NAD+ (100mg)

Search volume around "NAD peptide" is high enough that the label has stuck, but the chemistry doesn't support it. NAD+ has no amino acid backbone and no peptide bond anywhere in its structure. It's a dinucleotide: an adenine-based nucleotide and a nicotinamide-based nucleotide, each built on a ribose sugar and a phosphate group, linked by a shared pyrophosphate bridge.^[1][2] PubChem lists it under CID 5892, molecular formula C21H27N7O14P2, alongside the older name nadide.^[1]

Tetrava Labs does carry genuine peptides discussed in the same longevity and mitochondrial-research conversations as NAD+. MOTS-c is one: a 16-amino-acid, mitochondrially encoded signaling peptide with an actual sequence and peptide bonds. NAD+ and MOTS-c turn up in the same research literature because both sit inside mitochondrial and metabolic-aging biology, not because they're the same class of molecule.

NAD+/NADH is the electron-carrying pair that keeps glycolysis, the citric acid cycle, and oxidative phosphorylation moving, cycling between oxidized and reduced states as it shuttles electrons toward ATP production.^[2] That redox role alone would make NAD+ worth studying. It isn't the whole story.

NAD+ also gets consumed, not just recycled, by three enzyme families driving a lot of current aging research: the sirtuins (SIRT1 through SIRT7), which use NAD+ to strip acetyl groups off histones and other proteins; the PARPs, which burn NAD+ to build poly-ADP-ribose chains during DNA repair; and CD38, an immune-cell enzyme that degrades NAD+ into calcium-signaling metabolites.^[2] Sirtuins and PARPs compete for the same limited NAD+ pool. A cell under heavy DNA-damage load can starve its sirtuin activity of substrate, which is the mechanism researchers use to connect oxidative stress to aging phenotypes.^[2]

A separate line of research ties NAD+ to exercise physiology through AMPK, the cell's fuel-sensing enzyme. A 2009 study in mouse skeletal muscle found that AMPK activation raises cellular NAD+ levels, which in turn boosts SIRT1 activity. SIRT1 then deacetylates PGC-1α, FOXO1, and FOXO3a, three transcription factors that switch on mitochondrial biogenesis and oxidative-metabolism genes.^[3] That's the mechanistic chain researchers point to when they connect NAD+ to exercise adaptation and mitochondrial density, not a single "NAD+ raises energy" claim.

It's a mouse skeletal-muscle model, not a human trial, and it says nothing about whether an exogenous NAD+ reagent reproduces the same intracellular AMPK-SIRT1 signaling. Labs studying this pathway typically need an AMPK activator (AICAR or metformin are common choices in the literature) alongside NAD+ and SIRT1 readouts to isolate where in the chain an effect originates.^[3]

A 2012 study measured NAD+, PARP activity, and SIRT1 activity directly in human pelvic skin samples from 49 subjects ranging from newborn to age 77.^[4] NAD+ levels correlated negatively with age in both sexes. PARP activity rose with age and tracked inversely with tissue NAD+ levels, most strongly in males.^[4] The authors' interpretation: age-related oxidative DNA damage drives PARP into overdrive, and the resulting NAD+ consumption may be part of what limits energy production and DNA repair capacity as tissue ages.^[4]

That's a correlational human-tissue dataset, not a controlled intervention trial. It supports the hypothesis that preserving NAD+ pools matters for cellular aging, but it doesn't establish that supplementing NAD+ from outside the cell reverses any of it. A comparative aging model should treat NAD+ depletion as one variable among several, with PARP and sirtuin activity measured directly rather than assumed.

Most of the controlled human evidence on raising NAD+ levels doesn't test the intact dinucleotide. It tests precursors, smaller molecules like nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR), that cells convert into NAD+ through the salvage pathway.^[2] A 2021 randomized, placebo-controlled trial gave 25 postmenopausal women with prediabetes either 250 mg of oral NMN daily or placebo for 10 weeks. The NMN group showed increased NAD+ in blood cells and improved skeletal-muscle insulin signaling, with no NMN-attributed adverse events reported.^[5]

NAD+ is a large, charged molecule that doesn't cross cell membranes as readily as its smaller precursors, which is part of why the precursor route dominates the published human trial record.^[2] That gap in the literature is exactly why "how much NAD peptide should I take" and similar dosing questions don't have a published answer. The best-controlled human data measures a different, smaller molecule than the one in this vial.

Wellness clinics market NAD+ by IV infusion or injection for energy, recovery, and anti-aging claims. The tolerability data tells a rougher story than the marketing does. A 2026 retrospective study comparing commercial NAD+ IV against NR IV infusions found that every NAD+ IV participant reported moderate-to-severe abdominal cramping, nausea, vomiting, elevated heart rate, throat pain, and chest pressure during the infusion, all of which resolved once the infusion stopped.^[6] Average NAD+ IV infusion time ran 97 minutes, more than double the NR IV group's 37 minutes, largely because clinicians had to slow the drip rate to manage those reactions.^[6]

A separate 2024 randomized pilot study comparing acute NAD+ IV, NR IV, and oral NR found a measurable increase in white blood cell count and neutrophils in the NAD+ IV arm, consistent with an inflammatory response. NR IV raised blood NAD+ levels faster and higher than NAD+ IV did at the three-hour mark.^[7] Neither study is large enough to settle safety questions, and both call for more systematic research given how widely IV NAD+ is already marketed.^[6][7] Nothing in that literature describes a validated dosing chart, calculator, or injection-site protocol. This page doesn't publish one either.

"NAD+ serum" and "NAD+ patch" are marketing terms from the skincare and wellness industries, not chemistry terms with a shared research definition behind them. Nothing in the literature reviewed for this page tests a topical serum or transdermal patch route for NAD+.

That gap tracks with what's already known about the molecule: NAD+ is large and charged, the same membrane-permeability problem that pushes controlled human trials toward smaller precursors instead of the intact dinucleotide.^[2] Tetrava Labs doesn't sell a topical serum or a patch. This catalog listing is a lyophilized vial for laboratory reconstitution, nothing else.

NAD+ has no FDA-approved indication in any form. In a September 2019 proposed rule, FDA reviewed NAD among 26 nominated substances and proposed not to add it to the Section 503A Bulks List, the list that lets compounding pharmacies use a bulk substance without an individual patient prescription tied to an approved drug.^[8] Injectable NAD+ sold by clinics is compounded medication, prepared under FDA's interim compounding enforcement policy rather than as an approved drug product. Oral NMN and NR are marketed as dietary supplements under a completely different regulatory framework.^[2][8]

FDA has separately reminded compounders that food-grade NAD+ isn't suitable for sterile injectable use, since food-grade material isn't manufactured or tested to the sterility and endotoxin standards an IV product requires.^[9] Tetrava Labs' catalog listing is a Research Use Only laboratory reagent. It is not a compounded injectable, an IV product, or a dietary supplement.

NAD+ ships as a lyophilized powder, which keeps it stable in transport and storage. Store sealed vials at -20°C, away from light, and avoid repeated freeze-thaw cycling; NAD+ degrades under both heat and prolonged light exposure in solution.^[2] Reconstitute under sterile technique with a protocol-appropriate diluent immediately before use.

After reconstitution, hold working solutions at 4°C, minimize freeze-thaw cycles, and use them within the window your laboratory SOP sets. Because NAD+/NADH ratios are the actual readout in most redox assays, record diluent lot, reconstitution date, and time-to-assay in your ELN so preparation timing doesn't confound the ratio you're measuring. Keep those preparation notes matched to the batch Certificate of Analysis.