Igakkai Zasshi. 1998 Feb;35(2):139-44.
A 66-year-old woman with a 7-year history of Parkinsons' disease was admitted to our hospital because of a high fever and disturbance of consciousness. She had been treated with levodopa/benserazide hydrochloride and trihexyphenidyl hydrochloride until admission. On admission, the patient was comatose, her temperature was 40.5 degrees C, her blood pressure was 54/-mmHg, and her pulse rate was 130 beats/min. Laboratory tests showed leukocytosis, a high level of creatine kinase in serum and evidence of hyperosmolar non-ketotic diabetic coma (blood glucose, 1,080 mg/dl) and of disseminated intravascular coagulation (DIC). A continuous insulin infusion, antibiotics, nafamostat mesilate, and urinastatin were given, after which the DIC, hyperglycemia, and the level of consciousness were improved. However, levels of creatine kinase, myoglobin, transaminase, and amylase in serum continued to increase, and multiple organ failure was suspected. Furthermore, she became less responsive, diaphoretic, and tremulous; fever and mild rigidity developed. The peak creatine kinase and myoglobin were 11,095 U/l and 12,520 ng/ml, respectively. A diagnosis of malignant syndrome was made, and treatment with levodopa/carbidopa and dantrolene was begun. Within several days, the clinical and laboratory findings improved. We report here a rare case of malignant syndrome associated with DIC followed by diabetic coma in an elderly patient with Parkinsons' disease during L-dopa therapy. Timely diagnosis and treatment of malignant syndrome are important in the management of elderly patients with Parkinsons' disease, because DIC and multiple organ failure may occur in the early stages of malignant syndrome.
Role of thromboxane (Tx) A2 in guinea pig Forssman shock and the effect of OKY-046, Tx A2 synthetase inhibitor.[Pubmed:3470814]
Prostaglandins Leukot Med. 1987 Feb;26(2):133-41.
To study the role of thromboxane (Tx) A2 in Forssman systemic shock (FSS) in guinea pig, the effect of (E)-3-[p-(1H-Imidazol-1-ylmethyl)phenyl]-2-propenoic acid hydrochloride (OKY-046), a specific Tx A2 synthetase inhibitor, was studied. OKY-046 administered intravenously clearly prolonged survival time and protected against fatal shock. In shocked animals, definite decreases in serum complement hemolytic activity (CH50), leucocyte counts and platelet counts and an increase in lactate dehydrogenase (LDH) activity were observed. In addition, a significant increase of Tx B2 and incoagulability of blood were observed after shock. Whereas OKY-046 had no effect on the decreases in CH50, platelet counts and leucocyte counts, it inhibited the increase of Tx B2 and increased the amount of 6-keto PG F1 alpha. When Forssman antibody (half a lethal dose) was injected, a diphasic increase in airway resistance was observed. OKY-046 inhibited this diphasic increase in airway resistance. These data suggest a pathophysiological role for Tx A2 in FSS. OKY-046 inhibited the Forssman antibody induced respiratory disorders probably due to the inhibition of Tx A2 synthesis after shock.
