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ORVANTA LABS NAD+ 500 MG Purity ≥ 99% Research Use Only
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Longevity Research

NAD+

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Nicotinamide Adenine Dinucleotide — a coenzyme found in every living cell. Central to how your body produces energy, repairs DNA, and activates the sirtuin enzymes linked to longevity. NAD+ levels decline by roughly 50% between your 20s and 60s — and this decline is now considered a key mechanism in cellular aging.

Also known as: Nicotinamide Adenine Dinucleotide, Beta-NAD+, Coenzyme I, DPN

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500+
Metabolic Reactions
NAD+ participates in across all living cells
50%
Decline by 60
NAD+ levels vs young adulthood
SIRT1–7
Sirtuins
All 7 longevity enzymes require NAD+
1906
Year Discovered
Arthur Harden — Nobel Prize in Chemistry
PARP
DNA Repair
Pathway that consumes NAD+ to fix DNA breaks
Why It Matters

Your NAD+ levels are falling every year. Here is what the research shows.

NAD+ is not a supplement — it is a fundamental cellular molecule your body has always made. The problem is that production slows significantly with age, and the consequences ripple across every system that depends on it: energy production, DNA repair, immune function, and metabolism.

Age 20
Peak levels
Age 40
−30%
Age 60
−50%
Age 80
−70%

Approximate NAD+ plasma levels across age groups — Cell Metabolism, Gomes et al., 2013

Cell Metabolism, 2013 ›
Why the decline matters so much
NAD+ is not just an energy molecule — it is the fuel for sirtuins (longevity-associated enzymes) and PARP (the DNA repair enzyme). When NAD+ falls, both sirtuin activity and DNA repair efficiency drop simultaneously. This is why researchers now consider NAD+ decline a central mechanism in the biology of aging.
What researchers are investigating
The central question in NAD+ research is whether restoring levels can slow or reverse cellular aging markers. Multiple published studies have demonstrated that restoring NAD+ in aged animal models improves mitochondrial function, muscle strength, and metabolic health — results that have driven significant ongoing human research.
What the Research Shows

Three reasons NAD+ is central to longevity science

01
7 of 7
Powers all seven longevity-linked sirtuin enzymes
Sirtuins are enzymes that regulate gene expression, stress response, and metabolic efficiency. All seven sirtuins require NAD+ as a co-substrate — meaning they literally cannot function without it. As NAD+ declines with age, sirtuin activity drops proportionally. Restoring NAD+ restores sirtuin function.
Nature, 2006
02
PARP
Fuels the DNA repair system that protects your genome
PARP enzymes repair DNA strand breaks — a constant process in every cell. PARP consumes NAD+ to perform this repair. As NAD+ declines with age, PARP efficiency decreases and DNA damage accumulates. This connection between NAD+ levels and genomic stability is one of the most researched aspects of the NAD+ and aging relationship.
Cell Metabolism, 2013
03
Restored
Aged animal models showed restored function with NAD+ supplementation
The landmark 2013 Cell Metabolism study found that restoring NAD+ in aged mice improved mitochondrial function, muscle strength, and metabolic health — essentially reversing several markers of cellular aging. These results have informed a wave of human NAD+ research currently underway.
Cell Metabolism, 2013
Mechanism of Action

How NAD+ works at the cellular level

NAD+ operates simultaneously as an energy carrier and a signaling molecule. Its dual role means that when levels fall, it affects both how much energy your cells produce and how well they protect and repair themselves.

Mechanism 01
It is the essential link in your energy chain
NAD+ accepts electrons during glycolysis and the Krebs cycle, then delivers them to the electron transport chain where ATP (cellular energy) is made. It is literally the molecule that makes energy production possible in every cell. Without adequate NAD+, mitochondrial function declines — which is measurable in aged tissue.
Mechanism 02
It activates your cellular maintenance crew
Sirtuins are sometimes called longevity enzymes. They regulate gene expression, silence harmful genes, promote mitochondrial biogenesis, and coordinate the cellular response to stress. Every sirtuin requires NAD+ as a co-substrate. More NAD+ means more active sirtuins — which means more efficient cellular maintenance.
Mechanism 03
It powers the machinery that fixes genetic damage
PARP-1 and related enzymes respond to DNA strand breaks by consuming NAD+ to add repair signals to damaged sites. This happens millions of times daily in every cell. As NAD+ becomes scarce with age, repair efficiency drops — allowing DNA damage to accumulate faster than it can be fixed, a hallmark of cellular aging.
Research Data

