Details
Stereochemistry | ABSOLUTE |
Molecular Formula | C21H26N7O17P3.2Na |
Molecular Weight | 787.3687 |
Optical Activity | UNSPECIFIED |
Defined Stereocenters | 8 / 8 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
[Na+].[Na+].NC(=O)C1=CC=C[N+](=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=WSDDJLMGYRLUKR-WUEGHLCSSA-L
InChI=1S/C21H28N7O17P3.2Na/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;2*+1/p-2/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 |
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.
Originator
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
Target ID: CHEMBL4096 Sources: https://www.ncbi.nlm.nih.gov/pubmed/15509798 |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
---|---|---|---|---|
Primary | Enada Approved UseChronic fatigue syndrome |
|||
Primary | Unknown Approved UseUnknown |
PubMed
Title | Date | PubMed |
---|---|---|
Flavins inhibit human cytomegalovirus UL80 protease via disulfide bond formation. | 1996 May 7 |
|
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 |
|
Reactive oxygen species alter gene expression in podocytes: induction of granulocyte macrophage-colony-stimulating factor. | 2002 Jan |
|
[Effect of NADH against liver cell line L02 apoptosis induced by UVB irradiation]. | 2002 Mar |
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Crystal structures of Tritrichomonasfoetus inosine monophosphate dehydrogenase in complex with substrate, cofactor and analogs: a structural basis for the random-in ordered-out kinetic mechanism. | 2003 Feb 14 |
|
Expression profile of the transient receptor potential (TRP) family in neutrophil granulocytes: evidence for currents through long TRP channel 2 induced by ADP-ribose and NAD. | 2003 May 1 |
|
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 |
|
Competing roles of cytochrome P450 1A1/1B1 and aldo-keto reductase 1A1 in the metabolic activation of (+/-)-7,8-dihydroxy-7,8-dihydro-benzo[a]pyrene in human bronchoalveolar cell extracts. | 2005 Feb |
|
Inositol 1,4,5-trisphosphate receptor/GAPDH complex augments Ca2+ release via locally derived NADH. | 2005 Feb 1 |
|
Structure and function of poly(ADP-ribose) polymerase-1: role in oxidative stress-related pathologies. | 2005 Jul |
|
Polymorphisms in the mitochondrial aldehyde dehydrogenase gene (Aldh2) determine peak blood acetaldehyde levels and voluntary ethanol consumption in rats. | 2005 Jun |
|
PARP-10, a novel Myc-interacting protein with poly(ADP-ribose) polymerase activity, inhibits transformation. | 2005 Mar 17 |
|
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 |
|
Expression of a novel P275L variant of NADH:cytochrome b5 reductase gives functional insight into the conserved motif important for pyridine nucleotide binding. | 2006 Mar 1 |
|
TRPM2 activation by cyclic ADP-ribose at body temperature is involved in insulin secretion. | 2006 May 3 |
|
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 |
|
Protective role of estrogen receptor-alpha on lower chlorinated PCB congener-induced DNA damage and repair in human tumoral breast cells. | 2009 Jul 10 |
|
Reciprocal relationship between cytosolic NADH and ENOX2 inhibition triggers sphingolipid-induced apoptosis in HeLa cells. | 2010 Aug 15 |
|
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 |
|
Resveratrol modulates tumor cell proliferation and protein translation via SIRT1-dependent AMPK activation. | 2010 Feb 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 |
|
NADH fluorescence lifetime analysis of the effect of magnesium ions on ALDH2. | 2011 May 30 |
|
Elevated microRNA-34a in obesity reduces NAD+ levels and SIRT1 activity by directly targeting NAMPT. | 2013 Dec |
|
Catalytic contribution of threonine 244 in human ALDH2. | 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
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/24308914
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
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Edited
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by
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on
Sat Dec 16 08:38:15 GMT 2023
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Record UNII |
1ZCR3Z51KV
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Record Status |
Validated (UNII)
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Record Version |
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ACTIVE MOIETY |