Details
| Stereochemistry | ABSOLUTE |
| Molecular Formula | C21H26N7O17P3.Na.H |
| Molecular Weight | 765.3868 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 8 / 8 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
[H+].[Na+].NC(=O)C1=C[N+](=CC=C1)[C@@H]2O[C@H](COP([O-])(=O)OP([O-])(=O)OC[C@H]3O[C@H]([C@H](OP(O)([O-])=O)[C@@H]3O)N4C=NC5=C4N=CN=C5N)[C@@H](O)[C@H]2O
InChI
InChIKey=JNUMDLCHLVUHFS-QYZPTAICSA-M
InChI=1S/C21H28N7O17P3.Na/c22-17-12-19(25-7-24-17)28(8-26-12)21-16(44-46(33,34)35)14(30)11(43-21)6-41-48(38,39)45-47(36,37)40-5-10-13(29)15(31)20(42-10)27-3-1-2-9(4-27)18(23)32;/h1-4,7-8,10-11,13-16,20-21,29-31H,5-6H2,(H7-,22,23,24,25,32,33,34,35,36,37,38,39);/q;+1/p-1/t10-,11-,13-,14-,15-,16-,20-,21-;/m1./s1
| Molecular Formula | C21H26N7O17P3 |
| Molecular Weight | 741.3891 |
| Charge | -2 |
| Count |
|
| Stereochemistry | ABSOLUTE |
| Additional Stereochemistry | No |
| Defined Stereocenters | 8 / 8 |
| E/Z Centers | 0 |
| Optical Activity | UNSPECIFIED |
| Molecular Formula | Na |
| Molecular Weight | 22.9898 |
| Charge | 1 |
| Count |
|
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
| Molecular Formula | H |
| Molecular Weight | 1.0079 |
| Charge | 1 |
| Count |
|
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
NADIDE (NAD+) is a coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. NADIDE was marketed under the brand name Enada. Although Enada (NADH) is marketed as a nutritional supplement, Birkmayer
Pharmaceuticals has launched two clinical trials to prove scientifically that Enada is effective.
Before these studies could get started they had to also prove to the Food and Drug Administration (FDA) that the stable oral form of Enada (NADH) is a safe substance.
Since the mid-‘80s more than 3,000 parkinsonian patients have received NADH, either as
intravenous infusion or in the form of oral tablets. Enada (NADH) is the world‘s first and only stabilized, absorbable, patented, tablet-form
NADH dietary supplement. It is now available to everyone whose lifestyle demands increased
energy, vitality and mental clarity. In other words, it is beneficial not only for patients
suffering from chronic fatigue syndrome, Alzheimer‘s disease, depression or Parkinson‘s
disease, but for any normal, healthy individual whose lifestyle demands more energy. NADIDE (NADH) may be considered as a therapeutic adjunct for
cancer patients to protect them against the general toxic effects of substances such as
doxorubicin or cisplatin by stimulating the DNA repair system and by promoting normal cellular
biosynthetic responses after chemotherapy. NADH seems to exhibit a chemo preventive effect.
Approval Year
PubMed
| Title | Date | PubMed |
|---|---|---|
| [The effect of guanosyl-5'-monophosphate on metabolic processes in rats with experimental myocarditis]. | 1990 Sep-Oct |
|
| L-lactate dehydrogenase A4- and A3B isoforms are bona fide peroxisomal enzymes in rat liver. Evidence for involvement in intraperoxisomal NADH reoxidation. | 1996 Feb 16 |
|
| Flavins inhibit human cytomegalovirus UL80 protease via disulfide bond formation. | 1996 May 7 |
|
| Metabolism of retinaldehyde and other aldehydes in soluble extracts of human liver and kidney. | 1999 Nov 19 |
|
| Inactivation of aldophosphamide by human aldehyde dehydrogenase isozyme 3. | 2000 Aug 1 |
|
| Intrinsic alcohol dehydrogenase and hydroxysteroid dehydrogenase activities of human mitochondrial short-chain L-3-hydroxyacyl-CoA dehydrogenase. | 2000 Jan 1 |
|
| Ca(2+)-calmodulin antagonist chlorpromazine and poly(ADP-ribose) polymerase modulators 4-aminobenzamide and nicotinamide influence hepatic expression of BCL-XL and P53 and protect against acetaminophen-induced programmed and unprogrammed cell death in mice. | 2001 Aug 1 |
|
| Oxidative stress, metabolism of ethanol and alcohol-related diseases. | 2001 Jan-Feb |
|
| Poly(ADP-ribose) glycohydrolase mediates oxidative and excitotoxic neuronal death. | 2001 Oct 9 |
|
| Reactive oxygen species alter gene expression in podocytes: induction of granulocyte macrophage-colony-stimulating factor. | 2002 Jan |
|
| A candidate NAD+ transporter in an intracellular bacterial symbiont related to Chlamydiae. | 2004 Dec 2 |
|
| A new crystal structure of deoxyhypusine synthase reveals the configuration of the active enzyme and of an enzyme.NAD.inhibitor ternary complex. | 2004 Jul 2 |
|
| Acute ammonia intoxication induces an NMDA receptor-mediated increase in poly(ADP-ribose) polymerase level and NAD metabolism in nuclei of rat brain cells. | 2004 Jun |
|
| Human SirT1 interacts with histone H1 and promotes formation of facultative heterochromatin. | 2004 Oct 8 |
|
| Synthesis and antiviral evaluation of cis-substituted cyclohexenyl and cyclohexanyl nucleosides. | 2005 Jan 27 |
|
| Polymorphisms in the mitochondrial aldehyde dehydrogenase gene (Aldh2) determine peak blood acetaldehyde levels and voluntary ethanol consumption in rats. | 2005 Jun |
