The short version

Plain English first. Everything below this section is the same material with the sources, the numbers and the caveats attached.

What NAD+ is

Two nucleotides bolted together through their phosphates — adenine on one end, nicotinamide on the other. It is not a peptide, and that is a mechanical fact rather than a pedantic one. It sits in a peptide catalogue by market convention, not by chemistry.

Three consequences follow from not being a peptide, and they run through this whole page.

• Nothing about peptide handling transfers. There is no protease to worry about, no acetate or trifluoroacetate counterion question of the kind that afflicts most of this shelf, and no sequence to verify. The enzymes that destroy it are a glycohydrolase and a pyrophosphatase — they cut sugar and phosphate bonds, not peptide bonds.
• Charge and size are the barrier. Two phosphates plus a permanently charged ring is a large, heavily charged, highly polar molecule — the opposite of what drifts across a lipid membrane.
• The bonds that hold it together are the bonds that break. The chemical degradation products and the enzymatic degradation products are the same fragments. The molecule falls apart along the same two seams either way.

What a label saying “NAD+” is actually specifying

Two things worth knowing. Neither NAD+ nor NADH is the “active” form — they are two states of the same carrier, and marketing that calls one the energised form and the other the spent form is describing nothing. And they degrade under opposite conditions: NAD+ breaks down in alkaline solution, NADH in acidic. There is no single buffer that suits both, and a vendor giving identical storage advice for their NAD+ and their NADH has not read the chemistry.

What 1000 mg represents

1000 mg is 1,507.4 micromoles. If the vial is the monosodium salt rather than the free acid, it holds about 965.1 mg of NAD+ proper — a 3.5% shortfall, small but real, and the kind of thing a certificate should specify and usually does not.

The more interesting comparison is against physiology. Cytosolic NAD+ in a living cell is around 0.3 mmol/L. Reconstituted to the 200 mg/mL that compounded product is actually supplied at, this vial is 300 mmol/L — roughly a thousand times the concentration inside a cell, injected into the compartment outside it.

Our arithmetic from published weights and concentrations, not figures we found stated. The chemistry block rests on four concordant commercial and reference sources; the main chemical database would not render for us.

How it works, and why the route matters

This section is where the page turns, so start with what is not in dispute. NAD+ is the central redox carrier of metabolism. It drives ATP production. It is consumed as a substrate — not merely used as a catalyst — by sirtuins, by the PARP enzymes, and by CD38, which is why cells must continuously rebuild it. All of that is textbook and correct.

It is also entirely an argument about the inside of cells. The product is an injection into the outside.

Cells do not import finished NAD+

Unlike most questions in this library, this one has been tested directly. A 2019 experimental paper put NAD+ and each of its intermediates into human cell cultures and watched what happened to them:

The enzyme's active site points at the syringe

If you want one image for why injection is a strange route for this molecule, it is CD38. CD38 is an ecto-enzyme: it sits in the cell membrane with its catalytic site facing outward, into the extracellular space. Its apparent job is to police the concentration of exactly the molecules being injected. The review literature calls this the “NAD sink.”

And it is abundant in the compartment an infusion runs into: adult red blood cells express high levels of NAD+ glycohydrolase activity, and red cells are 40 to 45% of blood by volume. An intravenous NAD+ infusion runs directly into a suspension of cells coated in the enzyme that dismantles it. A second enzyme class attacks the other bond — the pyrophosphate bridge — so there is redundancy.

The twist that looks like a point for the marketing

A mammalian NAD+ transporter was identified, in Nature, in 2020. It is real, and the discovery date tells you how recently the field's basic transport questions were open.

One caveat we owe you. There is a published route by which intact NAD+ is reported to cross a plasma membrane — connexin 43 hemichannels, described in 2001. We could not open the paper and will not characterise its findings beyond the title. Two honest observations: those channels are large non-selective pores whose best-known role for NAD+ is efflux rather than uptake, and they are calcium-gated rather than constitutive. We mention it because the transporter literature is not quite uniformly negative, and saying so is more honest than pretending it is.

The line worth carrying

Pharmacokinetics

There is real human data here, and the one properly-run infusion study produced a result nobody would have designed for.

