Molecular Weight(MW): 269.69
L-NAME is a nonselective inhibitor of nitric oxide synthetases (NOS) for nNOS (bovine), eNOS (human), and iNOS (murine), with Ki of 15 nM, 39 nM and 4.4 μM, respectively.
Cited by 11 Publications
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(C) HOSS1 cells were grown in soft agar, in the presence or absence of L-NAME (10 mM), and treated as indicated with drugs, as indicated, for 6 h and 12 h. Cells were subjected to electrophoresis and stained. The tail moments of cells were measured and presented below each image (n = 4, ± SEM) *P < 0.05 less than corresponding value in vehicle-treated cells.
Cancer Biol Ther, 2014, 15(6):758-67. . L-NAME HCl purchased from Selleck.
(E) Western blot analysis of p-eNOS expression after 1 mM metformin and/or 1 mM l-NAME treatment (n = 3). (F) NO production measurement via Griess method after 1 mM metformin and/or 1 mM l-NAME treatment (n = 3). (G,H) Q-PCR analysis of vWF and CD31 expression after 1 mM metformin and/or 1 mM l-NAME treatment (n = 3). **p < 0.01 when comparison was performed between groups, ***p < 0.001 between groups.
Biochem Biophys Res Commun, 2015, 465(4):803-9. . L-NAME HCl purchased from Selleck.
(B) NO levels in cucumber leaves under normal conditions. L, L-NAME; N, NaN3; C, wild type and H2O was used as a control. The mean values of three independent samples and standard errors are shown, and the same letter above the column indicates no significant differences at P < 0.05.
Front Plant Sci, 2016, 7:1652.. L-NAME HCl purchased from Selleck.
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Choose Selective NOS Inhibitors
|Description||L-NAME is a nonselective inhibitor of nitric oxide synthetases (NOS) for nNOS (bovine), eNOS (human), and iNOS (murine), with Ki of 15 nM, 39 nM and 4.4 μM, respectively.|
NG-nitro-L-arginine methyl ester (L-NAME; at 0.1-100 mM) causes concentration-dependent inhibition of the Ca2(+)-dependent endothelial NO synthase from porcine aortae. L-NAME causes an endothelium-dependent contraction and an inhibition of the endothelium-dependent relaxation induced by acetylcholine (ACh) in aortic rings.  In another research, Viability of rMC-1 cells or BREC in 25 mM glucose is significantly less than at 5 mM glucose, and this cell death is inhibited by l-NAME in both cell types. 
|In vivo||L-NAME (0.03-300 mg kg-1, i.v.) induces a dose-dependent increase in mean systemic arterial blood pressure accompanied by bradycardia. L-NAME (100 mg kg-1, i.v.) inhibits significantly the hypotensive responses to ACh and bradykinin. The increase in blood pressure and bradycardia produced by L-NAME is reversed by L-arginine (30-100 mg kg-1, i.v.) in a dose-dependent manner. |
Enzyme Assay:The oxidation of L-arginine is monitored by the conversion of [3H]- or [14C]-arginine to L-citrulline which separates L-citrulline from L-arginine by Dowex 50x8-200 (Na) chromatography. Typical reaction mixtures (100 pL) contains 50 mM HEPES, pH 7.0, 8 pM tetrahydrobiopterin, 1 mM CaC12, 0.01 mg/mL calmodulin, 0.5 mM EDTA, 0.450 pM [14C]-arginine (30000 cpm), and 100-200 pM NADPH. The cNOS-catalyzed oxidation of NADPH to NADP+ is monitored by the reduction of absorbance at 340 nm with a Kontron 860 spectrophotometer in a volume of 300 pL. All reactions are at 30 ℃ unless otherwise indicated.
|In vitro||Water||54 mg/mL (200.22 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
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