NAD+ 500mg high purity - Atlas Lab

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What the parcel contains

One sealed vial of NAD+ 500mg, lyophilised, without individual labelling.

What you also need

Bacteriostatic water for reconstitution and 1 ml precision syringes graduated in 100 units, sold separately. The vial alone cannot be used as is.

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NAD+ (Nicotinamide Adenine Dinucleotide, MW 663.43 Da) is not strictly a peptide: it is a dinucleotide coenzyme present in every living cell, the obligatory catalyst of more than 500 enzymatic reactions linking energy metabolism, DNA repair, calcium signalling and epigenetics. It is also one of the best-documented biological markers of ageing: intracellular NAD+ levels drop by roughly 50 % between ages 20 and 60 in human tissues, and this erosion correlates directly with loss of mitochondrial function, insulin resistance, cognitive decline and frailty in older subjects.

NAD+ research exploded after 2013, when Shin-ichiro Imai, David Sinclair and their teams crystallised the NAD+/sirtuin hypothesis: restoring the NAD+ pool reactivates SIRT1-SIRT7, NAD+-dependent enzymes that deacetylate substrates as critical as PGC-1alpha, FOXO3, p53 and histone H3K9. Three supplementation strategies now coexist: oral precursors (NR nicotinamide riboside, NMN nicotinamide mononucleotide), direct subcutaneous injection of NAD+, and long clinical IV infusions (250-1000 mg over 2-8 hours). Subcutaneous injection of pure NAD+ offers a compromise between the limited bioavailability of oral forms (major hepatic first-pass effect) and the logistical burden of IV protocols.

This vial delivers 500 mg of high-purity NAD+ (>98 %, HPLC), type I glass, fluorinated butyl stopper, inert seal. Lyophilisation protects the molecule from hydrolysis: as anhydrous solid at -20 C, stability exceeds 24 months. After reconstitution in bacteriostatic water, the solution remains usable for 14 days refrigerated at 4-8 C, provided warming-cooling cycles and light exposure are minimised. In accordance with European regulations, this product is intended exclusively for in vitro research and preclinical studies on non-human models: it is neither a medicinal product, a food supplement, nor a medical device.

Science

01
Mechanism of action

NAD+ participates in four major families of enzymatic reactions. First, as a redox coenzyme: glycolysis, the Krebs cycle and beta-oxidation convert NAD+ into NADH, whose reducing equivalents feed the mitochondrial respiratory chain (complex I) to generate ATP. The cytoplasmic and mitochondrial NAD+/NADH ratio is a real-time metabolic sensor: a high ratio signals efficient energy status, a low ratio indicates metabolic saturation or relative hypoxia.

Second, NAD+ is the obligatory substrate of sirtuins (SIRT1 to SIRT7), deacetylases and ADP-ribosyltransferases described by Shin-ichiro Imai in 2000 (Nature). SIRT1 deacetylates PGC-1alpha (mitochondrial biogenesis), FOXO3 (longevity, autophagy), p53 (senescence) and numerous histones. SIRT3 is the major mitochondrial sirtuin: it deacetylates SOD2 (antioxidant defence), the respiratory chain and several Krebs cycle enzymes. When NAD+ falls, sirtuin activity collapses in cascade, accelerating the epigenetic and metabolic drift associated with ageing.

Third, NAD+ is consumed by PARPs (Poly-ADP-Ribose Polymerases) during DNA break repair. PARP1 can consume up to 100 NAD+ molecules per second during massive genotoxic stress, literally depleting the cellular pool. The PARP/sirtuin competition for NAD+ explains why chronic inflammatory states or radiation exposure accelerate NAD+ decline.

Fourth, NAD+ is hydrolysed by CD38, an ectonucleotidase expressed on immune cells and senescent tissues. CD38 increases with age (Camacho-Pereira 2016 Cell Metabolism), to the point of becoming the main driver of NAD+ decline in older subjects. CD38 inhibitors (apigenin, 78c) are studied as complementary strategies to NAD+ precursors.

After subcutaneous injection, NAD+ does not cross the cell membrane directly: it is hydrolysed into nicotinamide riboside (NR) and AMP by extracellular CD73/CD38, then precursors re-enter the cell via ENT/SLC transporters and are reconverted into intracellular NAD+ through the salvage pathway (NAMPT, NMNAT1-3). This indirect pharmacokinetics explains why plasma NAD+ rise is modest but tissue rise can be significant depending on the model.

