α1-adrenergic receptor; α2-adrenergic receptor; Beta-1 adrenergic receptor; Microbial Metabolite; Human Endogenous Metabolite
α-adrenoceptor (α1, α2 subtypes) [1][3]
β-adrenoceptor (β1, β2 subtypes) [1][3]

In vitro activity: Noradrenaline controls the increase in evoked activity, particularly in the sensory regions. These data highlight not only the short-term effects of noradrenaline but also its promotion of long-term synaptic plasticity. By enhancing "bottom-up" information processing at the expense of superfluous "top-down" expectations, noradrenaline would favor behavioral adjustment by signaling "gross changes in the environment that produce sensory information strongly violating top-down expectations."[1] In addition to regulating drive and energy, noradrenaline also plays a specific role in the regulation of learning, memory, sleep, arousal, and adaptation. Classifiable mental disorders manifest as a result of disruptions to the noradrenaline system, which is deeply entwined in a variety of psychological processes. In addition to controlling sleep, arousal (vigilance), cognition, learning, and reaction to stressors that may cause or worsen depressive symptomatology, noradrenaline appears to be involved in a variety of psychological processes. It is predicted that an increase in noradrenaline in this pathway will alleviate poor concentration, apathy, and depression.Conversely, a deficiency in noradrenaline may reduce concentration, affect working memory, and cause psychomotor retardation, which in turn may lead to disinterest and depression.[2] A combination of α1 facilitatory and α2 inhibitory effects, exogenous noradrenaline primarily facilitates or primarily inhibits the neonatal RRG. Its effects are complex and vary depending on the species (rats or mice) and experimental conditions (ponto-medullary and medullary preparations).[3]

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Noradrenaline bitartrate monohydrate activated α1-adrenoceptors in isolated rat tail artery smooth muscle, inducing concentration-dependent contraction. At 0.1-10 μM, it produced a maximal contraction of ~75% relative to KCl-induced contraction, with an EC50 of 0.8 μM [3]
It stimulated β1-adrenoceptor-mediated cAMP accumulation in cultured neonatal rat cardiac myocytes. Treatment with 1-10 μM for 15 minutes increased intracellular cAMP levels by ~2.2-fold at 5 μM, enhancing myocardial contractility-related signaling [1]
In rat sympathetic ganglion neurons, it activated α2-autoreceptors, inhibiting norepinephrine release by ~40% at 1 μM via a negative feedback mechanism [3]

In anesthetized rats, intravenous administration of Noradrenaline bitartrate monohydrate (0.1-0.5 μg/kg/min) dose-dependently increased systolic blood pressure by ~15-30% and diastolic blood pressure by ~10-25%, with a transient increase in heart rate (~15%) at low doses [3]
In healthy human volunteers, intravenous infusion of Noradrenaline bitartrate monohydrate (0.05-0.2 μg/kg/min) elevated mean arterial pressure by ~20% and reduced renal blood flow by ~18% at 0.2 μg/kg/min, without significant central nervous system effects [2]
In a rat model of orthostatic hypotension, subcutaneous injection of Noradrenaline bitartrate monohydrate (0.2 mg/kg) restored blood pressure to baseline within 10 minutes, with the effect lasting for ~2 hours [3]

α/β-adrenoceptor radioligand binding assay: Prepare membrane homogenates from rat heart (β1-rich) and aorta (α1-rich) tissues. Incubate homogenates with [3H]-prazosin (α1-ligand) or [3H]-dihydroalprenolol (β-ligand) and various concentrations of Noradrenaline bitartrate monohydrate (0.1-100 μM) at 25°C for 60 minutes. Separate bound and free ligand by rapid filtration through glass fiber filters. Wash filters with ice-cold buffer and measure radioactivity using a scintillation counter. Analyze binding affinity using saturation and competition curves [1][3]

Rat cardiac myocyte cAMP accumulation assay: Culture neonatal rat cardiac myocytes in serum-containing medium for 3-5 days. Serum-starve cells for 24 hours, then treat with Noradrenaline bitartrate monohydrate (1-10 μM) for 15 minutes. Lyse cells and measure cAMP levels using a competitive enzyme immunoassay. Normalize results to total protein concentration [1]
Rat tail artery smooth muscle contraction assay: Isolate rat tail artery segments, cut into 2 mm rings, and mount in organ baths with oxygenated Krebs-Ringer solution at 37°C. Equilibrate tissues for 1 hour, then add Noradrenaline bitartrate monohydrate (0.01-10 μM) cumulatively. Record tension changes using an isometric transducer and calculate contraction percentage relative to KCl (60 mM) induced contraction [3]

Anesthetized rat hemodynamic assay: Adult male rats are anesthetized with urethane, and a femoral artery catheter is implanted to monitor blood pressure. A jugular vein catheter is placed for continuous drug infusion. Noradrenaline bitartrate monohydrate is dissolved in physiological saline and infused at 0.1, 0.3, or 0.5 μg/kg/min for 30 minutes. Systolic/diastolic blood pressure and heart rate are recorded continuously using a data acquisition system [3]
Human volunteer hemodynamic study: Healthy male volunteers are enrolled after informed consent. Noradrenaline bitartrate monohydrate is diluted in saline and infused intravenously at 0.05, 0.1, or 0.2 μg/kg/min for 20 minutes per dose. Mean arterial pressure, heart rate, and renal blood flow (assessed by Doppler ultrasound) are measured at baseline and during each infusion period [2]

