Search peptides — top sellers first
Search peptides — top sellers first
Search peptides — top sellers first
$79$0.16/mg
Endogenous coenzyme — mitochondrial metabolism and aging research
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NAD+ · 500mg
Frequently bought together
Researchers usually add these to complete the protocol.
BAC Water · 3ml
Essential · Extras
GHK-CU · 50mg
Recovery
Melanotan 2 · 10mg
Tanning
Certificate of analysis
We don't publish a brand-wide spec sheet and call it a “COA.” The certificate you receive references the actual lot number stamped on your vial — with the raw chromatograms attached.
Vantage Analytical
Independent analytical lab
Certificate of Analysis
RESULT · PASS
Analytical results
HPLC Chromatogram
Purity ≥98%
Know your compound
Nicotinamide adenine dinucleotide (NAD+) is an endogenous pyridine dinucleotide coenzyme that functions as an obligate hydride-transfer cofactor in mitochondrial oxidative phosphorylation and as a substrate for sirtuin deacylases and poly(ADP-ribose) polymerase (PARP) enzymes. Cellular NAD+ abundance declines markedly with organismal age, a trajectory documented across multiple human tissue types.
The age-associated decline in NAD+ pools is mechanistically linked to impaired DNA damage responses, reduced sirtuin activity, and dysregulated mitochondrial biogenesis — connecting NAD+ homeostasis to the central hallmarks of aging. Restoration of intracellular NAD+ concentrations is consequently a primary investigative target in longevity, metabolic, and oncology research programs.
For research use only — not for human or veterinary use.
The research
The published findings behind this compound — the headline numbers, in plain terms, each cited to source. Preclinical results are directional (animal / in-vitro) and shown for context, not as therapeutic claims.
Published research on the reference compound class. Provided for scientific context only — not a claim about the product supplied.
In a human tissue cross-sectional analysis, NAD+ levels were approximately half as high by age 50 compared with young-adult baseline — a decline documented directly in human samples (Massudi et al., cited in Covarrubias et al., Nat Rev Mol Cell Biol, 2021).
Cross-sectional human tissue analysis; approximate values from Massudi et al., cited in Covarrubias et al. 2021.
In vitro and murine studies show that PARP-mediated DNA repair activity is directionally constrained by NAD+ availability — when NAD+ is depleted, repair signalling slows (Amjad et al., Mol Metab, 2021). No quantified human effect size is established.
Relative / directional representation only — no precise quantified values reported in source. In vitro and murine model systems; not a human effect size.
Across in vitro and murine model systems, sirtuin-family deacylase activity — which governs chromatin remodelling and metabolic adaptation — was directionally rate-limited by intracellular NAD+ concentration (Amjad et al., Mol Metab, 2021). The relationship is substrate-dependent, with no quantified human magnitude reported.
Directional representation only — source reports a substrate-rate relationship without a single quantified figure. In vitro and murine model systems; not a human effect size.
Mechanism
NAD+ is studied principally through three distinct molecular routes: as a hydride-transfer cofactor in redox metabolism, as a consumed substrate for sirtuin deacylases, and as the rate-limiting input to PARP-dependent DNA repair.
As the obligate electron acceptor in glycolysis and the TCA cycle, NAD+ is reduced to NADH and subsequently re-oxidized by the mitochondrial electron transport chain — a cycle whose efficiency is under investigation as a determinant of cellular energy output in aging and metabolic disease models.
Sirtuin enzymes (SIRT1–7) consume NAD+ stoichiometrically during deacylation of histones and metabolic regulatory proteins; because sirtuin activity is therefore directly limited by NAD+ availability, researchers study NAD+ pools as a node linking nutrient status to chromatin remodeling and transcriptional regulation.
Poly(ADP-ribose) polymerases consume NAD+ to synthesize poly(ADP-ribose) chains at sites of DNA strand breaks; in preclinical models, cellular NAD+ concentration has been shown to constrain the rate and completeness of PARP-dependent DNA repair, making it a focus of genotoxic-stress and oncology research.
For research use only. Mechanisms described reflect published preclinical and clinical literature.
The process
Synthesized
Produced under controlled manufacturing with documented, repeatable processes.
HPLC purity
An independent lab reports the exact purity of every lot — a number, never a 'passes'.
Mass-spec identity
Molecular weight confirms the exact sequence is what the label says.
COA published
The certificate is posted to the open library, by lot, before the vial ships.
Best sellers
FAQ
Common questions about NAD+
The COA guarantee
Have any lot independently re-tested. If the results don't match the published certificate, we refund the order in full — no returns, no questions.
Order with coverThird-party tested
An independent, accredited lab — no commercial interest in the result.
A COA on every lot
A lot-specific certificate ships with each vial, archived by batch.
Test it yourself → refund
Re-test any batch at any lab. A mismatch is a full refund.