Clinical data

02Clinical studies

The NAD+ and precursors literature exceeds 15,000 PubMed-indexed publications. Pivotal studies have established three data layers: NAD+ decline with age, precursor efficacy, and human clinical trials.

Massudi 2012 PLoS One first quantified human tissue NAD+ decline: skin biopsies from 30 subjects aged 20-60, mean 50 % drop, negative correlation r = -0.65 with age. Zhu 2015 PNAS showed by in vivo 31P MRS that brain NAD+ falls with age in healthy humans.

Gomes 2013 Cell (Sinclair lab) described the nuclear pseudohypoxia mechanism: the age-related NAD+ drop deactivates SIRT1, which stabilises HIF1alpha, which represses nucleus-encoded mitochondrial transcription, uncoupling mtDNA/nDNA. NMN administration (500 mg/kg IP 7 days) in aged mice restored NAD+ and mitochondrial function to young-mouse levels.

Mills 2016 Cell Metabolism conducted the most comprehensive long-term safety study: oral NMN 100-300 mg/kg/day for 12 months in mice, improved insulin sensitivity, bone density, ocular and muscle function, without detectable toxicity. Yoshino 2021 Science conducted the first human randomised trial: 250 mg/day oral NMN for 10 weeks in 25 prediabetic postmenopausal women, improved muscle insulin sensitivity (hyperinsulinemic clamp, +25 %).

Martens 2018 Nature Communications: randomised crossover trial, 1000 mg/day oral NR for 6 weeks in 30 healthy adults aged 55-79, blood NAD+ elevation of 60 %, systolic blood pressure decrease (-8 mmHg average in mildly hypertensive subjects). Trammell 2016 Nature Communications characterised human NR pharmacokinetics: plasma half-life 2.7 hours, bioavailability superior to nicotinamide, dose-dependent blood NAD+ rise.

Airhart 2017 PLoS One followed 8 heart failure patients on NR 1000 mg/day 9 weeks: blood NAD+ elevation, reduction of NLRP3 activation and pro-inflammatory cytokines. Elhassan 2019 Cell Reports: oral NR 500 mg/day 3 weeks in older men, muscle NAD+ elevation, drop in circulating inflammatory markers (IL-6, TNF-alpha, IL-2).

Regarding subcutaneous injection, human data come mainly from specialised clinics (Springfield Wellness Center, Paterick 2017): 100-500 mg IV or SC protocols in addiction withdrawal programmes, with reports of better mood, sleep and cognitive clarity from non-randomised cohorts. Preclinical studies on direct NAD+ SC injection are limited; most research focuses on oral NR/NMN precursors, whose bioavailability is better documented.

Critical limitation: long-term human trials on precursors remain short (3-12 weeks), cohorts small (<100 subjects), and data on pure NAD+ SC injection essentially observational. Generalisations to global anti-ageing indications are speculative.

1
VieillissementNAD+ in aging, metabolism, and neurodegeneration
Verdin E · Science · 2015
2
Molécules NADTherapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence
Rajman L, Chwalek K, Sinclair DA · Cell Metabolism · 2018
3
Précurseurs NADNAD+ Intermediates: The Biology and Therapeutic Potential of NMN and NR
Yoshino J, Baur JA, Imai SI · Cell Metabolism · 2018

The listed studies are provided for documentation and research purposes only. They do not constitute a therapeutic indication nor a recommendation for human use. This product is strictly for laboratory use only (RUO).

Lab workflow

03
Research protocols

Standard reconstitution: slowly inject 5 ml of bacteriostatic water into the 500 mg vial, creating a 100 mg/ml solution. Gently roll the vial between palms, never shake (NAD+ is sensitive to mechanical shear). The reconstituted solution must be clear, pale yellow to colourless; any opacity, precipitate or brown coloration indicates degradation (oxidation to ADP-ribose).

Typical working concentrations in research:
- Low dose (maintenance): 50 mg = 0.5 ml
- Medium dose (short protocol): 100 mg = 1.0 ml
- High dose (withdrawal/clinical protocol): 200-250 mg = 2.0-2.5 ml
- Clinical IV dose: 500 mg = 5 ml (diluted in 250 ml 0.9 % NaCl over 2-4 hours)

Typical frequency in research models: 2 to 5 times per week for maintenance protocols, daily for 5-10 days for intensive short protocols (withdrawal, post-stress recovery).

