NG,NG-Dimethylarginine dihydrochloride

NG,NG-Dimethylarginine dihydrochloride
Product Name NG,NG-Dimethylarginine dihydrochloride
CAS No.: 220805-22-1
Catalog No.: CFN90056
Molecular Formula: C8H20Cl2N4O2
Molecular Weight: 275.18 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Targets: NO
Source:
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price:
NG,NG-Dimethylarginine dihydrochloride is a reversible inhibitor of nitric oxide synthetase in vivo and in vitro.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    NG,NG-Dimethylarginine dihydrochloride

    Catalog No: CFN90056
    CAS No: 220805-22-1
    Price: Inquiry(manager@chemfaces.com)
    Lancet. 1992 Mar 7;339(8793):572-5.
    Accumulation of an endogenous inhibitor of nitric oxide synthesis in chronic renal failure.[Pubmed: 1347093]
    Nitric oxide (NO), synthesised from L-arginine, contributes to the regulation of blood pressure and to host defence.
    METHODS AND RESULTS:
    We describe in-vitro and in-vivo evidence that NO synthesis can be inhibited by an endogenous compound, NG,NG-dimethylarginine (asymmetrical dimethylarginine, ADMA). In man, this inhibitor is found in plasma and more than 10 mg is excreted in urine over 24 h. However, in patients with end-stage chronic renal failure, who have little or no urine output, elimination is blocked and circulating concentrations of the inhibitor rise sufficiently to inhibit NO synthesis.
    CONCLUSIONS:
    Accumulation of endogenous ADMA, leading to impaired NO synthesis, might contribute to the hypertension and immune dysfunction associated with chronic renal failure.
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