NADPH tetrasodium salt - CAS 2646-71-1
Catalog number: B0084-293179
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
NADPH tetrasodium salt is an ubiquitous coenzyme that acts as an electron donor in various biological reactions.
Nutritional supplement in health care products.
Ordering Information
Catalog Number Size Price Stock Quantity
B0084-293179 250 mg $199 In stock
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Solid powder
Soluble to 50 mg/ml in H2O
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -140℃ for long term (months to years).
Ingredient of health care products.
Shelf Life:
2 years
Data not available, please inquire.
Boiling Point:
1175.1ºC at 760 mmHg
Melting Point:
>250ºC (dec.)
2.28 g/cm3
Canonical SMILES:
1.Administration of L-arginine plus L-citrulline or L-citrulline alone successfully retarded endothelial senescence.
Tsuboi T;Maeda M;Hayashi T PLoS One. 2018 Feb 7;13(2):e0192252. doi: 10.1371/journal.pone.0192252. eCollection 2018.
L-citrulline and L-arginine supplementation has been shown to have several beneficial effects on the cardiovascular system. Nitric oxide (NO) protects against the progression of atherosclerosis and is synthesized by nitric oxide synthase (NOS), which converts L-arginine (L-Arg) into L-citrulline (L-Cit). Our previous study revealed that chronic administration of a combination of L-Cit and L- Arg has a better therapeutic effect on high cholesterol-induced atherosclerosis in rabbits. We investigated how L-Arg and L-Cit affect endothelial function, aging and atherosclerosis. Following a 3-day stimulation of human umbilical venous endothelial cells (HUVECs) with high glucose (HG: 22 mM) and L-Arg (300 μM), L-Cit (300 μM) or L-Arg plus L-Cit (LALC: each 150 μM) supplementation, endothelial senescence and function were evaluated. These amino acids were also administered to dyslipidemic type 2 diabetic (ZDFM) rats fed a high cholesterol diet. They were fed L-Arg or L-Cit or LALC for four weeks. Aortic senescence was investigated by measuring senescence-associated ß-galactosidase (SA-ß-gal), telomerase activity, DNA damage and p16INK4a protein expression. Only L-Cit and LALC supplementation retarded the HG-induced endothelial senescence, as evaluated by SA-ß-gal activity, a widely used marker of cellular senescence, p16INK4a expression, a senescence-related protein, and DNA damage.
2.Structural basis for the electron transfer from an open form of NADPH-cytochrome P450 oxidoreductase to heme oxygenase.
Sugishima M;Sato H;Higashimoto Y;Harada J;Wada K;Fukuyama K;Noguchi M Proc Natl Acad Sci U S A. 2014 Feb 18;111(7):2524-9. doi: 10.1073/pnas.1322034111. Epub 2014 Feb 3.
NADPH-cytochrome P450 oxidoreductase (CPR) supplies electrons to various heme proteins including heme oxygenase (HO), which is a key enzyme for heme degradation. Electrons from NADPH flow first to flavin adenine dinucleotide, then to flavin mononucleotide (FMN), and finally to heme in the redox partner. For electron transfer from CPR to its redox partner, the ''closed-open transition'' of CPR is indispensable. Here, we demonstrate that a hinge-shortened CPR variant, which favors an open conformation, makes a stable complex with heme-HO-1 and can support the HO reaction, although its efficiency is extremely limited. Furthermore, we determined the crystal structure of the CPR variant in complex with heme-HO-1 at 4.3-Å resolution. The crystal structure of a complex of CPR and its redox partner was previously unidentified. The distance between heme and FMN in this complex (6 Å) implies direct electron transfer from FMN to heme.
3.Pulmonary surfactant protein a inhibits macrophage reactive oxygen intermediate production in response to stimuli by reducing NADPH oxidase activity.
Crowther JE;Kutala VK;Kuppusamy P;Ferguson JS;Beharka AA;Zweier JL;McCormack FX;Schlesinger LS J Immunol. 2004 Jun 1;172(11):6866-74.
Alveolar macrophages are important host defense cells in the human lung that continuously phagocytose environmental and infectious particles that invade the alveolar space. Alveolar macrophages are prototypical alternatively activated macrophages, with up-regulated innate immune receptor expression, down-regulated costimulatory molecule expression, and limited production of reactive oxygen intermediates (ROI) in response to stimuli. Surfactant protein A (SP-A) is an abundant protein in pulmonary surfactant that has been shown to alter several macrophage (Mphi) immune functions. Data regarding SP-A effects on ROI production are contradictory, and lacking with regard to human Mphi. In this study, we examined the effects of SP-A on the oxidative response of human Mphi to particulate and soluble stimuli using fluorescent and biochemical assays, as well as electron paramagnetic resonance spectroscopy. SP-A significantly reduced Mphi superoxide production in response to the phorbol ester PMA and to serum-opsonized zymosan (OpZy), independent of any effect by SP-A on zymosan phagocytosis. SP-A was not found to scavenge superoxide. We measured Mphi oxygen consumption in response to stimuli using a new oxygen-sensitive electron paramagnetic resonance probe to determine the effects of SP-A on NADPH oxidase activity.
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CAS 2646-71-1 NADPH tetrasodium salt

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