Nafamostat

539.58

347.37

1806241-263-5

Y25LQ0H97D

DTXSID0048420

C96292

141

2

1.4±0.1 g/cm3

637.2°C at 760 mmHg

339.1±34.3 °C

1.694

Reported incidences of agranulocytosis, hyperkalemia, and anaphylaxis. The use of nafamostat has been reported to cause cardiac arrest in patients receiving dialysis due to a sudden change in the patient's condition such as dyspnea. A study suggests that the drug and its metabolites may inhibit the amiloride-sensitive sodium (Na) conductance at the collecting ducts, resulting in an inhibition of K secretion and hyperkalemia. Reported LD50 value from intravenous administration in rats is 16.4mg/kg.

Used as an anticoagulant in patients with disseminative blood vessel coagulation, hemorrhagic lesions, and hemorrhagic tendencies. It prevents blood clot formation during extracorporeal circulation in patients undergoing continuous renal replacement therapy and extra corporeal membrane oxygenation.

Nafamostat is a fast-acting proteolytic inhibitor used during hemodialysis to prevent the proteolysis of fibrinogen into fibrin by competitively inhibiting several serine proteases including thrombin. It improves acute pancreatitis and prevents blood clot formation during extracorporeal circulation and has an anti-inflammatory effect in vitro. A study suggets that nafamostat has a neuroprotective role during ischemia-induced brain injury from antithrombin activity.

Exogenous or endogenous compounds which inhibit SERINE ENDOPEPTIDASES. (See all compounds classified as Serine Proteinase Inhibitors.)|Agents that prevent BLOOD CLOTTING. (See all compounds classified as Anticoagulants.)|Compounds that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. (See all compounds classified as Complement Inactivating Agents.)|Serine proteinase inhibitors which inhibit trypsin. They may be endogenous or exogenous compounds. (See all compounds classified as Trypsin Inhibitors.)|Anti-inflammatory agents that are non-steroidal in nature. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions.They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects. (See all compounds classified as Anti-Inflammatory Agents, Non-Steroidal.)|Compounds which inhibit or antagonize biosynthesis or actions of proteases (ENDOPEPTIDASES). (See all compounds classified as Protease Inhibitors.)

Two metabolites of NM, p-guanidinobenzoic acid (PGBA) and 6-amidino-2-naphthol (AN), are renally excreted. Nafamostat accumulates in the kidneys.

Nafamostat is mainly hydrolyzed by hepatic carboxyesterase and long-chain acyl-CoA hydrolase in human liver cytosol. Main metabolites are p-guanidinobenzoic acid (PGBA) and 6-amidino-2-naphthol (AN) as inactive protease inhibitors.

Approximately 8 minutes

Nafamostat mesilate inhibits various enzyme systems, such as coagulation and fibrinolytic systems (thrombin, Xa, and XIIa), the kallikrein–kinin system, the complement system, pancreatic proteases and activation of protease-activated receptors (PARs). Nafamostat inhibits lipopolysaccharide-induced nitric oxide production, apoptosis, and interleukin (IL)-6 and IL-8 levels in cultured human trophoblasts. It is shown to act as an antioxidant in TNF-α-induced ROS production.

6'-amidino-2-naphthyl 4-guanidinobenzoate