
NAD+ dosage numbers in circulation almost always describe something other than the product being sold. The trials that generated them mostly administered oral precursors, principally nicotinamide riboside and nicotinamide mononucleotide, not injected NAD+, and a figure produced by an oral capsule does not transfer to a vial.
The vendor we point lifters to
NAD+ from Ascension Peptides
Independently assayed material, dispatched from the US. The vial drops by half with the code below.
Quoted per 100 mg because NAD+ is dosed in hundreds of milligrams, not the single milligrams a peptide vial holds. Buying 3, 5 or 10 takes 3%, 5% or 10% off the list price. Free shipping starts at $250.
- Two independent lab reports per batch
- Free delivery above $250
- Same-day dispatch on orders before 2pm CST
Research material, laboratory use only, not for human consumption. Affiliate links: we may earn a commission at no extra cost to you. Pricing verified August 20, 2026.
That is not a technicality. It is the single most important thing to understand about this compound, and it survives every other detail on this page.
Injected NAD+ has a far thinner evidence base than the size of the NAD literature suggests, and neither form has a muscle mass or strength outcome behind it in any species.
Three different products share one abbreviation
Search results collapse three separate things into one word.
The first is oral precursor supplementation: nicotinamide riboside or nicotinamide mononucleotide taken as a capsule, converted inside the body toward NAD+ through the salvage pathway. This is where nearly all of the human trial work sits.
The second is intravenous NAD+, delivered as a slow infusion in a clinic over hours. Different molecule entering the body, different route, and a much smaller published record.
The third is subcutaneous injection of NAD+ from a vial bought as research material. This has the thinnest record of the three, and no regulator has approved any injected NAD+ product as a medicine.
An amount that means something for the first tells you nothing about the second or third.
NAD+ dosage figures and what each one was measuring
| Intervention | Route | What human trials have measured | Muscle mass or strength outcome | Organism |
|---|---|---|---|---|
| Nicotinamide riboside | Oral | Blood NAD+ metabolite levels, tolerability, assorted metabolic markers | None reported | Human |
| Nicotinamide mononucleotide | Oral | Blood NAD+ metabolite levels, tolerability, some functional measures | None reported | Human |
| NAD+ by intravenous infusion | Intravenous | Very little in controlled trials; mostly clinic reports and small studies | None reported | Human |
| NAD+ by subcutaneous injection | Subcutaneous | Effectively nothing published in controlled form | None reported | Human |
| NAD+ manipulation in rodent models | Various | Mitochondrial and metabolic endpoints | Not a muscle mass endpoint | Mouse |
The right hand column is the same all the way down, and it is the column this site exists to ask about.
What the oral precursor trials actually established
They established one thing well: taking nicotinamide riboside or nicotinamide mononucleotide orally raises NAD+ related metabolites measured in blood in humans. That result has been reported repeatedly and is not seriously contested.
They established a second thing reasonably well: at the amounts used, both were generally tolerated in the trial populations, which is a statement about those populations over those durations rather than a general safety claim.
What they did not establish is that the raised measurement produced a functional benefit. Reported outcomes across this literature have been inconsistent, and where trials in older adults looked directly at skeletal muscle rather than blood, the picture was noticeably less impressive than the blood result. Some of that work reported that blood NAD+ metabolites rose while effects inside muscle were limited or absent.
For a reader whose interest is ageing muscle, that is the finding to carry away, and it comes from oral precursors in humans.
How a supplement label became an injection number
The path is short and entirely undocumented, which is why it is worth spelling out.
A trial administers an oral precursor and publishes the amount. A supplement manufacturer prints a comparable amount on a label, which is legitimate for an oral product. A forum post then discusses that amount alongside injectable NAD+, because both are filed mentally under the same three characters. A vendor listing quotes something in the same neighbourhood. By the fourth step, a figure generated by a capsule of a different molecule is being repeated as guidance for a syringe.
Nothing in that chain involved a study of the injected form, and no step in it was dishonest. Each transfer just dropped a qualifier, and the qualifiers were the informative part.