Six hours of infusion, and nothing happened for two of them

Eleven healthy men, NAD+ infused at 3 micromoles a minute for six hours. The finding, verbatim from the abstract:

By six hours, plasma NAD+ had risen about 398% over baseline — so something does eventually get through. Three readings, and the page owes you all three:

• The generous one. Given long enough, you can raise plasma NAD+ nearly fivefold. The infusion is not pharmacologically inert.
• The sceptical one. For the first two hours — longer than most commercial infusions run at all — the body erased it without a trace. A 500 mg drip over ninety minutes, on this data, plausibly produces no measurable change in plasma NAD+ whatsoever.
• The awkward one. Once plasma NAD+ finally did rise, NAD+ itself started appearing in the urine. That is not a picture of tissue uptake. It is a picture of overflow.

And the metabolite pattern confirms the mechanism from the other direction. What rose in parallel was nicotinamide and ADP-ribose — precisely the two halves you get when a glycohydrolase cuts NAD+ in two. The signature in human plasma is the CD38 signature.

Worth knowing about that study: its authors include the clinician behind the best-known commercial IV NAD+ protocol. They had every commercial reason to want a different result. That makes the two-hour finding more credible, not less.

The head-to-head, at half this vial's dose

One randomised, placebo-controlled study exists. It is a pharmacokinetic and tolerability study rather than an outcome trial — and it tested 500 mg intravenously, which is half of what this vial holds.

Caveats it deserves: a preprint, small, and funded by parties with an interest in the precursor. We are not burying it because it is the only randomised comparison anyone has run, and it points the same way as the mechanism and the same way as the infusion study.

On half-life: we could not source one, and we will not invent one

We searched specifically for a measured human plasma half-life and did not find one. A figure of “1 to 5 minutes” circulates on a commercial page with no citation we could follow. It is directionally consistent with everything else here and may well be about right — and we are not printing it, because we cannot source it.

What we can say instead, with a citation behind it: the only human infusion study found plasma NAD+ did not measurably rise for two hours of continuous infusion, and the metabolites that eventually appeared were the signature of the molecule being cut in half.

What the evidence shows

One rule governs this section and it has to be enforced without exception: NAD+ and its precursors are different products with different evidence bases, and almost every claim made for the injection is borrowed from trials of oral nicotinamide riboside or NMN.

For anti-ageing, energy, cognition or wellness: there is no controlled trial

Not a negative one. None. Two independent 2026 reviews say so:

The only randomised work involving IV NAD+ is the two pharmacokinetic and tolerability studies above, in both of which it came second.

For addiction and withdrawal — where the money is

This deserves care, because it is the claim most likely to reach someone vulnerable. The best-known protocol runs 500 to 1,500 mg a day, five to ten hours a day, for about ten consecutive days. Here is what sits under it:

A 2014 conference abstract. Sixty patients. Described by the operation itself as “retrospective pilot study (not randomized, not blinded, no control group).” Craving ratings fell from day 1 to day 10 on a self-report scale; 45% answered a follow-up survey a year or more later, reporting roughly halved relapse severity.

Where the real randomised evidence is: the oral precursors

Nicotinamide riboside has 25 published human clinical trials. This is a genuinely different evidential world, and being fair about it means being fair about the results too — which are more modest than the marketing.

The most careful critical review of the field puts it plainly: “oral nicotinamide riboside supplementation has displayed few clinically relevant effects” — with “an unfortunate tendency in the literature to exaggerate the importance and robustness of reported effects.”

Two figures worth recognising when you meet them. The famous “−9 mmHg blood pressure” result from NR is an uncorrected exploratory subgroup of thirteen people, in a trial whose actual cardiovascular outcomes were null. And NMN's eight-trial meta-analysis in 342 people found no significant effect on fasting glucose, insulin, HOMA-IR, HbA1c, triglycerides or cholesterol.

Parkinson's disease — the best work in the field, and it is all oral

A 30-patient randomised phase I of oral NR raised NAD+ in the brain measurable by magnetic resonance spectroscopy, with mild clinical improvement in the strongest responders. A 400-patient phase III of oral NR completed enrolment and was due to conclude in June 2025.

As of today we could not find published results from that phase III. We searched specifically. Treat it as pending, and do not let anyone imply the answer is known. And note: every trial in this programme is oral nicotinamide riboside. A vendor citing them in support of an injectable has changed both the molecule and the route.

Reconstitution

Two practical facts here, and neither appears on any protocol page we read.

