What is NAD+?

NAD+ is the oxidised form of nicotinamide adenine dinucleotide, a coenzyme that cells use to move electrons between chemical reactions. It has two forms: NAD+ accepts electrons and becomes NADH, the reduced form. ^[11] Cells build it from the amino acid tryptophan and from the forms of vitamin B3, nicotinic acid and nicotinamide. ^[12]

Arthur Harden and William John Young discovered it in 1906 in a yeast extract that sped up alcohol fermentation. ^[11] For most of the century that followed, researchers studied it as a redox carrier. A 2018 review in Cell Metabolism calls it "the cell's hydrogen carrier for redox enzymes" and notes that it has since emerged as a signalling molecule. ^[13]

NAD+ sits in our longevity range beside peptides studied in related pathways. Chemically it is a nucleotide. It has no amino acid sequence and no peptide bonds, so peptide measures such as sequence, length and net peptide content do not apply to it. NAD+ 500mg is in stock with a batch certificate, published under the batch number on the vial.

NAD+ works in two ways: as a reusable electron carrier, and as a substrate that some enzymes break apart. In the first role it accepts electrons during glycolysis, beta-oxidation and oxidative phosphorylation, and the NADH it forms carries them on. ^[11] This role recycles the molecule. In the second role, NAD+-dependent enzymes consume it. ^[2]

The 2000 Sir2 paper is where the modern interest began. Imai and colleagues showed that yeast and mouse Sir2 proteins are NAD-dependent histone deacetylases, which tied a metabolic coenzyme to gene silencing and yeast life span. ^[14]

Because consumption uses NAD+ up, cells must keep making it. In cell lines, isotope tracing showed NAD+ made from nicotinamide and consumed largely by PARPs and sirtuins. In mice, the liver made it from tryptophan and released nicotinamide into the blood for other tissues. ^[17] The enzyme NAMPT is the rate-limiting step of that recycling route. ^[18]

NAD+ is a dinucleotide of adenine and nicotinamide, with a formula of C21H27N7O14P2 and a molecular weight of 663.4 g/mol. ^[1] One nucleotide carries nicotinamide on a ribose sugar. The other is adenosine. A pyrophosphate linkage (two phosphate groups) joins them. The nicotinamide ring is the part that accepts electrons. In the oxidised form it carries a positive charge (PubChem names it a pyridin-1-ium ring), which gives NAD+ its "+".

We checked each value against PubChem on 29 September 2026. ^[1] Two details matter when you compare a certificate against this table. First, PubChem's CAS section returns 53-84-9 from most depositors and 64417-72-7 from one, so a supplier may quote either. Second, a mass spectrometry result can report the average molecular weight (663.4) or the monoisotopic mass (663.109), and the certificate should say which.

Research on NAD+ is deep in cells and mice and thin in people, and most human trials tested precursors taken by mouth. The 2026 systematic review identified 113 eligible studies from 2010 to October 2025: 80 in rodents and 33 human intervention studies, of which 28 were randomised. ^[3] The human trials mostly used nicotinamide riboside (NR) or nicotinamide mononucleotide (NMN).

Two of these papers have Australian links. The 6-hour infusion pilot was led from the Australasian Research Institute at Sydney Adventist Hospital, with University of New South Wales co-authors. ^[4] David Sinclair, an author of the 2018 Cell Metabolism review, lists a UNSW affiliation. ^[13]

Each finding above belongs to its own model and population. The mouse life span result used NR. The heart failure trial used intravenous NAD+ in hospital patients already on standard therapy.

The NAD+ evidence does not yet show what intravenous or oral NAD+ itself does in people over months or years. Four limits stand out.

1. Direct human trials of NAD+ are few and small. The 2026 systematic review found no eligible outcome trials of NAD+ given by vein or into muscle for ageing or wellness indications. It treated the infusion pilot as contextual evidence only. ^[3] The 2026 narrative review describes the human intravenous evidence as mostly small uncontrolled studies, observational work and case reports. ^[7]
2. Precursor results belong to the precursors. NR and NMN are different molecules with their own absorption and metabolism. In mice, oral NR and NMN reached tissues as nicotinamide after first-pass metabolism in the liver. ^[17] Infused NAD+ behaved differently again: in the Sydney pilot it was removed from plasma rapidly and completely for at least the first 2 hours. ^[4]
3. The human decline story is contested. A 2021 review states that NAD+ falls with age in rodents and humans. ^[2] The 2026 narrative review reports that recent large-scale human data show whole-blood NAD+ does not decline with healthy ageing as such. ^[7] Both statements are published. Tissue and blood measures differ, so neither settles the other.
4. Commercial ties are common. The first NR pharmacokinetic trial was sponsored by the NR supplier, and several authors held stock. ^[20] The authors of the 2026 clinic review were employed by the clinic operator. ^[6] Authors of the 2021 review declare research support from Napa Therapeutics. ^[2]

Identity and purity of a research vial are separate questions, and a batch certificate answers them.