|
| Mechanism of sirtuin inhibition by nicotinamide: altering the NAD(+) cosubstrate specificity of a Sir2 enzyme. | 2005 Mar 18 |
|
| Nutrient control of glucose homeostasis through a complex of PGC-1alpha and SIRT1. | 2005 Mar 3 |
|
| Molecular cloning of a novel type of rat cytoplasmic 17beta-hydroxysteroid dehydrogenase distinct from the type 5 isozyme. | 2006 Jun |
|
| Extracellular NAD+ is an agonist of the human P2Y11 purinergic receptor in human granulocytes. | 2006 Oct 20 |
|
| 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces oxidative stress, DNA strand breaks, and poly(ADP-ribose) polymerase-1 activation in human breast carcinoma cell lines. | 2007 Aug |
|
| Nicotinamide prevents NAD+ depletion and protects neurons against excitotoxicity and cerebral ischemia: NAD+ consumption by SIRT1 may endanger energetically compromised neurons. | 2009 |
|
| Mechanism of thiol-supported arsenate reduction mediated by phosphorolytic-arsenolytic enzymes: I. The role of arsenolysis. | 2009 Aug |
|
| Saline-linked surface radiofrequency ablation: a safe and effective method of surface ablation of hepatic metastatic colorectal cancer. | 2009 Jul |
|
| Prevention of hepatocarcinogenesis and increased susceptibility to acetaminophen-induced liver failure in transaldolase-deficient mice by N-acetylcysteine. | 2009 Jun |
|
| Identification of the aryl hydrocarbon receptor target gene TiPARP as a mediator of suppression of hepatic gluconeogenesis by 2,3,7,8-tetrachlorodibenzo-p-dioxin and of nicotinamide as a corrective agent for this effect. | 2010 Dec 10 |
|
| Triazole-linked inhibitors of inosine monophosphate dehydrogenase from human and Mycobacterium tuberculosis. | 2010 Jun 24 |
|
| Biochemical mechanism of caffeic acid phenylethyl ester (CAPE) selective toxicity towards melanoma cell lines. | 2010 Oct 6 |
|
| Disruption of adaptive energy metabolism and elevated ribosomal p-S6K1 levels contribute to INCL pathogenesis: partial rescue by resveratrol. | 2011 Mar 15 |
|
| NADH fluorescence lifetime analysis of the effect of magnesium ions on ALDH2. | 2011 May 30 |
|
| NAD(P)H:quinone oxidoreductase 1 (NQO1) competes with 20S proteasome for binding with C/EBPα leading to its stabilization and protection against radiation-induced myeloproliferative disease. | 2012 Dec 7 |
|
| Regulation of FOXOs and p53 by SIRT1 modulators under oxidative stress. | 2013 |
|
| Resveratrol induces a mitochondrial complex I-dependent increase in NADH oxidation responsible for sirtuin activation in liver cells. | 2013 Dec 20 |
|
| Catalytic contribution of threonine 244 in human ALDH2. | 2013 Feb 25 |
|
| Biocatalytic production of alpha-hydroxy ketones and vicinal diols by yeast and human aldo-keto reductases. | 2013 Feb 25 |
|
| Ruthenium complexes as inhibitors of the aldo-keto reductases AKR1C1-1C3. | 2015 Jun 5 |
Patents
Sample Use Guides
Dosage requirements and response time vary from individual to individual. Optimal dosage
should be established individually. A daily dosage of 2.5 mg shows results in healthy people;
people with neurological disorders may require higher amounts. Enada tablets should always
be taken whole with half a glass of water only on an empty stomach, 20-30 minutes before a
meal, preferably in the morning.
Enada is available as a dietary supplement in the U.S.A. in 2.5 mg and 5 mg tablet form.
Nutritional and Energy Enhancement
2.5 to 5 mg daily or every other day depending upon individual response.
Therapeutic Treatment
10 to 15 mg daily, depending upon individual requirements and the guidance of your
physician or health-care professional.
Route of Administration:
Oral
Oochlear organotypic cultures were treated with different doses of Mn (0.5-3.0 mM) alone or combined with 20 mM NADIDE (NAD). Results demonstrate that the percentage of hair cells, auditory nerve fibers (ANF) and SGN decreased with increasing Mn concentration. The addition of 20 mM NAD did not significantly reduce hair cells loss in the presence of Mn, whereas the density of ANF and SGN increased significantly in the presence of NAD. NAD suppressed Mn-induced TUNEL staining and caspase activation suggesting it prevents apoptotic cell death.
| Substance Class |
Chemical
Created
by
admin
on
Edited
Sat Dec 16 05:00:57 GMT 2023
by
admin
on
Sat Dec 16 05:00:57 GMT 2023
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| Record UNII |
NR2O7P57YA
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| Record Status |
Validated (UNII)
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| Record Version |
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NR2O7P57YA
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2724369
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DTXSID30861580
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20273
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PARENT -> SALT/SOLVATE |
