Camostat mesylate (FOY-S980) is a trypsin-like protease inhibitor and inhibits airway epithelial sodium channel (ENaC) function.

ENaC:50 nM

Camostat mesilate, at a concentration of 1 mg/g, is effective in preventing pancreatic atrophy and improving exocrine function in rats with DBTC-induced chronic pancreatitis. This compound also inhibits chronic inflammation and fibrosis in the pancreas caused by DBTC. It suppresses the development of pancreatic fibrosis and PSC activation, as well as monocyte infiltration and the expression of MCP-1 in serum and pancreatic tissues. When administered at a dose of 100 mg/kg, Camostat mesilate significantly increases body and pancreatic wet weight, and effectively reduces inflammatory changes and fibrosis in the pancreas by inhibiting gene expression of PAP, p8, and cytokines in chronic pancreatitis. In rats treated with pig serum, Camostat mesilate (1-2 mg/g in diet) notably decreases the levels of hepatic plasmin and TGF-β and inhibits HSC activation and liver fibrosis, without noticeable systemic or local side effects. Additionally, at a dose of 100 μg/kg intratracheally, Camostat prolongs the attenuation of ENaC activity in guinea pig tracheas.

At a concentration of 2 mM, Camostat mesilate inhibits the production of MCP-1 and TNF-α in activated rat monocytes and the proliferation of rat pancreatic stellate cells (PSCs) along with MCP-1 production. In the presence of 20 mM Camostat mesilate, there is a notable reduction in blood glucose levels when combined with insulin and administered via the large intestine, effectively decreasing insulin degradation in the rat's small intestine and its homogenate. A 30 μM concentration of Camostat prolongs the decay of ENaC function in a human respiratory epithelial cell model, which can be reversed by adding excess trypsin. At 500 mM, Camostat mesilate inhibits the generation of TGF-β by suppressing plasmin activity and reduces the activity of TGF-beta, thereby blocking the ex vivo activation of hepatic stellate cells (HSC).