L-NAME hydrochloride inhibits NOS with an IC₅₀ of 70 μM. L-NAME is a precursor to NOS inhibitor L-NOARG which has an IC₅₀ value of 1.4 μM.

L-arginine analogues are widely used inhibitors of nitric oxide synthase (NOS) activity, with N^w-nitro-L-arginine methyl ester (L-NAME) being at the head. Freshly dissolved L-NAME is a 50 fold less potent inhibitor of purified brain NOS (mean IC₅₀= 70 μM) than L-NOARG (IC₅₀= 1.4 μM), but the apparent inhibitory potency of L-NAME approached that of L-NOARG upon prolonged incubation at neutral or alkaline pH. HPLC analyses reveal that NOS inhibition by L-NAME closely correlated with hydrolysis of the drug to L-NOARG.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

L-NAME infusion significantly decreases NKT-leukocyte level, tumor-necrosis factor (TNF)-alpha production by T-splenocytes and macrophages, and IFNγ production by T-leukocytes, monocytes, and T-splenocytes, as well as increased interleukin-6 production by T-leukocytes and monocytes and nitrate/nitrite production by T-leukocytes. There is increasing evidence that nitric oxide may be involved in learning and memory. l-NAME produces a task-dependent impairment of fear extinction, and implies that nitric oxide signaling is involved in memory process of certain fear extinction tasks^[4]. Chronic L-NAME administration induces cardiac hypertrophy in rodent models. Six weeks L-NAME administration induces significant cardiac hypertrophy compared to control hearts^[5].

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

L-NAME infusion significantly decreases NKT-leukocyte level, tumor-necrosis factor (TNF)-alpha production by T-splenocytes and macrophages, and IFNγ production by T-leukocytes, monocytes, and T-splenocytes, as well as increased interleukin-6 production by T-leukocytes and monocytes and nitrate/nitrite production by T-leukocytes. There is increasing evidence that nitric oxide may be involved in learning and memory. l-NAME produces a task-dependent impairment of fear extinction, and implies that nitric oxide signaling is involved in memory process of certain fear extinction tasks^[4]. Chronic L-NAME administration induces cardiac hypertrophy in rodent models. Six weeks L-NAME administration induces significant cardiac hypertrophy compared to control hearts^[5].

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

• . Pfeiffer S, et al. Inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME): requirement forbioactivation to the free acid, NG-nitro-L-arginine. Br J Pharmacol. 1996 Jul;118(6):1433-40.  [Content Brief]

  . Kopincová J, et al. L-NAME in the cardiovascular system - nitric oxide synthase activator? Pharmacol Rep. 2012;64(3):511-20.  [Content Brief]

  . Lo HC, et al. The Nitric Oxide Synthase Inhibitor NG-Nitro-L-Arginine Methyl Ester Diminishes the Immunomodulatory Effects of Parental Arginine in Rats with Subacute Peritonitis. PLoSOne. 2016 Mar 23;11(3):e0151973.  [Content Brief]

  [4]. Luo H, et al. Effect of nitric oxide synthase inhibitor L-NAME on fear extinction in rats: a task-dependent effect. Neurosci Lett. 2014 Jun 20;572:13-8.  [Content Brief]

  [5]. Ocsan RJ, et al. Chronic NG-nitro-l-arginine methyl ester (L-NAME) administration in C57BL/6J mice induces a sustained decrease in c-kit positive cells during development of cardiac hypertrophy. J Physiol Pharmacol. 2013 Dec;64(6):727-36.  [Content Brief]