Specific points of vigilance for injectable NAD+:
1. Injection site pain: concentrated NAD+ is notoriously painful on SC or rapid IV injection. Inject VERY SLOWLY (1 ml over 2-3 minutes). Dilution in 0.9 % NaCl reduces pain.
2. Flush and chest sensation: rapid IV infusions trigger facial warmth, chest tightness and transient dyspnoea. Slow the flow rate.
3. Nausea: frequent at high doses (>200 mg), mitigated by dividing the dose or injecting after a light meal.
4. Maintain cold chain: reconstituted solution must stay at 4 C, never at prolonged room temperature.

Documented research synergies: protocols combining oral precursors (NMN/NR 500-1000 mg/day) and SC NAD+ injections 2-3x/week are most used in specialised clinics, with the hypothesis that oral maintains baseline tone and injection creates tissue peaks. Combinations with SS-31 (mitochondrial health) or MOTS-c (insulin sensitivity) are explored but interaction data are limited.

This product is not intended for human use. The protocols described are examples drawn from scientific literature and documented clinical practices, provided strictly for informational purposes for research work on non-human models.

Reconstitution for this format (500 mg)Standard volumes used in laboratory settings

Water added	Concentration	Reading marker
3 ml	166,67 mg/ml	10 UI = 16,67 mg
5 ml	100 mg/ml	10 UI = 10 mg

The volume of water does not change the product, only its concentration. Introduce the water slowly along the vial wall, never directly onto the lyophilisate, then swirl without shaking. Markers given on a 1 ml syringe graduated in 100 units.

Asepsis

Disinfect surfaces and stoppers (70% alcohol).

Solvent

Draw the required volume of bacteriostatic water.

Introduction

Inject gently against the vial wall (avoid direct jet on powder).

Solubilization

Roll the vial gently. Do not shake vigorously (degradation risk).

Solution storageOnce reconstituted: 2-8°C (refrigerator).

WarningTheoretical tool for chemical handling. Does not constitute medical advice.

I open the dilution calculator

What is normal on arrivalThe observations that worry customers, and are not defects

The amount of powder looks tiny. A lyophilisate takes up a few millimetres at the bottom of the vial, sometimes just a translucent film. The stated weight is there.
The powder is compact, stuck to the wall or to the stopper. Transport moves the freeze-dried cake around. It changes nothing to reconstitution.
The vial carries no individual label. That is our standard packaging, not a downgraded vial.
After reconstitution, deposits or filaments appear. This is common, especially with small molecules. Let it settle and roll the vial between your palms, never shake it.
The parcel is plain. Nothing on the outside indicates the contents or the brand name.

What is not normal: a cracked vial, an uncrimped cap or a stopper that moves, powder that has liquefied or changed colour. In those specific cases, write to us with a photo and we take the vial back.

Handling

04Storage & handling

Sealed unreconstituted vial: storage at -20 C in a laboratory freezer, certified stability 24 months from production date (see COA). At 4 C, stability is 6-9 months according to internal stability studies. At room temperature (20-25 C), do not store beyond 30 days; beyond, NAD+ oxidation to ADP-ribose accelerates.

After reconstitution in bacteriostatic water (0.9 % benzyl alcohol):
- 4-8 C (standard laboratory refrigerator): optimal stability 14 days, acceptable up to 21 days if the vial has not been repeatedly taken out and returned.
- -20 C (freezing): NOT RECOMMENDED for NAD+ in solution. Unlike short peptides, NAD+ is a dinucleotide sensitive to freeze-thaw cycles, which cause crystallisation and partial hydrolysis.
- Light: keep protected from light in an opaque box or wrapped in aluminium. NAD+ absorbs in UV (maximum 260 nm) and degrades under prolonged UV exposure.
- pH: the reconstituted solution has a natural pH around 5.5-7.5. Avoid any contact with strongly alkaline solutions (pH >9), which accelerate pyrophosphate bond hydrolysis.

Visual signs of degradation to check before each draw:
1. Colour: shift from pale yellow to amber brown = advanced oxidation.
2. Opacity or precipitate: formation of insoluble aggregates = structural degradation.
3. Odour: appearance of ammonia smell = release of free nicotinamide (hydrolysis).

If in doubt, discard the vial. The cost of a reconstituted vial is negligible compared to research time lost on data corrupted by degraded product. Rigorously document reconstitution date, lot, draws performed and storage conditions in a laboratory logbook.

01Is NAD+ a peptide?

No. NAD+ is a dinucleotide (nicotinamide + adenine + two riboses + two phosphates), MW 663 Da. It is sold in peptide catalogues by historical convention linked to injectable practices, but biologically it is a redox coenzyme, not a polymer of amino acids.

02Why inject NAD+ rather than take oral NR or NMN?

