α-Fluoromethylhistidine dihydrochloride

α-Fluoromethylhistidine (dihydrochloride) (3 mg/kg per h; subcutaneous; continuous infusion; 6 weeks) depletes ECL cell histamine, reduces ECL cell secretory vesicle and microvesicle numbers, and alters secretory vesicle size, but does not affect ECL cell hypertrophy or granule ultrastructure in female Sprague-Dawley rats^[1].
α-Fluoromethylhistidine (dihydrochloride) (3 mg/kg per h; subcutaneous; continuous infusion; 6 weeks) depletes ECL cell histamine, abolishes omeprazole-induced ECL cell vacuole formation, reduces ECL cell secretory vesicle and microvesicle numbers and volume density, but does not affect omeprazole-induced ECL cell hypertrophy or granule ultrastructure in female Sprague-Dawley rats with omeprazole-induced hypergastrinemia^[1].
α-Fluoromethylhistidine (dihydrochloride) (3 mg/kg per h; subcutaneous; 24 h) reduces mouse oxyntic mucosal histamine by ~65%, depletes ECL cell secretory vesicles by ~84%, and increases plasma gastrin levels by 130%^[2].
α-Fluoromethylhistidine (dihydrochloride) (3 mg/kg per h; subcutaneous; 24 h) reduces rat oxyntic mucosal histamine by ~83%, depletes ECL cell secretory vesicles by ~88%, increases plasma gastrin levels by 143%, and does not affect other gastric oxyntic endocrine cell types^[2].
α-Fluoromethylhistidine (dihydrochloride) (3 mg/kg per h; subcutaneous; 24 h) reduces hamster oxyntic mucosal histamine by ~91%, depletes ECL cell secretory vesicles by ~89%, and reduces ECL cell profile size by ~33%, with no effect on plasma gastrin levels^[2].
α-Fluoromethylhistidine (dihydrochloride) (5 mg/kg/h; s.c.; continuous; 24 hours) produces 80% depletion of oxyntic mucosal histamine via irreversible inhibition of HDC, while leaving oxyntic mucosal pancreastatin-LI concentrations unaltered in male Sprague-Dawley rats^[3].
α-Fluoromethylhistidine (3 mg/kg/h, 50 mg/kg; s.c., p.o.; continuous infusion, single dose; 2-6 days, 2 hours before testing) reduces oxyntic mucosal histamine by 80%, inhibits basal gastric acid secretion by over 60%, and almost abolishes gastrin-17-stimulated acid secretion, but does not alter histamine-stimulated or vagally induced (insulin or pylorus ligation) gastric acid secretion in female Sprague-Dawley rats^[4].