Volume — use 5 mL

The rest of this section is why, because the number quoted everywhere for NAD+ is 50 mg/mL and it does not mean what it appears to. It comes from supplier product sheets, and the phrasing matters: “soluble in water (50 mg/ml), yielding a clear, colorless solution.” That is a tested working concentration, not a measured saturation point — and treating it as a ceiling gives the wrong answer, because licensed compounding pharmacies demonstrably supply NAD+ at 100 and 200 mg/mL.

pH — and a genuine formulation trap

The free acid at 50 mg/mL measures pH 3.0. The sodium salt at the same strength measures pH 4 to 6. Physiological pH is 7.4, so a pH 3 solution is roughly 25,000 times more acidic in hydrogen-ion terms.

Three things follow. It will sting, and the reason is ordinary acid irritation rather than anything exotic. The salt form changes the pH by up to three units, which is a thousandfold in hydrogen-ion concentration — so “free acid or sodium salt?” is the single most practically consequential unanswered question about any given vial.

Stability — and here, unusually, there is real data

A 43-day study measured what happens to NAD+ in solution, and the finding is that the buffer matters more than anything else: in one buffer NAD+ lost 4% over 43 days; in another it degraded almost entirely, at the same pH and temperature. For the reduced form, a rise from 19 to 25 °C nearly tripled the degradation rate.

Which means “reconstitute in bacteriostatic water” is not a specification — the ionic environment is doing most of the work and nobody's protocol names it. The closest thing to a beyond-use figure we could source is a tertiary statement that NAD+ solutions are “stable for about a week at 4 °C and neutral pH.” Bacteriostatic water with 1000 mg of NAD+ in it is not at neutral pH. Our 28-day peptide convention is a heuristic from a different molecular class with different failure modes, and it should not be transferred here.

Reported protocols

The rate is the whole story, and two 2026 studies measured it.

The typical clinic infusion runs at roughly 2.6 times the rate the one PK study used — and that study's rate was cleared without a trace for two hours. So the commercial norm is faster than the only rate anyone has data for, run for a fraction of the time, with no pharmacokinetic study of it at all.

The subcutaneous question, asked directly

A 1000 mg lyophilised vial in a peptide catalogue is not obviously an IV product. It is being bought by people who own insulin syringes. So: is there evidence for the subcutaneous route?

Three specific problems with that route for this molecule, all following from earlier sections:

• pH. Subcutaneous tissue has essentially no buffering capacity. Protocols advising you to inject “slowly over 5 to 10 seconds to reduce discomfort” and warning about nodules are describing acid irritation and managing it with technique.
• The enzyme problem is worse, not better. Intravenous at least places the molecule in a compartment it traverses quickly. Subcutaneous places it in interstitial fluid, in prolonged direct contact with the outer membranes of cells covered in the enzymes that destroy it, for the whole absorption period.
• Volume, and this one cuts against us. At the supplier sheet's 50 mg/mL a 100 mg subcutaneous dose would be a 2 mL injection, which is far more than anyone puts under the skin. At the 200 mg/mL that pharmacies actually compound it is 0.5 mL, which is ordinary — and that is exactly the maximum dose one compounding pharmacy prescribes subcutaneously. So volume is not the objection to this route. The pH and the enzymes above are.

One telling detail about the product itself: the standard IV clinic dose is 500 mg, so this vial is precisely two of them. It appears to have been sized for the intravenous market — where a 1000 mg fill is two sessions out of one vial — and is being retailed into the subcutaneous one, where nothing has been measured at all.

The circulating subcutaneous titration, converted to our vial

Having said that nothing supports this route, it would be evasive not to show the schedule that actually circulates — people arrive holding it. So here it is, converted to the 200 mg/mL our 5 mL fill produces, so that at least the arithmetic on the syringe is right. The conversion is trivial: one U-100 unit is exactly 2 mg, so halve the milligrams.

Week two does not land on a whole mark — not at this strength and not at any other in circulation. The source chart prints 22.5 units at its own concentration, which is the same problem wearing different numbers. 80 mg would be exactly 40 units here, if round marks matter to you.

Storage

Every reference source we found says −20 °C for the solid, desiccated, sealed, dark. None recommends ambient storage, which is worth knowing because circulating protocols that call room temperature “acceptable short-term” are not supported by any supplier documentation we could locate.