SC injection bypasses hepatic first-pass (oral precursors undergo partial hepatic conversion) and guarantees immediate systemic bioavailability with high plasma peaks. In return, it is more constraining and painful. Specialised clinics often combine both approaches.

03Why is NAD+ injection painful?

Concentrated NAD+ solution is acidic at its natural pH (5.5-6.5) and irritating to subcutaneous tissue. Injecting very slowly (1 ml over 2-3 minutes), diluting in 0.9 % NaCl (0.5-1 ml extra) and applying cold before injection can significantly reduce pain.

04Can the reconstituted solution be frozen?

Not recommended. Unlike classical peptides, NAD+ is a dinucleotide sensitive to freeze-thaw cycles: crystallisation and partial hydrolysis occur. Store at 4 C and reconstitute small volumes (1-2 ml) to optimise usage freshness.

05Does injectable NAD+ extend lifespan?

No randomised clinical trial in humans on injectable NAD+ or its precursors has demonstrated lifespan extension. Data come from animal models (rodents) over short durations and from health markers (insulin sensitivity, inflammation) over 3-12 weeks in humans. Longevity generalisations are speculative.

06What are the reported side effects?

Pain/redness at injection site, transient facial flush, chest tightness (rapid IV infusion), nausea at high doses, paradoxical fatigue in the first days. Serious systemic effects are rare in observational cohorts but long-term data are insufficient.

07Can injectable NAD+ be combined with SS-31 or MOTS-c?

The three target distinct layers of mitochondrial biology: NAD+ the coenzyme pool and sirtuins, SS-31 membrane cardiolipin, MOTS-c AMPK signalling. Combinations are theoretically complementary and empirically documented in integrative medicine clinics, but no randomised trial has validated combination superiority versus each agent alone.

08Should NAD+ be cycled?

Documented protocols suggest 5-10 day intensive cycles followed by maintenance periods (2x/week) or 2-4 week pauses. This reflected tolerance concerns (pain, cost) more than formal scientific data on downregulation. The NAD+ pool is globally maintained as long as supply compensates for PARP/CD38/sirtuin consumption.

Benchmark

Similar peptides

Injectable NAD+ differs radically from oral precursors and other metabolic strategies. Versus oral NR (Nicotinamide Riboside): NR 500-1000 mg/day is very well documented (Trammell 2016, Martens 2018, Elhassan 2019) but undergoes partial hepatic conversion and intracellular bioavailability depends on ENT transporters. NR is the most studied form in human clinical trials but requires 3-6 weeks to significantly elevate tissue NAD+.

Versus oral NMN (Nicotinamide Mononucleotide): NMN 250-500 mg/day has shown clinical effects (Yoshino 2021 Science) but its absorption pathway is still debated (Slc12a8 transporter proposed by Grozio 2019, controversial). NMN is increasingly available as a dietary supplement in the USA (after the FDA removed it from NDI category in 2022).

Versus direct NAD+ injection: SC NAD+ bypasses hepatic first-pass metabolism, but NAD+ does not directly cross the cell membrane and must be hydrolysed into precursors by extracellular CD38/CD73. Plasma rise is rapid and robust but tissue uptake depends on the same salvage pathways as oral precursors. The main injection advantage is guaranteed systemic bioavailability and high plasma peaks.

Versus metformin and resveratrol: metformin activates AMPK and lowers the NAD+/NADH ratio through complex I inhibition (paradoxically beneficial), resveratrol activates SIRT1 without increasing NAD+. Neither restores the NAD+ pool: they act downstream. Strategies are complementary.

Versus caloric restriction and intermittent fasting: these interventions physiologically increase NAD+ and activate sirtuins without supplementation. NAD+ precursors are often described as partial mimetics of caloric restriction, without reproducing all its benefits (autophagy, ketones, mTOR signalling).

Versus the mitochondrial trilogy (SS-31, MOTS-c, Urolithin A): NAD+ acts at the redox coenzyme pool and sirtuin level. SS-31 protects mitochondrial membranes via cardiolipin. MOTS-c activates AMPK and metabolic signalling. Urolithin A induces mitophagy. These four strategies are not redundant: they target distinct nodes of mitochondrial biology. Experimental protocols combining NAD+ + MOTS-c + SS-31 are empirically documented but not yet validated in randomised trials.

Final limitation: no NAD+ precursor (nor direct NAD+) has demonstrated in randomised human trials prolongation of lifespan, prevention of major chronic diseases, or reversal of biological ageing markers over durations >12 months. Data are promising but preliminary.

Longevity

Asepsis

Solvent

Introduction

Solubilization

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