ABH (hydrochloride)

ABH (hydrochloride) is an orally active arginase inhibitor (K_i = 8.5 nM). ABH hydrochloride promotes NO production and reduces the expression of inflammatory response-related molecules (ICAM-1, VCAM-1, MCP-1). ABH hydrochloride improves erectile function, reduces lung damage, promotes wound healing, reduces arterial blood pressure, and improves vascular fibrosis^{[1][2][3][4][5][6][7][8][9][10][11]}. In Vitro:ABH (100 μM; pretreatment for 1 h, hypoxia for 12-24 h) hydrochloride partially prevents the hypoxia-induced reduction in in-vitro tube-like structure formation in bovine aortic endothelial cells and increased vascular endothelial growth factor (VEGF) expression^[2].
ABH (0-10 μM; 3 h) hydrochloride effectively inhibits arginase from multiple Bacillus anthracis spore strains^[3].
ABH (0.01-1 mM; pretreatment for 1 h) hydrochloride significantly reduces arginase activity in mouse dermal fibroblasts, with 0.1 mM ABH reducing arginase activity by 35% and 1 mM ABH reducing arginase activity by 54%^[5].
ABH (100 μM; pretreatment for 1 h) hydrochloride can inhibit the increase in arginase 1 (A1) expression and activity in mouse aortic endothelial cells induced by high glucose/palmitic acid, maintain NO production, reduce the expression of inflammatory response-related molecules (ICAM-1, VCAM-1, MCP-1), and inhibit monocyte adhesion^[7].
ABH (100 µM; 2 h) hydrochloride inhibits Ang II-induced proliferation of rat aortic smooth muscle cells, ODC activity and expression, and the increase in type I collagen and hydroxyproline levels^[10].
In Vivo:ABH (400 μg/day; p.o.; once daily; 25 days) hydrochloride can reduce arginase activity in the penile tissue of aged rats, improve erectile function, and make erectile hemodynamic indicators close to the level of young rats^[4].
ABH (0.1 mM, 0.1 mL; topical application; once every 8 hours; 14 days) hydrochloride can significantly promote wound healing in mice^[5].
ABH (5 mg/kg; s.c.; once 1 hour before surgery; single administration) hydrochloride can increase plasma nitrite levels in rats with pneumoperitoneum, maintain nitric oxide synthase (NOS) activity, reduce oxidative stress and inflammatory response, and reduce the severity of lung injury^[6].
ABH (10 mg/kg; p.o., drinking water; once daily) hydrochloride can inhibit the increase of arginase activity and A1 expression in vascular endothelial cells of obese mice induced by a high-fat and high-sugar diet, reduce inflammation and pathological remodeling of visceral adipose tissue (VAT), including reducing inflammatory monocyte infiltration, macrophage polarization to M1 type, improving adipocyte size, fibrosis and capillary density^[7].
ABH (100 mg; i.p.; once at 24, 48, 60, 70 h after infection or continuously administered until day 3 after infection) hydrochloride can increase NO production in the lungs of mice infected with Pseudomonas aeruginosa, improve L-arginine availability, reduce L-ornithine concentration, and do not increase the levels of lung inflammatory markers^[8].
ABH (400 µg/kg/day; subcutaneous osmotic pump injection; once/day; 21 days) hydrochloride can reduce the mean arterial blood pressure and improve the vascular reactivity of the carotid and femoral arteries in a rat model of hypertension induced by chronic intermittent hypoxia (CIH)^[9].
ABH (10 mg/kg/day; drinking water administration; continuous administration; 6 months) hydrochloride can improve endothelial function, reduce aortic stiffness and fibrosis, and reduce plasma and aortic arginase activities in a mouse model of obesity-related type 2 diabetes induced by a high-fat and high-sugar diet^[10].
ABH (400 µg/day; subcutaneous osmotic pump administration; continuous administration) hydrochloride can preserve the total volume of the fetal lung, prevent excessive proliferation of pulmonary vascular smooth muscle cells, and improve the number of pulmonary vessels and lung morphology in a rat model of congenital diaphragmatic hernia (CDH) induced by Nitrofen (HY-B1877)^[11].