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]}.

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

211.45

C₆H₁₅BClNO₄

194656-75-2

Solid

White to off-white

O=C([C@H](CCCCB(O)O)N)O.[H]Cl

Room temperature in continental US; may vary elsewhere.

4°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

• [1]. Vadon-Legoff S, et al. Improved and high yield synthesis of the potent arginase inhibitor: 2 (S)-amino-6-boronohexanoic acid. Organic process research & development, 2005, 9(5): 677-679

  [2]. Wang L, et al. Arginase inhibition enhances angiogenesis in endothelial cells exposed to hypoxia. Microvasc Res. 2015 Mar;98:1-8.  [Content Brief]

  [3]. Tsai P, et al. Effect of the mammalian arginase inhibitor 2(S)-amino-6-boronohexanoic acid on Bacillus anthracis arginase. Curr Microbiol. 2012 Apr;64(4):379-84.  [Content Brief]

  [4]. Segal R, et al. Chronic oral administration of the arginase inhibitor 2(S)-amino-6-boronohexanoic acid (ABH) improves erectile function in aged rats. J Androl. 2012 Nov-Dec;33(6):1169-75.  [Content Brief]

  [5]. Kavalukas SL, et al. Arginase inhibition promotes wound healing in mice. Surgery. 2012 Feb;151(2):287-95.  [Content Brief]

  [6]. Cho JS, et al. The effects of arginase inhibitor on lung oxidative stress and inflammation caused by pneumoperitoneum in rats. BMC Anesthesiol. 2015 Sep 28;15:129.  [Content Brief]

  [7]. Yao L, et al. Obesity-induced vascular inflammation involves elevated arginase activity. Am J Physiol Regul Integr Comp Physiol. 2017 Nov 1;313(5):R560-R571.  [Content Brief]

  [8]. Mehl A, et al. Effect of arginase inhibition on pulmonary L-arginine metabolism in murine Pseudomonas pneumonia. PLoS One. 2014 Mar 3;9(3):e90232.  [Content Brief]

  [9]. Krause BJ, et al. Chronic Intermittent Hypoxia-Induced Vascular Dysfunction in Rats is Reverted by N-Acetylcysteine Supplementation and Arginase Inhibition. Front Physiol. 2018 Jul 24;9:901.  [Content Brief]

  [10]. Bhatta A. Involvement of arginase upregulation in diabetes-and angiotensin II-induced vascular dysfunction. 2015.

  [11]. Toso A, et al. Congenital diaphragmatic hernia: phosphodiesterase-5 and Arginase inhibitors prevent pulmonary vascular hypoplasia in rat lungs. Pediatr Res. 2024 Mar;95(4):941-948.  [Content Brief]