H-HoArg-OH

H-HomoArg-OH (L-Homoarginine) is an orally active endogenous non-protein amino acid. H-HomoArg-OH acts as a weak alternative substrate for NOS and interferes with NO production, selectively inhibits tissue-nonspecific alkaline phosphatase (TNAP), and suppresses the uptake of arginine by y⁺-type transporters (system y⁺). H-HomoArg-OH increases tissue hArg concentrations in vivo, regulates amino acid homeostasis, and improves renal function and pathological features of diabetic nephropathy. H-HomoArg-OH can be used in studies related to diabetes and cardiomyopathy^{[1][2][3][4][5]}. In Vitro:H-HomoArg-OH (5-50 µM; 1 h) is not degraded by slices from male and female pig and rat tissues including small intestine, large intestine, liver, pancreas, spleen, heart, brain, kidney, skeletal muscle, white adipose tissue, thymus, mesenteric lymph nodes, skin, testes, and ovaries when incubated in the presence of physiological amino acid concentrations (excluding lysine)^[3]. In Vivo:H-HomoArg-OH (10 mg/rat; i.p.; single bolus administration) causes an immediate and transient decrease in exocrine pancreatic secretion parameters in BPJ shunt rats, but exerts no effect on normal rats^[1].
H-HomoArg-OH (19 g/kg diet; oral administration; daily; for 4 consecutive days) inhibits exocrine pancreatic hypertrophy and protease production in biliopancreatic jejunostomy (BPJ)-diverted rats induced by a high-protein diet^[1].
The recovery rate of H-HomoArg-OH (1-10 mg/kg; p.o.; single administration) in the urine of healthy pigs and rats is approximately 95-96% of the oral dosage, indicating that the compound undergoes limited catabolism in vivo^[3].
Supplementation with H-HomoArg-OH (50 mg/L; oral administration; ad libitum drinking; 12 weeks) or (0.72 mg/kg/day; subcutaneous injection; continuous infusion via mini-osmotic pump; 12 weeks) alleviates specific features of diabetic nephropathy in Ins2^Akita mice, including reduction of albuminuria, improvement of glomerular injury, attenuation of inflammation and oxidative stress, and restoration of renal nitrate + nitrite levels^[2].
H-HomoArg-OH (20-440 mg/kg; intraperitoneal injection; single bolus) dose-dependently increases tissue free hArg concentrations, regulates amino acid homeostasis, and shifts the reaction equilibrium catalyzed by AGAT without integrating into tissue proteins in isoproterenol-induced stress cardiomyopathy Sprague-Dawley rats^[5].