Benefits
Vitamin B3 activity without the niacin flush
Niacinamide is a full form of vitamin B3 and counts toward the daily requirement (16 mg for men and 14 mg for women, as niacin equivalents). Unlike nicotinic acid, it does not cause skin flushing. It also does not change cholesterol levels, because it does not act on the receptors behind nicotinic acid's effects on blood lipids.
Sun-damaged skin in high-risk dermatology patients
In a 12-month trial of 386 adults who had already had at least two non-melanoma skin cancers, 500 mg twice daily lowered the rate of new non-melanoma skin cancers by 23% and of actinic keratoses (rough sun-damage patches) by 11 to 20% versus placebo. The difference disappeared after people stopped. These were high-risk patients under dermatologist care, so the result is not evidence for people without that history.
Skin results in later trials and pooled analyses
A trial of the same dose in 158 organ-transplant recipients, stopped early because of slow recruitment, found no fewer skin cancers or actinic keratoses than placebo. Two meta-analyses disagree: one rated the overall reduction in skin cancers as moderate-certainty evidence, while a later one, pooling fewer trials, judged the evidence insufficient.
Skin immune response to UV light in healthy volunteers
In a crossover trial in healthy volunteers, one week of 500 or 1,500 mg daily lessened the drop in skin immune responses caused by low doses of simulated sunlight. Two later 30-day studies at 2,000 mg daily, with no placebo group, gave mixed results: no protection against UVB redness or DNA damage, and less UVA redness without less DNA damage. It is not a substitute for sunscreen.
Inner retinal function in eye-clinic studies
In two placebo-controlled crossover trials in people already treated for glaucoma (57 and 53 participants), 12 weeks at 1 to 3 g daily improved electrical signals from the inner retina, measured by electroretinography: on nicotinamide but not on placebo in one trial, and more than on placebo in the other. Visual-field results were weaker, with a possible gain in one trial and no significant difference in the other.
NAD+ precursor role
The body converts niacinamide into NAD+, the coenzyme behind energy metabolism and DNA maintenance. In a 14-day trial in 65 healthy adults, 500 mg daily caused only a brief rise in blood NAD+ markers after each dose and did not raise circulating NAD+ over two weeks, unlike nicotinamide riboside (NR) and NMN at 1 g daily.
Mechanism of action
Feeds the NAD+ salvage pathway
Absorbed niacinamide is converted into NAD+ and NADP+, coenzymes that carry electrons in energy metabolism and that DNA-repair and signalling enzymes consume. The liver methylates any excess into N1-methyl-nicotinamide and related compounds, which are excreted in urine. In a human trial, a daily dose caused only a brief rise in blood NAD+ markers rather than a sustained one.
Supports skin-cell energy and DNA repair after UV (lab work)
In skin cells grown in the lab and in donated human skin samples, nicotinamide helped cells keep up their energy supply after UV exposure and sped the repair of two types of UV-induced DNA damage. These are laboratory findings; a later study in healthy volunteers taking 2,000 mg daily did not detect less UV-induced DNA damage in skin.
No action on the niacin lipid receptor
Nicotinic acid changes blood lipids by binding specific receptors and also causes flushing. Niacinamide does not bind the receptors behind the lipid effects and does not cause flushing, which is why it has a different benefit and side-effect profile from niacin and is not a cholesterol treatment.
Clinical trials
Phase 3, double-blind, randomized, placebo-controlled trial of nicotinamide 500 mg twice daily for 12 months, with dermatologist skin checks every 3 months for 18 months; funded by Australia's National Health and Medical Research Council (Chen et al. 2015, N Engl J Med).
386 Australian adults who had had at least two non-melanoma skin cancers in the previous 5 years.
At 12 months the rate of new non-melanoma skin cancers was 23% lower than placebo (95% CI 4 to 38, P=0.02). Basal-cell carcinomas were 20% lower (not significant, P=0.12) and squamous-cell carcinomas 30% lower (P=0.05). Actinic keratoses were 11 to 20% lower at each 3-month check. Adverse events were similar, and there was no benefit after the tablets were stopped. A high-risk patient group, not evidence for healthy people.
Phase 3, randomized, placebo-controlled trial of nicotinamide 500 mg twice daily for 12 months; stopped early because of poor recruitment (Allen et al. 2023, N Engl J Med).
158 immunosuppressed solid-organ transplant recipients who had had at least two keratinocyte skin cancers in the past 5 years.
