Norepinephrine (hydrochloride)


CAS No. : 329-56-6

(Synonyms: Levarterenol (hydrochloride); L-Noradrenaline (hydrochloride))

329-56-6
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Cat. No. : HY-13715A
M.Wt: 205.64
Formula: C8H12ClNO3
Purity: >98 %
Solubility: DMSO : 50 mg/mL (ultrasonic);H2O : 100 mg/mL (ultrasonic)
Introduction of 329-56-6 :

Norepinephrine (Levarterenol; L-Noradrenaline) hydrochloride is a potent adrenergic receptor (AR) agonist. Norepinephrine activates α1, α2, β1 receptors[1][2][3][4]. In Vitro:Norepinephrine (Levarterenol; L-Noradrenaline) hydrochloride is generally considered to be a β1-subtype selective adrenergic agonist over β2-adrenoceptor. Norepinephrine(NE) hydrochloride also has direct activity at the β2-adrenoceptor in higher concentrations[2].
Adipocytes from the inguinal fat pad (iWA) or the interscapular fat pad (BA) are isolated from neonatal wild-type C57BL/6J mice and cultured. To examine the effect of activating AT2 upon β-adrenergic signaling, cAMP production is first assessed in response to Norepinephrine (NE, 10 μM) with or without CGP (10 nM) co-treatment.
Norepinephrine (NE) increases cAMP as expected in iWA, and CGP does not alter this effect
Norepinephrine (NE) is also known to induce lipolysis, and liberated fatty acids are required to functionally activate UCP1 protein and to stimulate heat production. CREB phosphorylation at Ser133 is increased after Norepinephrine (NE) treatment and significantly attenuated with CGP co-treatment in mouse iWA[3]. 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.

Norepinephrine hydrochloride can be used to induce cardiomyopathy[5][6]
Induced Cardiomyopathy Model[5][6]
Background
Norepinephrine hydrochloride is a potent growth factor for cardiomyocytes. Long-term infusion of subhyperbaric doses of Norepinephrine hydrochloride in animals can cause increases in myocardial mass and left ventricular wall thickness. Norepinephrine hydrochloride activates the Raf-1 kinase/MAP kinase cascade through α1- and β-adrenergic stimulation, and signaling pathways from both receptors synergistically induce cardiomyocyte hypertrophy.
Specific Modeling Methods
Rat: Spragues-Dawley rats • adult (6 months old) • male Administration: Continuously injected via an osmotic minipump • 100 μg/kg/h or 200 μg/kg/h (Norepinephrine)
Modeling Indicators
Molecular changes: Left ventricular Dnmt activity ↑; ROS generation ↑; lactate dehydrogenase release ↑; dystrophin expression ↑; FHL2 protein expression ↓
Gene Expression: Expression of Dnmt1, 3a, and 3b ↑; mRNA expression of fetal genes ANP, BNP, and βMHC in left ventricle ↑
Phenotypic observation: Myocardial infarction area ↑; blood pressure continues to rise; left ventricular mass ↑; left ventricular development pressure ↓; cardiac contractility ↓. Cardiac hypertrophy.
Opposite Product(s): 5-Aza-2’-deoxycytidine (HY-A0004), Prazosin (HY-B0193), Propranolol (HY-B0573B)

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