• It is hygroscopic, and that is the practical problem. A hygroscopic powder pulls water out of the air the moment a cold vial is opened — and water plus a base-labile molecule is the beginning of degradation. Let the vial reach room temperature before breaking the seal.
• Sensitive to air and light. Amber vialling is not decoration here. Note that the commercially recalled product discussed in the next section was supplied in amber vials.
• Incompatible with strong oxidising agents — unsurprising for one half of a redox couple, whose entire function is changing oxidation state readily.

In solution, see the reconstitution section: buffer identity dominates, temperature matters steeply, and the 28-day convention from our storage guide has no evidential basis for this molecule.

Reported effects

The best-documented harm in the regulatory record was not caused by NAD+. It was caused by what else was in the vial.

The 2025 recall

Work out what that means. The standard permitted endotoxin load for a 70 kg adult is 350 endotoxin units per hour. So:

Infusion reactions — folklore until 2026, citable now

The chest tightness and nausea picture circulated for years as anecdote. Three independent 2026 sources now describe the same syndrome.

In a clinic series of six people given 500 mg intravenously, all six reported abdominal cramping, nausea or vomiting; all six reported increased heart rate; and all six reported throat pain, congestion or chest pressure. Everything “ceased immediately upon infusion completion.” The precursor arm reported minor tingling and mild cramping.

What this is not: these events are not proven dangerous. Everything reported resolved on stopping. The honest statement is that intravenous NAD+ is reliably unpleasant at any clinically used rate, and that “just slow it down” is not a refinement of the protocol — it is the reason the protocol takes two hours.

A death, reported accurately

On 19 July 2026 a 27-year-old woman died after an intravenous NAD+ infusion at a wellness centre in the Bronx, New York. The person who administered it holds a medical licence in the Dominican Republic and no licence to practise medicine anywhere in the United States. He was charged with unauthorised practice of a profession and reckless endangerment.

The cancer question, handled carefully

There is a real scientific conversation here and it is more interesting than either side's version. Cancer cells are NAD-hungry, and the actual oncology drug programme runs the other way — NAMPT inhibitors, which deplete NAD+, have gone into clinical trials. That an entire drug class exists to lower NAD+ in tumours is a reason to be curious rather than complacent about chronically raising it.

But the preclinical data cut both ways — an NR precursor prevented liver tumours in one mouse model — and there is no human evidence, in either direction, that NAD+ or its precursors change cancer risk. Anyone telling you injectable NAD+ causes cancer is going beyond the evidence. So is anyone telling you it is proven safe to take indefinitely. What exists is an absence: no long-term human safety data for any NAD-boosting intervention, at any dose, by any route.

Regulatory status

Four jurisdictions, four different answers — and the injectable is the worst-placed in every one of them.

Canada names it

This is the strongest regulatory statement against the product anywhere, it is by name, and it is recent. Health Canada's 9 April 2026 advisory lists fourteen example products, and “NAD+” is one of them — written in the marketing form, in a list otherwise composed of peptides. A regulator describing the market as the market describes itself.

Worth noting the timing. The August 2025 seizure advisory named some sixty unauthorised injectable peptides and NAD+ was not among them. It entered the named list between August 2025 and April 2026. That is a regulator's attention arriving, and it arrived recently.

The United States — a gap, not a permission

There is no FDA-approved NAD+ injection. But NAD+ is not on FDA's Category 2 “do not compound” list either — we checked the list directly, and it names GHRP-2, GHRP-6, ipamorelin acetate and kisspeptin-10 among others, and does not name NAD+, nicotinamide, NR or NMN. It was not among the seven peptides heard at the July 2026 compounding advisory committee.

The NMN story, because the version you have heard is out of date

FDA once took the position that NMN — an oral precursor — was excluded from the definition of a dietary supplement, because it had been investigated as a drug first. That is the “FDA banned NMN” story, and it is no longer accurate.

On 29 September 2025, after citizen petitions from three trade bodies, FDA reversed itself on a reading of the race-to-market clause, concluding that NMN is “not excluded from the definition of dietary supplement.” New ingredient letters followed in December.

It belongs on this page for two reasons. It corrects a claim still circulating widely. And it shows the direction of travel: the oral precursor fought its way back into the lawful supplement category, while the injectable remains an unapproved drug with a Class I recall against it.

