Evidence Grade B — Strong clinical evidence. 46332 published studies, 14665 human. 236 registered clinical trials.
Medically reviewed by a licensed medical professional
NAD+ is a molecule essential for cellular energy production — it is not a peptide. It is included in this database because NAD+ precursors (NMN, NR) and intravenous NAD+ infusions are commonly encountered alongside peptide compounds in longevity and wellness markets. While NAD+ biology is well-established in basic science, no pharmaceutical has been approved for any therapeutic use of NAD+.
NAD+ (Peptide-Adjacent) is also known by these brand and alternate names:
46,332 published studies: 14665 human, 14710 animal, 5404 in-vitro, 4250 reviews
NAD+ has no pharmaceutical marketing authorisation for any therapeutic indication. Meta-analyses of NMN (an NAD+ precursor) randomised controlled trials have found that while supplementation elevates blood NAD+ levels, clinically relevant outcomes were not significantly different from placebo across metabolic endpoints.
NAD+ biology is well-established in basic science. The gap between established biochemistry and clinical therapeutic benefit remains unresolved. NAD+ is not a peptide. Intravenous NAD+ infusions marketed through wellness clinics have not been evaluated in rigorous clinical trials.
NAD+ is a well-characterised coenzyme that participates in hundreds of cellular reactions. Its role in energy metabolism is established biochemistry. The therapeutic hypothesis is that restoring declining NAD+ levels with age may improve cellular function, but this hypothesis has not been validated through clinical outcomes in human trials.
Research suggests that NMN and NR supplements consistently raise blood NAD+ levels across multiple randomised trials. However, the translation from striking animal results to human clinical benefit has been disappointing — two 2024 meta-analyses explicitly cautioned against exaggerated benefit claims, finding that clinically relevant outcomes were not significantly different from placebo across metabolic endpoints. Most human trials are small (20-80 participants), short (2-16 weeks), and show high individual variability. No large-scale trial (over 500 participants) exists, and no data extend beyond 6 months. Safety appears favourable for oral supplementation. A theoretical cancer concern exists because rapidly dividing cells (including cancer cells) also require NAD+. Intravenous NAD+ infusions marketed through wellness clinics have not been evaluated in rigorous trials.
PeptideTrace tracks 236 registered clinical trials for NAD+ (Peptide-Adjacent) sourced from ClinicalTrials.gov.
Shared Decision Making for Antipsychotic Medications
Validation of NAD+ Measurements for Human Clinical Studies
Edaravone Dexborneol for Post-Stroke Epilepsy
Neoadjuvant Letrozole in Postmenopausal Women With Hormone Receptor-Positive, HER2-Negative, Node Positive, Early-Stage Breast Cancer.
Research On Nicotinamide Riboside Supplement Support in MDS (ROSS Trial)
EMA Marketing Authorisation
NAD+ (nicotinamide adenine dinucleotide) is a dinucleotide coenzyme, not a peptide, included in peptide databases due to overlapping markets. Its molecular weight is 663.43 Da with molecular formula C21H27N7O14P2 (CAS 53-84-9). NAD+ exists in oxidized (NAD+) and reduced (NADH) forms. Circulating NAD+ has a very short plasma half-life (approximately 30 minutes). Key precursors include NMN (nicotinamide mononucleotide, MW 334.22 Da) and NR (nicotinamide riboside, MW 255.25 Da). NAD+ levels decline with age, and this decline is implicated in aging-related metabolic dysfunction.
NAD+ is an essential substrate for sirtuins (SIRT1-7), NAD+-dependent protein deacetylases that regulate mitochondrial biogenesis, DNA repair, inflammation, and stress resistance. SIRT1 deacetylates PGC-1alpha, p53, NF-kB, and FOXO transcription factors. NAD+ is consumed by poly(ADP-ribose) polymerases (PARP1/PARP2) during DNA repair and by CD38, a major NADase whose expression increases with age. In the electron transport chain, the NAD+/NADH couple shuttles electrons through Complex I. Biosynthesis occurs through salvage (nicotinamide via NAMPT to NMN to NAD+), Preiss-Handler (nicotinic acid), and NR kinase (NRK1/NRK2) pathways.
A meta-analysis of 12 NMN RCTs (Zhang et al. 2024, N=513) found NMN elevated blood NAD+ but concluded most clinically relevant outcomes were not significantly different from control. A second meta-analysis (Chen et al. 2024, 8 NMN RCTs, N=342) found no significant benefit on fasting glucose, insulin, HbA1c, HOMA-IR, or lipids. Yoshino et al. (2021, Science, N=25) showed 25.5% increased muscle insulin sensitivity with 250 mg NMN/day (p=0.04). Martens et al. (2018, Nature Communications, N=24) showed NR at 1000 mg/day increased whole blood NAD+ by approximately 60%. A direct IV NAD+ pilot (2024) found that NAD+ IV failed to alter whole blood NAD+ levels, while NR IV successfully raised them.
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
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Linaclotide is marketed as Linzess (approved August 2012). It is taken as a daily oral capsule on an empty stomach, at least 30 minutes before the first meal. The recommended dose is 290 mcg for IBS-C and 72 or 145 mcg for chronic constipation. In clinical trials, approximately 34% of IBS-C patients met the composite improvement endpoint compared to 17% on placebo. Diarrhoea is the most common side effect (approximately 20%) and the leading reason for discontinuation. Linaclotide has a boxed warning against use in children under 6 years due to deaths in young mice, though no such events have been reported in humans. It competes with plecanatide (which targets the same pathway) and other IBS-C treatments.
Elamipretide (Forzinity) was approved by the FDA for Barth syndrome based on the TAZPOWER trial. The randomised crossover phase (12 patients) did not meet its primary endpoints, but the open-label extension (168 weeks) demonstrated durable improvements in walking distance and muscle strength that formed the basis for approval. Barth syndrome affects approximately 1 in 300,000–400,000 births. A larger Phase III trial in primary mitochondrial myopathy (218 patients, MMPOWER-3) did not meet its primary endpoint, and the drug was not approved for that broader indication. Elamipretide remains approved exclusively for Barth syndrome. See also SS-31 (#158) for the research compound context.
Palopegteriparatide is marketed as Yorvipath (Ascendis Pharma, approved August 2024). It is the first FDA-approved PTH replacement therapy for hypoparathyroidism, a condition that previously had no approved hormone replacement and was managed only with high doses of calcium supplements and active vitamin D — an approach that does not fully normalise calcium metabolism. In the PaTHway trial, 79% of patients achieved independence from calcium and active vitamin D supplements while maintaining normal blood calcium levels, compared to 5% on placebo. This represents a fundamental shift in managing hypoparathyroidism — from supplementation to actual hormone replacement. Patients also showed improvements in kidney function markers and bone metabolism parameters.
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This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.
