Nicotinamide Adenine Dinucleotide, NAD+
Evidence Grade B — Strong clinical evidence. 45893 published studies, 14513 human. 247 registered clinical trials.
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+.
45,893 published studies: 14513 human, 14654 animal, 5335 in-vitro, 4178 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.
Shared Decision Making for Antipsychotic Medications
Neoadjuvant Letrozole in Postmenopausal Women With Hormone Receptor-Positive, HER2-Negative, Node Positive, Early-Stage Breast Cancer.
NAD Augmentation to Prevent or Reverse Alzheimer's Disease in People With Down Syndrome
Validation of NAD+ Measurements for Human Clinical Studies
Brain NAD in Alzheimer's Disease
EMA Marketing Authorisation
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.
Exenatide was the first GLP-1 receptor agonist approved anywhere, reaching the market as Byetta in April 2005. The once-weekly formulation Bydureon followed in 2012. Clinical trials showed blood sugar reductions (HbA1c) of 1.6–1.9% and modest weight loss of 2–4 kg. The EXSCEL cardiovascular outcomes trial, involving over 14,700 patients, showed a trend toward cardiovascular benefit but narrowly missed statistical significance. While exenatide was groundbreaking as the first in its class, it has been largely overtaken by newer GLP-1 treatments that offer greater efficacy, less frequent dosing, and proven cardiovascular benefits. It remains available and in clinical use, particularly in combination products.
Lixisenatide was marketed as Adlyxin in the US (approved July 2016), though it has since been discontinued in the US market. The ELIXA cardiovascular trial, involving over 6,000 patients, was the first cardiovascular outcomes trial for any GLP-1 medication to report results. It showed a neutral cardiovascular profile — neither harmful nor beneficial — meeting safety requirements but not demonstrating the heart benefits later shown by semaglutide and liraglutide. Lixisenatide found its primary clinical role in combination with basal insulin, marketed as Soliqua (lixisenatide plus insulin glargine). This combination addresses both fasting blood sugar (via insulin) and post-meal spikes (via lixisenatide) in a single daily injection. As a standalone treatment, it has been largely superseded by more potent GLP-1 medications.
Pramlintide is marketed as Symlin (approved March 2005) and remains the only approved amylin-based treatment. It is used alongside mealtime insulin in both type 1 and type 2 diabetes. Clinical trials showed modest blood sugar improvements (HbA1c reductions of 0.2–0.6%) and approximately 2.3 kg of weight loss — less dramatic than GLP-1 treatments but meaningful as an add-on therapy. Symlin carries a boxed warning for severe hypoglycaemia, particularly when combined with insulin, and requires careful dose adjustment. Practical uptake has been limited by the need for separate injections at each meal alongside existing insulin injections. Despite its modest clinical impact, pramlintide remains the only medication that addresses the amylin deficiency in diabetes, filling a distinct biological role that GLP-1 treatments do not cover.