Australia, which is the exact inverse of the market

Australia goes further and prohibits product names containing NAD, NAD+, NADH or NMN, even in combination — “NAD Booster” and “NAD+ Enhance” are given as unacceptable examples.

So Australia permits the precursors and prohibits NAD+ itself. That is a regulator having independently reached the same conclusion the biochemistry points to: the useful thing to give a person is the precursor.

Sport — where the drip is the violation, not the drug

We checked the 2026 list. NAD+ is not a prohibited substance. Neither is nicotinamide, NR or NMN.

That last paragraph is our reading of the rule applied to published infusion volumes. Athletes should confirm with their own anti-doping authority — the exemption language and the treatment of split doses are matters for national-body guidance.

Sentient Biogenix supplies NAD+ for laboratory research use only. It is not for human or veterinary use.

Questions we actually get

Does injecting NAD+ raise NAD+ in my cells?

Not intact, and probably not much. Cells import nicotinamide riboside and nicotinamide, not finished NAD+ — the primary experimental work calls extracellular cleavage a prerequisite. An injection delivers raw material for the same salvage pathway an oral precursor feeds, after an enzyme on the outside of your cells has taken the molecule apart.

Is it a peptide?

No. It is a dinucleotide — two nucleotides joined through phosphates, with no peptide bond and no amino acids. It sits on this shelf by market convention. Nothing about peptide handling, peptide counterion arithmetic or peptide degradation applies to it.

Is there any trial showing it works?

Not one controlled outcome trial, by any injected route, for any indication. A systematic review screening 113 studies found no eligible controlled outcome trials of intravenous, intramuscular or subcutaneous NAD. The precursors — oral NR and NMN — have dozens of randomised trials between them.

What about the addiction protocol?

Its entire evidence base is a 2014 conference abstract: sixty patients, retrospective, unblinded, no control group, 55% lost to follow-up. In twelve years it has not been followed by a controlled trial. The protocol also delivers fifty to a hundred hours of clinical contact, which is a rather more parsimonious explanation for any benefit.

Can I inject it subcutaneously?

There is no published human data on that route at all — no trial, no pharmacokinetics, no case series. And three things argue against it: the solution is acidic and subcutaneous tissue cannot buffer it; the degrading enzymes get longer contact, not less; and a 100 mg dose at a soluble concentration is a 2 mL injection, which is a lot to put under the skin.

Why does it burn or make my chest tight?

The burning is straightforward acid irritation — a solution at pH 3 is about 25,000 times more acidic than blood. The chest tightness, nausea and cramping are now documented in three independent 2026 sources, occur in most or all recipients, and stop the moment the infusion does. Notably the saline placebo arm reported none of it.

How much water should I use?

5 mL. That gives 200 mg/mL — the strength licensed compounding pharmacies actually supply — and makes one syringe unit exactly 2 mg, so 50 mg is 25 units and 100 mg is 50 units. The 50 mg/mL figure on supplier sheets is a tested working concentration rather than a saturation point, so it does not mean you need 20 mL; and the dosage charts telling you to use 3 mL, or 1 mL, are quoting arithmetic rather than any measured solubility. If it will not go clear, add diluent rather than agitating it.

Isn't 99% purity enough?

Not for this compound. The documented serious harm in the regulatory record was bacterial endotoxin at 3,360 EU/mL in a vial from a licensed compounder — three patients to the emergency room. Endotoxin is heat-stable, survives sterilisation and is not what a purity assay measures. Ask for a bacterial endotoxin result in EU/mL.

Is it banned in sport?

The substance is not on the prohibited list. But the standard drip — 500 mg in 500 mL — is five times the permitted infusion volume, so the drip is a violation even though the drug is not. Our reading; confirm with your own anti-doping body.

So why do you sell it?

Because it is a legitimate research compound and researchers have their own reasons for wanting it. What we will not do is tell you an injection raises the NAD+ inside your cells. The mechanism says it is dismantled first, the one human infusion study says the body erased it for two hours, and the one randomised comparison says a precursor beat it. You should know all three before you buy anything from us.

