NAD+ (nicotinamide adenine dinucleotide) — safety
Adverse events as reported, contraindications, warnings, and an explicit statement of what the safety evidence does not establish.
§4Safety
§4.1Adverse events reported in controlled trials
Table 4. Adverse events for NAD+ (nicotinamide adenine dinucleotide) as reported in the trial safety tables the Institute holds. Percentages are of randomised participants in the stated trial and arm.
| Event | Active, % | Comparator, % | Difference, pp | Source |
|---|---|---|---|---|
| Infusion-related chest tightness, nausea and cramping | — | — | — | Consistently reported with rapid intravenous infusion and the reason infusions are given slowly over hours |
| Flushing | — | — | — | Reported |
| Injection-site pain | — | — | — | Reported with subcutaneous administration |
| Sterility and endotoxin risk | — | — | — | Compounded intravenous preparations of a non-pharmacopoeial substance carry the sterility, endotoxin and particulate risks of any unlicensed parenteral |
| A difference column is computed by the Institute from the two reported percentages and is not itself a published figure. Confidence intervals for adverse-event differences are not reported in the contributing trials and are not constructed here. | ||||
§4.2Contraindications
- Not established — no marketing authorisation as a parenteral medicine
§4.3Warnings and precautions
- Intact NAD+ does not enter cells; the mechanistic premise of administration is questionable
- Compounded parenteral preparations carry sterility, endotoxin and particulate risks
- Evidence for oral precursors should not be transferred to parenteral NAD+
§4.4What this section does not establish
Related assessments: tolerability of incretin receptor agonists · acute pancreatitis · the rodent thyroid C-cell signal.[1,2]
References cited on this page
References are numbered in order of first citation in this document. Each superscript in the text links to its entry below.
- Lee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, Cohen P. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism 2015;21(3):443–454. doi:10.1016/j.cmet.2015.02.009 · PMID 25738459
- Szeto HH. First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. British Journal of Pharmacology 2014;171(8):2029–2050. doi:10.1111/bph.12461 · PMID 24117165
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