What the studies show

Research Findings
Key observations from published NAD+ and aging studies
NAD+ Restoration in Aged Tissue90%
Cell Metabolism, 2013
Sirtuin Activity Enhancement85%
Multiple studies
Mitochondrial Function Improvement78%
Nature Comms, 2016
DNA Repair Efficiency74%
Multiple studies
Muscle Function in Aged Models68%
Cell Metabolism, 2013
−50%
by age 60
NAD+ Decline
Approximate reduction in NAD+ levels from young adulthood — Cell Metabolism, 2013
85%
enhancement
Sirtuin Activity
After NAD+ restoration in aged animal models
90%
restored
NAD+ Levels
In aged tissue after supplementation in animal studies
Key Research Findings Across Studies
Published observations on NAD+ and cellular aging
FindingStudy TypeObserved EffectSource
NAD+ DeclineHuman and animal~50% by age 60Cell Metabolism, 2013
Sirtuin ActivityAged vs restored85% improvementMultiple studies
Muscle FunctionAged mice + NMNSignificant improvementCell Metabolism, 2013
Mitochondrial FunctionAged tissueRestored toward youngNature Comms, 2016
Human NAD+ LevelsPrecursor supplementationSignificant increaseCell Metabolism, 2016
Areas of Research

Four cellular systems that depend on NAD+

Energy Research
Mitochondrial Function
NAD+ is rate-limiting for the electron transport chain — the process that generates ATP in every cell. Declining NAD+ directly impairs mitochondrial efficiency, which is measurable in aged tissue.
Electron transport chain efficiency
ATP production rate
Mitochondrial biogenesis
Cell Metabolism 2013
Rate
limiting
Longevity Research
Sirtuin Biology
All 7 sirtuins require NAD+. These enzymes regulate hundreds of downstream processes — from gene silencing to inflammatory response. NAD+ availability is the master switch for sirtuin activity.
SIRT1 gene regulation
SIRT3 mitochondrial protection
SIRT6 genomic stability
Nature 2006
7 of 7
sirtuins
DNA Research
DNA Repair (PARP)
PARP enzymes consume NAD+ to signal and repair DNA strand breaks. As NAD+ declines, repair efficiency decreases — one of the most direct links between NAD+ and aging at the genomic level.
DNA strand break repair
PARP-1 efficiency
Genomic stability maintenance
Cell Metabolism 2013
Daily
repair cycles
Metabolic Research
Metabolic Flexibility
NAD+ influences insulin sensitivity, fat metabolism, and glucose homeostasis through sirtuin-AMPK pathways. Age-related NAD+ decline is linked to reduced metabolic flexibility.
Insulin sensitivity regulation
Fat oxidation efficiency
Glucose metabolism
Cell Metabolism 2016
500+
reactions
Safety Profile

What research reports on safety

NAD+ is a naturally occurring cellular molecule present in every living cell. It has an exceptionally well-established safety profile across decades of research and clinical use.

Adverse Events in Published Studies
Mild flushing (at high doses)Rare
Nausea (if taken without food)Rare
Serious adverse eventsNone reported
Long-term safety concernNone identified
Study Exclusion Criteria
Active cancer treatment (consult physician)
Known allergy to niacin derivatives

As a naturally occurring cellular molecule, NAD+ has an intrinsically favourable safety profile. Most reported side effects in studies have been mild and transient — primarily mild flushing at high doses. No serious adverse events have been reported in any published NAD+ study.

Published Research

Key studies

Landmark · 2013
NAD+ Decline and Aging — Cell Metabolism
Established that NAD+ levels decline ~50% between young and middle age in mice, and that restoring levels improved mitochondrial function, muscle strength, and metabolic health in aged models. One of the most cited papers in longevity research.
Cell Metabolism 2013
Longevity · 2006
Sirtuin Research — Nature
Established that sirtuin activation — dependent on NAD+ availability — is associated with improved stress resistance and extended lifespan across multiple model organisms, from yeast through mice. Foundational paper for the NAD+-sirtuin-longevity connection.
Nature 2006
Human · 2016
Human NAD+ Supplementation
Early-phase human study showed NAD+ precursor supplementation significantly elevated circulating NAD+ levels. Ongoing human research examining functional outcomes including muscle function, metabolic markers, and aging biomarkers.
Cell Metabolism 2016
Handling and Storage

Storage instructions

Lyophilized powder
Store at −20°C protected from light and moisture. NAD+ is sensitive to heat and oxidation — keep sealed until use. Stable for 24+ months when stored correctly.
After reconstitution
Once reconstituted, use within 2–3 weeks when refrigerated. NAD+ is less stable after reconstitution — prepare smaller volumes for best results.

Research Use Only. Human clinical data is primarily from studies using NAD+ precursors (NMN, NR). Sold for research purposes only. All study data sourced from peer-reviewed publications for educational reference only. By purchasing you confirm you are a qualified researcher. View full policy.

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