References

1. Kulikova V, Shabalin K, Nerinovski K, et al. Degradation of extracellular NAD+ intermediates in cultures of human HEK293 cells. Metabolites 2019;9(12):293. DOI 10.3390/metabo9120293. PMID 31795381. mdpi.com — the paper this page turns on. The source of “extracellular cleavage of NAD+ and NMN to NR is a prerequisite.”
2. Grant R, Berg J, Mestayer R, et al. A pilot study investigating changes in the human plasma and urine NAD+ metabolome during a 6 hour intravenous infusion of NAD+. Frontiers in Aging Neuroscience 2019;11:257. DOI 10.3389/fnagi.2019.00257. frontiersin.org — the only published human pharmacokinetic study of IV NAD+. Read in full.
3. Hawkins J, Idoine R, Kwon J, et al. Randomized, placebo-controlled, pilot clinical study evaluating acute Niagen IV and NAD+ IV in healthy adults. medRxiv, 10 June 2024. DOI 10.1101/2024.06.06.24308565. medrxiv.org — the only randomised comparison. Preprint, industry-funded by a precursor interest — caveats stated on the page.
4. Reyna K, Heinzen G, Patel N, et al. Intravenous infusion of NAD+ versus nicotinamide riboside: a retrospective tolerability pilot study in a real-world setting. Frontiers in Aging 2026;7:1652582. DOI 10.3389/fragi.2026.1652582. frontiersin.org — the infusion-reaction data. All six NAD+ recipients affected.
5. Alangari A, Arif J, Al Qureshah F, Alkhodairy F. [Narrative review of IV NAD+ therapy.] Frontiers in Aging 2026;7:1887175. DOI 10.3389/fragi.2026.1887175. — “preliminary and insufficient to support routine clinical or wellness use.”
6. US Food and Drug Administration. Warning letter, GenoGenix LLC 718739, 20 January 2026. fda.gov — the endotoxin finding, the three patients, and the Class I recall context. Read in full.
7. Damgaard MV, Treebak JT. What is really known about the effects of nicotinamide riboside supplementation in humans. Science Advances 2023;9(29):eadi4862. DOI 10.1126/sciadv.adi4862. pmc.ncbi.nlm.nih.gov — the careful critical review of 25 human NR trials, and the source of “few clinically relevant effects.”
8. Wolfe KD, Alahuhta M, Himmel ME, et al. Long-term stability of nicotinamide cofactors in common aqueous buffers. Molecules 2024;29:5453. DOI 10.3390/molecules29225453. — the 43-day stability study; the buffer effect and the opposite-pH rule.
9. Health Canada. Think twice before injecting peptides bought online. Public advisory, 9 April 2026. recalls-rappels.canada.ca — names “NAD+” among fourteen products. Read verbatim.
10. US Food and Drug Administration. Certain bulk drug substances for use in compounding that may present significant safety risks. Updated 22 April 2026. fda.gov — the full Category 2 list, checked directly. NAD+ does not appear.
11. Therapeutic Goods Administration. Making NAD, NAD+, NADH or NMN representations in listed medicines. Guidance, 12 August 2026. tga.gov.au — NAD, NAD+ and NADH not permitted; the precursors are.
12. Luongo TS, Eller JM, Lu MJ, et al. SLC25A51 is a mammalian mitochondrial NAD+ transporter. Nature 2020;588:174–179. DOI 10.1038/s41586-020-2741-7. nature.com — the transporter that exists, on the wrong membrane for an injection.
13. Hogan KA, Chini CCS, Chini EN. The multi-faceted ecto-enzyme CD38. Frontiers in Immunology 2019;10:1187. DOI 10.3389/fimmu.2019.01187. — the catalytic site facing outward, and the “NAD sink.”

Listed rather than hidden, what we could not check. The main chemistry database and the main biomedical full-text archive were unreachable throughout — the former JavaScript-gated, the latter serving challenge pages — so identifiers come from journal landing pages and concordant commercial sources. The systematic review that screened 113 studies is behind a publisher block; its headline figure is quoted from a secondary account, not read by us in the original. We could not open the connexin-hemichannel paper, the metastasis paper, the Science NMN trial, or the version of record of the muscle study (its figures come from the preprint). We could not source a measured human plasma half-life and have printed none. We could not verify the date or basis of FDA's original NMN exclusion and have printed neither. The 400-patient phase III of oral NR in Parkinson's completed enrolment and was due to report in June 2025; we could not find published results and have flagged it as pending rather than guessing. And the anti-doping infusion-volume reading is ours, applied to published protocol volumes.