NAD+ Injection (500 mg): What It Is, Where to Get It Prescribed, and What It Costs

Pepti supplies NAD+ as an injection in two vials. Both are 10 mL with the same directions: 0.83 mL, three times a week. The difference is what is dissolved in each millilitre. The standard NAD+ Injection is 100 mg/mL, so a 0.83 mL dose carries 83 mg of NAD+. This vial is 50 mg/mL, so the same 0.83 mL carries 41.5 mg: half the milligrams per injection, everything else unchanged.

That is the whole product difference. The 500 mg vial exists so a physician has a lower per-dose amount to prescribe without changing how the medication is drawn or given, and it is priced lower because it contains half as much active ingredient.

NAD+ is nicotinamide adenine dinucleotide. It is not a peptide. It is a coenzyme — two nucleotides joined through a pyrophosphate bridge, one carrying nicotinamide, a form of vitamin B3, the other adenine. Every living cell makes it and uses it continuously. It sits alongside the peptides on this site because it is compounded and prescribed the same way, not because it is one.

The body makes it from tryptophan, from niacin, and — the main route in adult tissue — by recycling nicotinamide through nicotinamide mononucleotide (NMN); nicotinamide riboside (NR) is another entry into that loop. NMN and NR are the "precursors" sold as supplements, and most of the human trial literature is about them.

It is not a vitamin, though it is built from one. It is not a hormone, a growth factor or a stimulant, and it does not bind a receptor the way a peptide does. It is not NMN or NR, so precursor results cannot simply be transferred to it. It has no approved indication for any disease. And it is not a "starter" product in any clinical sense: nothing in the literature describes a loading phase or threshold for NAD+ injection. It is a lower-dose presentation, and whether a lower dose is right for you is a physician's judgement.

The plus sign marks the oxidised form. NAD+ collects electrons from the breakdown of glucose and fatty acids, becomes NADH, and hands them to the mitochondrial electron transport chain, where ATP is made — then it is NAD+ again, thousands of times a second. This is textbook metabolism, and why extreme deficiency, pellagra, is a recognised disease. The injection contains the oxidised form.

Sirtuins are seven enzymes, SIRT1 to SIRT7, that remove acetyl groups from proteins and consume one NAD+ each time they act. A 2015 review in Science by Verdin set out the case, from animal and cell work, that declining NAD+ with age constrains sirtuin function — a mechanism argument, not a human outcome. PARP enzymes respond to DNA damage by assembling chains of ADP-ribose at the break, each unit costing one NAD+; a 2017 review in Trends in Molecular Medicine by Fang and colleagues describes how PARPs and sirtuins draw on the same limited pool, so heavy repair demand can starve mitochondrial maintenance in cells and in animal models of accelerated ageing. The pool is also reported to shrink with age: a 2012 study in PLOS ONE by Massudi and colleagues measured NAD+ in human skin across age groups and reported lower NAD+ and higher oxidative-stress markers in older tissue. That is human data, and it is observational — it shows the decline exists, not that reversing it changes anything.

NAD+ is a large, charged molecule and does not simply diffuse into cells. The only published study of NAD+ given directly to people — a 2019 pilot in Frontiers in Aging Neuroscience by Grant and colleagues, a six-hour intravenous infusion in healthy participants — reported that plasma NAD+ and its metabolites did not rise at all for the first two hours: the molecule was cleared as fast as it arrived, with a metabolite profile consistent with the enzymes that break NAD+ down. The likeliest reading is that injected NAD+ is broken down outside cells into fragments, including nicotinamide and NMN, which tissues rebuild through the same salvage pathway a precursor uses. That is a hypothesis from one small study; nothing equivalent exists for the subcutaneous route at either strength.

The trials are mixed. A 2018 trial in the American Journal of Clinical Nutrition by Dollerup and colleagues gave 40 obese, insulin-resistant men NR or placebo for 12 weeks and reported no improvement in insulin sensitivity, glucose metabolism, energy expenditure or body composition. A 2021 trial in Science by Yoshino and colleagues gave postmenopausal women with prediabetes NMN or placebo for 10 weeks and reported increased skeletal-muscle insulin sensitivity on clamp testing — positive, in a small selected group. A 2023 GeroScience trial in 80 healthy middle-aged adults compared 300, 600 and 900 mg of daily NMN with placebo over 60 days and reported dose-dependent rises in blood NAD+, with six-minute walk distances higher than placebo in all three dose groups. Beyond metabolism, the NADPARK study in Cell Metabolism 2022 reported raised brain NAD on MR spectroscopy in 30 newly diagnosed Parkinson's patients after 30 days of NR, with the clinical change described as mild, and the 2024 NICE trial in Nature Communications reported a 17.6-metre between-group difference in six-minute walk distance in 90 people with peripheral artery disease after six months of NR, with a confirmatory trial called for. In sum: precursors reliably raise blood NAD+; functional effects are small, inconsistent, and most visible in older or impaired participants.

