L-NAME (hydrochloride)


CAS No. : 51298-62-5

(Synonyms: NG-Nitroarginine methyl ester hydrochloride)

51298-62-5
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Cat. No. : HY-18729A
M.Wt: 269.69
Formula: C7H16ClN5O4
Purity: >98 %
Solubility: H2O : 100 mg/mL (ultrasonic)
Introduction of 51298-62-5 :

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-NAME hydrochloride requires hydrolysis of the methyl ester by cellular esterases to become a fully functional inhibitor. L-NAME hydrochloride can be used to induce hypertension and preeclampsia models. IC50 & Target:IC50: 70 μM (NOS)[1] In Vitro:L-arginine analogues are widely used inhibitors of nitric oxide synthase (NOS) activity, with Nw-nitro-L-arginine methyl ester (L-NAME) being at the head[2]. 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[1]. In Vivo:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

L-NAME hydrochloride can be used to induce hypertension models[6].

Induction of hypertension Model[6]
Background
L-NAME hydrochloride decreases nitric oxide (NO) release with an inhibition competence in endothelial nitric oxide synthase (eNOS) in animals.
Specific Modeling Methods
Mice: Swiss Webster • male • 6-week-old
Administration: 400 mg/kg • ip • once daily for 7 days
Modeling Indicators
Body quality changes: Induced hypertension with body weight loss and high blood pressure.

2. Induction of preeclampsia[8]
Background
L-NAME induces preeclampsia by reducing the production of nitric oxide through inhibiting nitric oxide synthase, triggering a series of changes such as vasoconstriction, placental dysfunction, inflammatory response, and anti-angiogenesis.
Specific Modeling Methods
Mice: CBA x C57BL/6 pregnant female mice • 6-16 weeks old
Administration: subcutaneous injection • 50 mg/kg/day • E7.5 to E17.5
Modeling Indicators
Elevated blood pressure, impaired fetal and placental growth, and increased circulating endothelin-1 (vasoconstrictor), soluble fms-like tyrosine kinase-1 (anti-angiogenic factor), and C-reactive protein (inflammatory marker).

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