Studies of intravenous NAD+ reported gastrointestinal symptoms, increased heart rate and chest pressure during infusion. In the 2026 retrospective review, clients who received IV NAD+ reported moderate to severe gastrointestinal symptoms, increased heart rate and chest pressure during infusions. All symptoms resolved when the infusion finished. ^[6]

The same review recorded these results:

• Infusion time: the symptoms lengthened NAD+ infusions to an average of 97 minutes, against 37 minutes for IV NR. ^[6]
• Comparator group: IV NR recipients reported minor tongue, jaw and arm tingling and mild cramping. ^[6]
• Blood markers: alkaline phosphatase fell in the NAD+ group while staying within normal reference ranges, and HDL cholesterol fell in the NAD+ group. ALT, AST, hsCRP, BUN/creatinine and TSH did not change significantly. ^[6]

The 2026 narrative review lists nausea, cramping, flushing and chest discomfort as reported adverse effects and states that long-term safety data are lacking. ^[7] In the 6-hour Sydney pilot, the authors observed no adverse events in either the NAD+ or the saline group. ^[4] The abstract of the 180-patient heart failure trial reports no adverse-event data. ^[5]

Precursor trials report their own events. In NR-SAFE, a 20-person phase 1 trial of oral NR in Parkinson's disease, the authors reported no moderate or severe adverse events and a slight initial rise in serum homocysteine among NR recipients. ^[25] Those observations describe NR in that population.

NAD+ is not named in the Poisons Standard. We searched the June 2026 instrument (F2026L00633, in force from 1 June 2026) and found no entry for NAD+, nadide or nicotinamide adenine dinucleotide. ^[8] The only related text is nicotinamide, which appears as an exception to the Schedule 3 and Schedule 4 entries for nicotinic acid.

The TGA addresses NAD+ directly in a safety alert on NAD, NAD+, NADH and NMN products. It states that NAD, NAD+ and NADH are currently not permitted ingredients in listed medicines. It warns that supplying therapeutic goods that refer to them without ARTG inclusion, exemption or authorisation is likely to breach the law. ^[10] NMN is treated differently: it entered the Permissible Ingredients Determination on 10 December 2025 under specific conditions, and the TGA updated the alert on 3 February 2026 to say so. ^[10]

For sport, NAD+ is not named on the WADA 2026 Prohibited List, which took effect on 1 January 2026. ^[9] Prohibited Method M2.2 still applies to how any substance is given: it covers intravenous infusions of more than a total of 100 mL per 12-hour period, apart from those legitimately received in hospital treatment, surgery or clinical diagnostic investigations. ^[9] WADA revises the List every year, so check the current edition.

Legal status in Australia depends on the compound. Our guide to Australian peptide law and the Poisons Standard explains each schedule.

NAD+ is a moisture-sensitive solid that degrades in warm or alkaline solution, so keep the powder sealed, dry and cold, and keep solutions cool and near neutral pH. PubChem records it as a highly hygroscopic white solid. ^[1] A 2019 study notes that NAD+ spontaneously decomposes at elevated temperatures and basic pH. ^[26]

Buffer choice changes solution stability. A 2024 study tracked NAD+ and NADH in sodium phosphate, HEPES and Tris buffers at 19 and 25 °C for up to 43 days. Both were highly stable in Tris. Degradation was faster in sodium phosphate and HEPES, and the small rise in temperature had a significant effect. ^[27]

A practical handling sequence for a research vial:

1. Match the batch number on the vial to its certificate before opening it.
2. Keep the sealed lyophilised powder cold, dry and away from light until use.
3. Reconstitute with a named solvent and record the solvent and the mg per mL concentration on the label.
4. Keep the solution cold and use it within a set window, since warmth speeds breakdown.

NAD+ dissolves readily in water; PubChem lists a water solubility of 752.5 mg/mL from the Human Metabolome Database. ^[1] We stock BAC Water (sterile water with 0.9% benzyl alcohol) for laboratory reconstitution. Our guides on how to reconstitute a lyophilised vial and peptide storage temperatures and freeze-thaw apply the same principles to NAD+.

NAD+ is the end product, and NR, NMN and nicotinamide are precursors that cells convert into it. The distinction matters because most human trials in the table above used a precursor.

No published trial compares research-grade NAD+ with a precursor. NAD+ sits in our longevity research range with peptides studied in similar pathways; the MOTS-C explainer sets out the structure and research record of one of them.

Peptides Collective sells NAD+ for laboratory research use only, in 500mg vials from A$94. Stock ships from Western Australia with tracking.

Every batch is tested by an independent lab before it goes on sale. The certificate reports purity by HPLC and identity by mass spectrometry, and it is published under the batch number printed on the vial. You can search the certificate of analysis library by that batch number and match the report to the vial in your hand.

Read the certificate against the structure table above. The identity result should correspond to 663.4 g/mol (or 663.109 Da as a monoisotopic mass), and net peptide content does not apply to a nucleotide. Our guide on how to read a certificate of analysis explains the HPLC trace and the mass spectrum, and the NAD+ product page links the certificate for the current batch.

NAD+ is a 663.4 g/mol dinucleotide coenzyme that cells use as an electron carrier and as fuel for sirtuins, PARPs and CD38. Its research record is broad in cells and mice, and the human trials mostly tested oral precursors; direct human data on NAD+ are limited to small intravenous studies and one 180-patient trial. In Australia it has no Poisons Standard entry, the TGA does not permit it in listed medicines, and WADA does not name it. For a research vial, the batch certificate is the evidence that settles identity and purity.