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  4. Norepinephrine tartrate

Norepinephrine tartrate  (Synonyms: Levarterenol tartrate; L-Noradrenaline tartrate)

Cat. No.: HY-13715C Purity: 99.45%
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Norepinephrine (Levarterenol; L-Noradrenaline) tartrate is a potent adrenergic receptor (AR) agonist. Norepinephrine tartrate activates α1, α2, β1 receptors.

For research use only. We do not sell to patients.

Norepinephrine tartrate Chemical Structure

Norepinephrine tartrate Chemical Structure

CAS No. : 51-40-1

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Based on 32 publication(s) in Google Scholar

Other Forms of Norepinephrine tartrate:

Top Publications Citing Use of Products

30 Publications Citing Use of MCE Norepinephrine tartrate

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WB

    Norepinephrine tartrate purchased from MedChemExpress. Usage Cited in: Cardiovasc Res. 2018 Feb 1;114(2):300-311.  [Abstract]

    Knockdown of GATA4 ameliorated morphology and functional changes in a Meox1 cell line with NE stimulation. Immunodetection of actin in HL-1 cells. Actin staining appeared green, and sections are counterstained blue with DAPI (40,6-diamidino-2-phenylindole).

    Norepinephrine tartrate purchased from MedChemExpress. Usage Cited in: J Nutr Biochem. 2018 May 1;58:110-118.  [Abstract]

    PASMCs are pretreated with or not Norepinephrine (50 μM) or ICI 118,551 (5 nM), and α-SMA (D) are analyzed.

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    Description

    Norepinephrine (Levarterenol; L-Noradrenaline) tartrate is a potent adrenergic receptor (AR) agonist. Norepinephrine tartrate activates α1, α2, β1 receptors[1][2][3][4].

    IC50 & Target[1]

    α1-adrenergic receptor

     

    α2-adrenergic receptor

     

    Beta-1 adrenergic receptor

     

    Microbial Metabolite

     

    Human Endogenous Metabolite

     

    In Vitro

    Norepinephrine (Levarterenol; L-Noradrenaline) tartrate is generally considered to be a β1-subtype selective adrenergic agonist over β2-adrenoceptor. Norepinephrine(NE) tartrate 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].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    RT-PCR[2]

    Cell Line: Subcutaneous preadipocytes Adipocytes.
    Concentration: 10 μM.
    Incubation Time: 6 hours.
    Result: AT2 activation suppressed Norepinephrine induced UCP1 in white adipocytes (iWA)
    In Vivo

    Induction of cardiomyopathy[5][6]

    Background
    Norepinephrine is a potent growth factor for cardiomyocytes, and long-term infusion of sub-hypertensive doses of Norepinephrine in animals can cause an increase in myocardial mass and left ventricular wall thickness. Norepinephrine activates the raf-1 kinase/MAP kinase cascade through α1 and β-adrenergic stimulation, and the signaling pathways from these two receptors work synergistically to induce cardiomyocyte hypertrophy.
    Specific Mmodeling Methods
    Rat: Spragues-Dawley rats • adult (6 months old) • Male &bull.
    Administration: Each rat was continuously injected with 100 μg/kg/h (Norepinephrine; HY-13715) or 200 μg/kg/h (Norepinephrine; HY-13715) through an osmotic minipump.
    Note
    Modeling Record
    Molecular changes: Significantly increased Dnmt activity and the expressions of Dnmt1, 3a, and 3b in the left ventricle.
    Significantly increased the mRNA expressions of fetal genes ANP, BNP, and βMHC in the left ventricle.
    Significantly increased ROS production in the left ventricle and increased global genomic DNA methylation and gene-specific CpG methylation at the Egr-1 binding site of the left ventricular PKCε promoter region in a concentration-dependent manner.
    Increased lactate dehydrogenase release in a concentration-dependent manner.
    Significantly reduced the left ventricular developed pressure and dP/dtmax, inducing the upregulation of myotrophin and downregulation of four-and-a-half LIM domains protein 2 (FHL2).
    Phenotype observations: Increased the myocardial infarction area and sustained the elevation of blood pressure.
    Induced cardiac hypertrophy and reduced cardiac contractility.
    Increased the left ventricular weight.
    Correlated Product(s): 5-Aza-2’-deoxycytidine (HY-A0004), Prazosin (HY-B0193), Propranolol (HY-B0573B)

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Clinical Trial
    Molecular Weight

    319.26

    Formula

    C12H17NO9

    CAS No.
    Appearance

    Solid

    Color

    White to off-white

    SMILES

    OC1=CC=C([C@@H](O)CN)C=C1O.OC([C@H](O)[C@@H](O)C(O)=O)=O

    Structure Classification
    Initial Source
    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

    4°C, protect from light, stored under nitrogen

    *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)

    Purity & Documentation
    References
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    • Do most proteins show cross-species activity?

      Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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    Product Name:
    Norepinephrine tartrate
    Cat. No.:
    HY-13715C
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