This is why the sentence "NAD+ has been studied extensively in humans" is misleading rather than false. The literature is genuinely large. Most of it is about precursors taken by mouth, and the person reading that sentence is usually holding a vial.
What injected NAD+ has behind it
Much less, and the gap is not a matter of degree.
The mechanistic question is unresolved. NAD+ is a large, charged dinucleotide, and there is published biochemistry arguing that extracellular NAD+ is broken down by cell surface enzymes into smaller pieces, including nicotinamide riboside and nicotinamide, before anything is taken up. If that is what happens, injecting NAD+ delivers precursors by an expensive route rather than delivering NAD+ into cells.
That is a mechanistic argument, not a settled finding, and it should be read as one. But it means the case for injection cannot simply borrow the oral precursor trials, since those trials would then be describing a partly overlapping intervention at best.
No approved injected NAD+ product exists. There is no label, no defined amount and no regulator who has judged the balance.
Why no figure here is aimed at muscle
No trial of oral precursors or of injected NAD+, in any species, has reported an increase in muscle mass or in strength as an outcome. Not a small effect, not a mixed effect. The endpoint was largely not chosen, and where muscle was examined the interesting results concerned mitochondrial and metabolic measures rather than tissue mass.
There is also nothing in the mechanism that would predict growth. NAD+ is a coenzyme in energy metabolism and a substrate for enzymes including sirtuins and PARPs. It is not a signal that instructs muscle to enlarge, and it has no described relationship with myostatin, satellite cell activity or muscle protein synthesis.
The plausible story for this audience is narrower and worth keeping: mitochondrial function matters to training capacity and it declines with age in humans. Whether raising a blood measurement changes anything inside an ageing muscle fibre is exactly what the human work has struggled to demonstrate.
The one input with muscle evidence behind it
There is a version of this subject with real human data attached, and it is not for sale.
Skeletal muscle maintains its own NAD+ supply largely through the salvage pathway, and exercise training has been reported in humans to increase expression of the salvage pathway enzyme NAMPT in skeletal muscle. In other words, the intervention with the best evidence for acting on muscle NAD handling is training, in the tissue that matters, measured directly.
That is not a reason to be smug about it, and it is not a claim that training makes supplementation pointless, because nobody has tested the combination properly. It is a reason to be precise about what is established and what is being sold. A lifter asking about an amount of injected NAD+ already performs, weekly, the intervention with the stronger evidence in the relevant tissue.
It also reframes the dosage question. Before asking how much of something to inject, it is worth asking what measurable problem the injection is meant to solve, and whether anyone has shown it solves it.
What would have to exist for an amount to mean anything
A trial of the injected form specifically, since that is what is being sold. A controlled design with a placebo group, since anything involving perceived energy is highly susceptible to expectation. Skeletal muscle as the tissue examined rather than blood, because the blood result is already known and has not predicted the muscle one. Body composition and strength as endpoints. And a dose ranging structure, so that an amount could be attached to an effect rather than to a habit.
None of that exists. Until it does, any number quoted for this compound is a description of what someone did, not evidence of what it achieved.
Questions about these figures
Is there an established NAD+ dose for injection?
No. There is no approved injected NAD+ product in any market, so there is no established amount, no label and no defined population.
Do the oral precursor amounts convert to an injection?
No. They describe a different molecule taken by a different route, and the conversion steps inside the body differ. Treating one as a guide to the other is the specific error this page exists to flag.
Does raising blood NAD+ mean the amount worked?
It means the marker moved. Trials in humans have shown blood NAD+ metabolites rise with oral precursors while muscle level effects were limited, so the marker has already failed once as a proxy for the outcome people want.
Would more of it do more for muscle?
There is no muscle outcome to scale. No trial of either form in any species has reported muscle mass or strength as a result, so there is no dose response curve to be on.
Does a clinic infusion schedule count as a protocol?
It counts as a description of what that clinic does. Clinic practice is not trial evidence, and slow infusion rates in that setting exist mainly to manage the discomfort the infusion itself causes.