For NAD+ given directly, the honest summary is short. There is the 2019 intravenous pilot, which measured what happens to the molecule in blood and urine and tested no clinical outcome. There are no randomised controlled trials of subcutaneous NAD+ injection in humans, at any strength, and no randomised trial of NAD+ by any injected route with a clinical endpoint.

• It does not establish that subcutaneous NAD+ injection raises tissue NAD+ in humans, by how much, or for how long.
• It does not establish a dose–response for injected NAD+. The only dose-ranging work is oral NMN; nobody has compared a 41.5 mg injection with an 83 mg one, or either with placebo.
• It does not establish an effect on fatigue, cognition, longevity or any ageing marker from injected NAD+. Where those endpoints were tested, the molecule was an oral precursor and the results were small and mixed.
• It does not establish efficacy for any condition as an approved treatment. NAD+ is not approved for anything.

Nicotinamide adenine dinucleotide (NAD) sits in Category 1 — "Bulk Drug Substances Under Evaluation" — of the FDA's list of substances nominated for the 503A bulks list, in the version updated 14 May 2026. Under the FDA's interim policy, the agency does not intend to take action against a compounder for compounding with a Category 1 substance while its evaluation is pending, provided the conditions in the guidance are met. That is the basis on which a state-licensed 503A pharmacy compounds NAD+ to a prescription today.

The nomination was for fatigue in multiple sclerosis. At the Pharmacy Compounding Advisory Committee meeting on 8 May 2017 the FDA's reviewers recommended against listing, citing the molecule's instability — it degrades with light, moisture, alkaline pH and room temperature — and the absence of published studies for that use, and the committee voted not to include it. A September 2019 proposed rule carried that position forward and has not been finalised for NAD as of September 2026, which is why the substance remains in Category 1.

On 15 April 2026 the FDA removed twelve peptides from Category 2, and on 23–24 July 2026 the advisory committee reviewed several of them. NAD+ was not among the twelve, because it was never in Category 2. Separately, on 30 October 2024 the FDA reminded compounders that food-grade NAD+ ingredients are not suitable for sterile injectable compounding without appropriate processing, after adverse-event reports consistent with excessive endotoxin. That is about ingredient sourcing, not NAD+ as a molecule; Pepti's sourcing and testing is on the quality page.

So the accurate description today is: nominated, under FDA evaluation, compoundable under the interim policy. It is not an FDA-approved drug product, and compounded medications never are.

The most consistently reported early experience is not a benefit but a sensation: flushing, tightness in the chest or abdomen, or nausea during the injection, fading within minutes. Prescribers describe it as tracking how much NAD+ enters the circulation and how fast — one practical reason a physician may choose the 500 mg vial for a first course, since at the same injection speed half the milligrams are arriving. Some people notice nothing at all on either vial. Neither says anything about the course.

If anything is reported subjectively, prescribers describe it in this window — usually a change in how tiring ordinary days feel, or in sleep. That is consistent with the precursor trials, where blood NAD+ was raised by day 30, and equally with placebo.

Because both vials share the same volume and schedule, changing the amount per dose means changing the vial, not the directions. Some prescribers describe a first course on the 500 mg vial and a decision at the first refill to continue, move to the standard 1,000 mg vial, or stop; others start on the higher strength. No published data favours either sequence. Stopping is uneventful: NAD+ has no receptor to downregulate and no feedback loop to suppress, so nothing in the literature describes withdrawal or rebound.

The directions are written in millilitres and in insulin-syringe units because that is what you can read off the barrel. 0.83 mL is 83 units on a U-100 syringe. You are not calculating anything — the number is printed on your medication, and it is the same on both NAD+ vials.

This is the one place the two vials part ways. At 50 mg/mL, 0.83 mL contains 41.5 mg of NAD+, about 125 mg a week; twelve doses use the 500 mg in the vial. At 100 mg/mL the identical draw contains 83 mg, about 250 mg a week. If you are switched between vials, your technique does not change; the label does. This product comes in one strength; the 1,000 mg and 2,000 mg strengths belong to the standard NAD+ Injection.

Subcutaneous means into the fat layer, not the muscle. Abdomen and thigh are the usual sites, rotated. With NAD+ specifically, prescribers consistently advise injecting slowly: the flushing and nausea described under safety track with how fast the molecule enters the circulation. The reaction is described as milder at this concentration, but slow injection is still the advice. Your directions will say.

12 doses at three times per week is four weeks, which is why refills run on a 28-day cycle. One vial per fill, always — not a stockpile. A 500 mg vial does not last longer than a 1,000 mg vial; both are used up in twelve draws.

Refrigerated, and it ships that way in insulated packaging with ice packs. Storage matters more than usual here: the FDA's own review describes the molecule as degrading with light, moisture, alkaline pH and room temperature. Keep it in the fridge, out of light, and follow the beyond-use date on the label, which runs from first puncture. How to store peptides covers the general rules.