222638-67-7
S-(2-boronoethyl)-L-cysteine hydrochloride
CAS: 222638-67-7
Molecular Formula: C5H13BClNO4S
222638-67-7 - Names and Identifiers
222638-67-7 - Physico-chemical Properties
| Molecular Formula | C5H13BClNO4S |
| Molar Mass | 229.48 |
| Solubility | Soluble in DMSO |
| Storage Condition | Inert atmosphere,Store in freezer, under -20°C |
| Use | BEC, also known as S-(2-boronoethyl)-L-cysteine, is an a slow-binding and competitive Arginase II inhibitor with Ki of 0.31 μM (ph 7.5). BEC significantly enhances NO-dependent relaxation of human penile corpus canvernosum smooth muscle in vitro at concentrations between 0.1-1.0 mM. S-(2-boronoethyl)-L-cysteine binds to arginase as a transition state analogue and enhances smooth muscle relaxation in human penile corpus cavernosum. |
| In vitro study | BEC results in a significant enhancement of NO-dependent smooth muscle contraction. In cardiomyocytes, BEC enhances Ca(2)-dependent NOS activity and NO production while increasing its basal contractility. BEC also inhibits the proliferation of human pulmonary artery smooth muscle cells by reducing the expression levels of cyclin D1 and CDK4, increasing the expression of p27 and partially reducing the phosphorylation of Akt and ERK. |
| In vivo study | In a mouse model with allergic inflammation, BEC enhances the perivascular and subvascular inflammatory response, resulting in enhanced NF-κB DNA binding and NF-κB-dependent inflammatory gene expression, at the same time, the content of NOx is increased. In a rat model of pulmonary hypertension, BEC reduced right ventricular systolic pressure. |
222638-67-7 - Reference
| Reference Show more | 1: Kim NN, Cox JD, Baggio RF, Emig FA, Mistry SK, Harper SL, Speicher DW, Morris SM Jr, Ash DE, Traish A, Christianson DW. Probing erectile function: S-(2-boronoethyl)-L-cysteine binds to arginase as a transition state analogue and enhances smooth muscle relaxation in human penile corpus cavernosum. Biochemistry. 2001 Mar 6;40(9):2678-88. PubMed PMID: 11258879. 2: Kim SH, Langford ML, Boucher JL, Testerman TL, McGee DJ. Helicobacter pylori arginase mutant colonizes arginase II knockout mice. World J Gastroenterol. 2011 Jul 28;17(28):3300-9. doi: 10.3748/wjg.v17.i28.3300. PubMed PMID: 21876618; PubMed Central PMCID: PMC3160534. 3: Martens CR, Kuczmarski JM, Lennon-Edwards S, Edwards DG. Impaired L-arginine uptake but not arginase contributes to endothelial dysfunction in rats with chronic kidney disease. J Cardiovasc Pharmacol. 2014 Jan;63(1):40-8. doi: 10.1097/FJC.0000000000000022. PubMed PMID: 24084210. 4: You H, Gao T, Cooper TK, Morris SM Jr, Awad AS. Arginase inhibition: a new treatment for preventing progression of established diabetic nephropathy. Am J Physiol Renal Physiol. 2015 Sep 1;309(5):F447-55. doi: 10.1152/ajprenal.00137.2015. PubMed PMID: 26041444; PubMed Central PMCID: PMC4556892. 5: You H, Gao T, Cooper TK, Morris SM Jr, Awad AS. Arginase inhibition mediates renal tissue protection in diabetic nephropathy by a nitric oxide synthase 3-dependent mechanism. Kidney Int. 2013 Dec;84(6):1189-97. doi: 10.1038/ki.2013.215. PubMed PMID: 23760286; PubMed Central PMCID: PMC3783645. |
222638-67-7 - Preparation solution concentration reference
| 1mg | 5mg | 10mg | |
|---|---|---|---|
| 1 mM | 4.357 ml | 21.787 ml | 43.575 ml |
| 5 mM | 0.871 ml | 4.357 ml | 8.715 ml |
| 10 mM | 0.436 ml | 2.179 ml | 4.357 ml |
| 5 mM | 0.087 ml | 0.436 ml | 0.871 ml |
Last Update：2024-01-02 23:10:35
222638-67-7 - Reference Information
| biological activity | BEC HCl is a slow-binding, competitive arginase inhibitor with Ki values for Arginase II and rat Arginase I of 0.31 μM (pH7.5) and 0.4-0.6 μM respectively. |
| target | TargetValue Arginase II 0.31 μM(Ki) rat Arginase I <0.6 μM(Ki) |
| Target | Value |
| Arginase II | 0.31 μM(Ki) |
| rat Arginase I | <0.6 μM(Ki) |
| In vitro studies | BEC led to a significant increase in NO-dependent smooth muscle contraction. In cardiomyocytes, BEC enhanced Ca(2 +)-dependent NOS activity and NO production while increasing its basal contractility. BEC also inhibited 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 partially decreasing the phosphorylation of Akt and ERK. |
| In vivo studies | In a mouse model with allergic inflammation, BEC enhances the inflammatory response around the vessels and vessels, leading to enhanced NF-κB DNA binding and NF-κB-dependent inflammatory gene expression, while increasing NOx content. In a rat model of pulmonary arterial hypertension, BEC reduced right ventricular systolic pressure. |
Last Update：2024-04-09 15:16:39
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View History
222638-67-7
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220497-48-3
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760952-88-3
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卡前列甲酯