Highly selective and potent inhibitor of nNOS (Ki = 57 nM). Displays 3158-fold and 149-fold selectivity over iNOS and eNOS respectively. Hypotensive in vivo. Kakoki et al (2001) The influence of nitric oxide synthase 1 on blood flow and interstitial nitric oxide in the kidney. Am.J.Physiol.Regul.Integr.Comp.Physiol. 281 R91 PMID:11404282 |Zhang et al (1997) Potent and selective inhibition of neuronal nitric oxide synthase by Nω-propyl-L-arginine. J.Med.Chem. 40 3869 PMID:9397167
L-Arginine-15N4 ((S)-(+)-Arginine-15N4) hydrochloride, the 15N-labeled variant of L-Argininehydrochloride ((S)-(+)-Argininehydrochloride), serves as the nitrogen donor in the synthesis of nitric oxide. This potent vasodilator is crucial, especially during a sickle cell crisis where its levels are notably diminished.
MRTX9768 hydrochloride is a potent, orally active PRMT5 inhibitor. MRTX9768 hydrochloride is a synthetic lethal-based inhibitor binding the PRMT5-MTA complex[1]. MRTX9768 inhibits SDMA and cell proliferation in HCT116 MTAP-del cells (SDMA IC50 3 nM; prolif. IC50 11 nM) with marked selectivity over HCT116 MTAP-WT cells (SDMA IC50 544 nM; prolif. IC50 861 nM)[1].MRTX9768 selectively targets MTAP CDKN2A-deleted tumors[2][1]. In xenograft studies, oral administration of MRTX9768 demonstrates dose-dependent inhibition of SDMA in MTAP-del tumors, with less SDMA modulation observed in bone marrow[1]. [1]. Christopher R. Smith, et al. Abstract LB003: Fragment based discovery of MRTX9768, a synthetic lethal-based inhibitor designed to bind the PRMT5-MTA complex and selectively target MTAP CDKN2A-deleted tumors. AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA.[2]. Yingqing Chen, et al. Targeting protein arginine methyltransferase 5 in cancers: Roles, inhibitors and mechanisms. Biomed Pharmacother. 2021 Oct 4;144:112252.
NG,NG-dimethyl-L-arginine-d6 (ADMA-d6) (hydrochloride) is intended for use as an internal standard for the quantification of NG,NG-dimethyl-L-arginine by GC- or LC-MS. ADMA is an endogenous inhibitor of nitric oxide synthase (NOS). It is formed from arginine by protein arginine methyltransferases (PRMTs) and degraded by dimethylarginine dimethylaminohydrolases (DDAHs) and alanine-glyoxylate aminotransferase 2 (AGXT2). ADMA levels are increased concomitant with an increase in blood pressure in Dahl salt-sensitive rats fed a high-salt diet. ADMA levels are increased in the plasma in a variety of endothelial dysfunction-related diseases, including hypertension, congestive heart failure, and end-stage renal disease.