Description | BEC hydrochloride (BEC HCl) is a competitive arginase inhibitor, which bind slowly. Ki of BEC HCl is 0.31 μM (pH7.5) for Arginase II, and is 0.4-0.6 μM for rat Arginase I. |
In vitro | BEC causes significant enhancement of NO-dependent smooth muscle relaxation. [2] In myocytes, BEC augments Ca(2+)-dependent NOS activity and NO production, and increases basal contractility. [3] BEC also inhibits the proliferation of human pulmonary artery smooth muscle cells by decreasing the expression levels of cyclin D1 and CDK4, increasing the expression of p27, and partly reducing the phosphorylation of Akt and ERK. [5] |
In vivo | In mice with allergic inflammation (OVA/OVA), BEC enhances peribronchiolar and perivascular inflammation, leads to enhanced NF-κB DNA binding and NF-κB-dependent inflammatory gene expression, and causes an increase in the content of NOx. [4] In rats with pulmonary arterial hypertension, BEC reduces the right ventricle systolic pressure. [5] |
Target activity | Arginase II:0.31 μM(Ki) |
Synonyms | BEC HCl |
molecular weight | 229.49 |
Molecular formula | C5H12BNO4S·ClH |
CAS | 222638-67-7 |
Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year |
Solubility | DMSO: 42 mg/mL (183 mM) Ethanol: 42 mg/mL (183 mM) H2O: 41 mg/mL (178.7 mM) |
References | 1. Colleluori DM, et al. Biochemistry. 2001, 40(31), 9356-9362. 2. Kim NN, et al. Biochemistry. 2001, 40(9), 2678-2688. 3. Steppan J, et al. Proc Natl Acad Sci U S A. 2006, 103(12), 4759-4764. 4. Ckless K, et al. J Immunol. 2008, 181(6), 4255-4264. 5. Jiang W, et al. Mol Med Rep. 2015, 12(3), 4743-4749. |