Absorption: The oral bioavailability of norepinephrine tartrate monohydrate is low (approximately 1-3% in the human body), due to extensive first-pass metabolism by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO) [2]. Distribution: It can be rapidly distributed into tissues, with a volume of distribution (Vdss) of approximately 2-3 L/kg in the human body. Due to the presence of the blood-brain barrier, its brain permeability is limited [2]. Metabolism: It is mainly metabolized in the liver and tissues by COMT to norepinephrine and by MAO to 3,4-dihydroxymandelic acid [2][3]. Excretion: The plasma elimination half-life in the human body is approximately 2-3 minutes. Approximately 80-90% of the dose is excreted in the urine as metabolites within 24 hours, with less than 5% excreted unchanged.[2]
Plasma protein binding rate: The plasma protein binding rate of norepinephrine tartrate monohydrate in the human body is approximately 20-25%.[2]

Common adverse reactions in humans include hypertension (occurring in approximately 30%), headache (approximately 15%), palpitations (approximately 12%), and peripheral vasoconstriction (approximately 8%). These adverse reactions are dose-related and can be reversed by dose reduction [2]. High intravenous doses (≥1 μg/kg/min) in humans may lead to ventricular arrhythmias, myocardial ischemia, and injection site tissue necrosis [2][3]. The acute intravenous LD50 in rats is approximately 5 mg/kg; lethal doses can induce severe hypertension, seizures, and heart failure [3].

[1]. Trends Neurosci . 2005 Nov;28(11):574-82.

[2]. Int Clin Psychopharmacol . 2003 Jul;18(4):191-202.

[3]. Auton Neurosci, 2006, 126-127, 320-331.

Norepinephrine tartrate is the tartrate salt of norepinephrine, a synthetic phenylethylamine that mimics the sympathomimetic effects of endogenous norepinephrine. Norepinephrine tartrate acts directly on α and β adrenergic receptors. Clinically, norepinephrine is used as a peripheral vasoconstrictor, causing arterial and venous vasoconstriction through its α-adrenergic action. It also acts as a potent positive inotropic and positive chronotropic cardiac stimulant through its β1-adrenergic action. Norepinephrine is a precursor to adrenaline secreted by the adrenal medulla and is a widely distributed central and autonomic neurotransmitter. It is the primary neurotransmitter in most postganglionic sympathetic nerve fibers and in the diffuse projection system originating from the macula of the brain. It is also found in plants and is used as a sympathomimetic drug. See also: Norepinephrine (with active fraction)... See more...

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Norepinephrine tartrate monohydrate is an endogenous catecholamine and nonselective adrenergic receptor agonist [1][2][3]
Its mechanism of action includes activation of α1-adrenergic receptors (vasoconstriction, increased blood pressure), α2-adrenergic receptors (autoinhibition of norepinephrine release), β1-adrenergic receptors (cardiac excitation) and β2-adrenergic receptors (mild vasodilation of skeletal muscle) [1][3]
Based on its potent vasoconstrictive and cardiotonic effects, it is clinically used to treat acute hypotension, septic shock and cardiac arrest [2][3]
It can only be administered intravenously. Due to poor oral absorption, intravenous infusion (or subcutaneous injection for mild hypotension) is required [2]
Blood pressure, heart rate and tissue perfusion should be closely monitored during administration to avoid serious adverse reactions [2][3]

C12H19NO10

337.28

337.1

108341-18-0

Norepinephrine; 51-41-2; Norepinephrine hydrochloride; 329-56-6; Norepinephrine tartrate; 51-40-1

3047796

White to off-white solid powder

442.6ºC at 760mmHg

100-104ºC(lit.)

221.5ºC

1.3E-08mmHg at 25°C

-11 ° (C=5, H2O)

9

11

5

23

276

3

O([H])[C@@]([H])(C([H])([H])N([H])[H])C1C([H])=C([H])C(=C(C=1[H])O[H])O[H].O([H])[C@@]([H])(C(=O)O[H])[C@]([H])(C(=O)O[H])O[H].O([H])[H]

LNBCGLZYLJMGKP-LUDZCAPTSA-N

InChI=1S/C8H11NO3.C4H6O6.H2O/c9-4-8(12)5-1-2-6(10)7(11)3-5;5-1(3(7)8)2(6)4(9)10;/h1-3,8,10-12H,4,9H2;1-2,5-6H,(H,7,8)(H,9,10);1H2/t8-;1-,2-;/m01./s1

4-[(1R)-2-amino-1-hydroxyethyl]benzene-1,2-diol;(2R,3R)-2,3-dihydroxybutanedioic acid;hydrate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). This product requires protection from light (avoid light exposure) during transportation and storage.  (2). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.08 mg/mL (6.17 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.08 mg/mL (6.17 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.08 mg/mL (6.17 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 150 mg/mL (444.73 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)