There were 207 new keratinocyte cancers on nicotinamide and 210 on placebo (rate ratio 1.0, 95% CI 0.8 to 1.3, P=0.96). Squamous-cell, basal-cell and actinic keratosis counts and quality of life also did not differ. Adverse events and blood and urine tests were similar in both groups. The primary outcome was null.
Systematic review and meta-analysis of randomized controlled trials of nicotinamide by any route and for any indication, searched to October 2020 (Mainville et al. 2022, J Cutan Med Surg).
29 trials with 3,039 patients overall; 5 trials (552 patients) reported skin-cancer counts.
Nicotinamide was linked to fewer skin cancers than control (rate ratio 0.50, 95% CI 0.29 to 0.85; moderate strength of evidence, with heterogeneity explained by risk of bias). Effects on actinic keratoses and melanoma were not significant. Digestive side effects were more common with nicotinamide (risk ratio 1.78, very low certainty), while skin and laboratory side effects did not differ from control. A later meta-analysis that pooled fewer trials found the skin-cancer evidence insufficient.
Randomized, double-blind, placebo-controlled crossover study using the Mantoux skin-immunity model after low-dose solar-simulated UV on 3 consecutive days (Yiasemides et al. 2009, Carcinogenesis).
Healthy volunteers taking nicotinamide (500 or 1,500 mg daily) or placebo for 1 week each.
On placebo, UV suppressed the skin's immune reaction in a dose-dependent way; both nicotinamide doses significantly reduced this suppression, with no effect on immune reactions in skin that was not irradiated. Nicotinamide was well tolerated. This is a short experimental skin measure, not a test of sunburn or skin health over time.
Double-masked, randomized, placebo-controlled crossover trial at two tertiary eye centres, with no washout between periods (Hui et al. 2020, Clin Exp Ophthalmol).
57 people diagnosed with and already treated for glaucoma; nicotinamide 1.5 g/day for 6 weeks then 3.0 g/day for 6 weeks, or placebo.
The main electroretinogram measure (PhNR Vmax) improved by 14.8% within the nicotinamide period (P=0.02) versus 5.2% within the placebo period (not significant), and the Vmax ratio by 12.6% versus 3.6%. In visual-field testing, 27% improved by at least 1 dB on nicotinamide and fewer worsened than on placebo (P=0.02), which the authors called a trend. Short-term functional measures in patients on standard treatment, not evidence of slowed disease.
Double-masked, placebo-controlled, randomized crossover trial without washout; funded by Hanlim Pharm, and one co-author is a named inventor on a patent for nicotinamide treatment in glaucoma (Ha et al. 2026, Br J Ophthalmol).
53 people with normal-tension glaucoma already on eye-pressure-lowering treatment; nicotinamide 1 g/day for 6 weeks then 2 g/day for 6 weeks, or placebo.
After 12 weeks, two electroretinogram amplitudes (PhNR peak-to-trough and B-wave) rose more on nicotinamide than placebo (P=0.045 and P=0.032). Visual-field measures (mean deviation, pattern standard deviation and visual field index) did not differ between groups. Small, short and in patients.
Randomized, open-label, placebo-controlled study by Nestle researchers comparing three NAD+ precursors over 14 days (Christen et al. 2026, Nat Metab).
65 healthy adults (mean age about 35) analysed; nicotinamide 0.5 g/day (17 people), NR 1 g/day, NMN 1 g/day or placebo.
After 14 days, NR and NMN raised circulating NAD+ to a similar degree, but nicotinamide did not. Nicotinamide was the only precursor that acutely and briefly changed the whole-blood NAD+ metabolome after a dose. Each nicotinamide dose also briefly raised blood homocysteine, which the authors linked to its methylation. Industry-run and open-label, and it measured blood markers, not health outcomes.
Randomized, double-blind, placebo-controlled trial in 18 European countries, Canada and the USA testing modified-release nicotinamide 1.2 g/m2 of body surface per day for 5 years (Gale et al. 2004, Lancet).
552 first-degree relatives of people with type 1 diabetes who had islet-cell antibodies but normal glucose tolerance.
Diabetes developed in 82 people on nicotinamide and 77 on placebo (adjusted hazard ratio 1.01, P=0.97), so the primary outcome was null. Serious adverse events did not differ between groups, and nicotinamide did not affect children's growth or first-phase insulin secretion. Its main value here is long-term safety data at gram doses.