Educational reference, not medical advice. This page summarizes information from published research and regulatory filings for educational purposes. It is not a recommendation to use any compound and should not replace guidance from a licensed healthcare provider. Most peptides discussed here are not approved for the uses described.
What it is
NAD+ — nicotinamide adenine dinucleotide — is not a peptide. It is a coenzyme made of two nucleotides (one carrying adenine, the other nicotinamide) joined through their phosphate groups. It is included in this library because injectable and intravenous NAD+ have become a common adjunct in the same longevity and recovery clinics that handle peptides, and the reconstitution mechanics overlap.
NAD+ is the principal electron carrier in cellular metabolism and a required substrate for the sirtuin family of enzymes, the poly(ADP-ribose) polymerases (PARPs), and the CD38 ectoenzyme. Tissue NAD+ levels decline with age in most measured tissues, which is the central rationale for NAD+ supplementation strategies.
History
Arthur Harden and William John Young first isolated the coenzyme in 1906, calling it a "coferment" of yeast fermentation. Its modern name and structure were established in the 1930s by Otto Warburg, Hans von Euler-Chelpin, and others.
The injectable use that drives most current interest traces to the 1960s, when Paul O'Hollaren published case-series reports of intravenous NAD+ for opioid and alcohol withdrawal. That work remained on the fringe of mainstream medicine for decades. Interest revived in the 2010s alongside the broader sirtuin-and-longevity research wave led by David Sinclair's group at Harvard, Shin-ichiro Imai's group at Washington University, and others. Oral precursors (nicotinamide riboside, nicotinamide mononucleotide) are now widely sold as supplements; injectable NAD+ itself is handled through compounding pharmacies.
Regulatory status
NAD+ injection is not an FDA-approved drug. Compounded NAD+ is prepared by 503A pharmacies under physician orders, but its bulk substance status has been contested. In 2020 the FDA placed NAD+ on a list of substances under review for inclusion or exclusion from the 503A bulks list; as of the most recent guidance the status remains unsettled. The FDA has issued warning letters to compounding pharmacies marketing NAD+ for addiction recovery, anti-aging, and neurodegenerative indications. NAD+ is not licensed for medical use in the United Kingdom.
How researchers describe its action
The biochemistry is well established. NAD+ shuttles electrons in glycolysis, the citric acid cycle, and oxidative phosphorylation; it is consumed (not catalytically recycled) by sirtuins, PARPs, and CD38. The therapeutic hypothesis is that age-related NAD+ decline limits these consumer enzymes' activity, and that restoring NAD+ — by precursor supplementation or direct administration — improves mitochondrial function, DNA repair, and metabolic flexibility.
A 2019 pilot study from Grant and colleagues directly measured plasma and urine NAD+ metabolites during a 6-hour intravenous NAD+ infusion in healthy volunteers and found that the parent molecule appeared in urine essentially intact, with downstream metabolites rising in plasma — suggesting most administered NAD+ is broken down to constituent nucleotides before tissue uptake. This is the central uncertainty around the modality: whether direct NAD+ infusion delivers a meaningful advantage over oral precursors.
Half-life and dosing intervals
Published estimates of intracellular NAD+ half-life vary by compartment: roughly 1 to 4 hours overall, 2 hours in cytoplasm, and 4 to 6 hours in mitochondria. Circulating NAD+ after infusion is cleared rapidly — within minutes to hours.
In clinic settings, NAD+ is most often given as a slow intravenous infusion: 250 to 1000 mg over 2 to 8 hours, with the slow rate driven by the flushing, chest pressure, and gastrointestinal sensation reported at faster rates. Subcutaneous compounded NAD+ is also sold for at-home use at doses of 50 to 200 mg per injection, typically daily or several times per week. Subcutaneous use is not supported by published pharmacokinetic data on tissue distribution.
Reconstitution example
Compounded NAD+ for subcutaneous use is supplied lyophilized in vials of 100 mg to 1000 mg, or pre-formulated in a multi-dose vial with bacteriostatic water. A 500 mg lyophilized vial reconstituted with 5 mL of bacteriostatic water yields 100 mg/mL. On a 1 mL U-100 insulin syringe, 50 units (0.5 mL) delivers 50 mg. Vial's calculator handles the conversion when vial mass and water volume are entered.
What to know
- Not a peptide. NAD+ is a dinucleotide coenzyme. It is included here because it shares administration channels with peptide protocols.
- Infusion side effects are common. Flushing, chest tightness, abdominal cramping, and dyspnea during fast infusion are dose-rate dependent and resolve when the rate is slowed.
- Tissue delivery is uncertain. Most administered NAD+ appears to be metabolized to nucleotide precursors before tissue uptake; whether infusion meaningfully outperforms oral nicotinamide riboside or NMN remains an open clinical question.
- Regulatory status is unsettled. Compounded NAD+ is sold widely but is not an FDA-approved drug, and the bulks list status has been under review.
- Storage. Lyophilized vials: refrigerate, protect from light. Reconstituted: refrigerate; degradation accelerates at room temperature and the solution may yellow.
Sources
- 1.Rajman L, Chwalek K, Sinclair DA (2018). Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. Cell Metabolism.
- 2.Grant R et al. (2019). A Pilot Study Investigating Changes in the Human Plasma and Urine NAD+ Metabolome During a 6 Hour Intravenous Infusion of NAD+. Frontiers in Aging Neuroscience.
- 3.Yoshino J, Baur JA, Imai SI (2018). NAD+ Intermediates: The Biology and Therapeutic Potential of NMN and NR. Cell Metabolism.
- 4.Conlon N, Ford D (2022). A systems-approach to NAD+ restoration. Biochemical Pharmacology.