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MOTS-c 10 mg
Peptide Library · Profile
MOTS-c 10 mg
There is a real and interesting human literature on MOTS-c. Almost all of it measured the peptide people already had, in people who were given nothing. No completed trial has ever administered it to a human being — the first one started in February 2026 and reports in 2027 — and the dose the market sells is about a twentieth of what the mouse studies would scale to.
Molecular weight2,174.6Da · 16 residues, MRWQEMGYIFYPRKLR
Trials that have reportedNoneone Phase 2a began February 2026
Measured half-lifeNonein any species, by any route
WADA 2026ProhibitedS4.4.1, named, at all times
The short version
Plain English first. Everything below this section is the same material with the sources, the numbers and the caveats attached.
What it is
A 16-residue peptide encoded in mitochondrial DNA rather than in the cell nucleus, which is genuinely unusual biology.
What has actually been measured
A real and interesting human literature — almost all of it measuring the MOTS-c people already had, in people who were given nothing.
What has not been measured
Giving it to anyone. No completed trial has ever administered it to a human being. The first started in February 2026 and reports in 2027. No half-life has been measured in any species.
What most people get wrong
Two things. The dose sold is roughly a twentieth of what the mouse studies scale to. And it is prohibited in sport at all times, named directly on WADA’s list rather than caught by a catch-all.
What MOTS-c is
MOTS-c is a sixteen-residue peptide your own mitochondria encode. That is not marketing language — it is genuinely unusual, and it is the reason the compound is interesting even though almost nothing about it has been tested in a person.
| Value | |
|---|---|
| Sequence | MRWQEMGYIFYPRKLR — 16 amino acids |
| Formula | C101H152N28O22S2 |
| Molecular weight | 2,174.6 g/mol, free base |
| CAS | 1627580-64-6 |
| Encoded in | A 51-base-pair open reading frame inside mitochondrial 12S rRNA |
One detail almost every page gets wrong
You will read that MOTS-c is "made inside the mitochondrion." It is not. The gene sits in mitochondrial DNA, but the peptide is built in the cytoplasm using the standard genetic code. Read with the mitochondrial code instead, that same stretch of DNA produces tandem stop codons and no peptide at all. Encoded in one place, translated in another. It is a small point and it is the difference between a page that has read the literature and one that has read other pages.
Check the numbers on whatever you are buying
We compared the chemistry published by five suppliers of this compound. Two of them are wrong, and one is wrong in a way you can catch without a laboratory.
One vendor prints the correct sixteen-residue sequence — which contains two methionines, each carrying a sulfur atom — alongside a molecular formula with no sulfur in it at all, and a molecular weight of 1,789. The formula and the sequence on that page cannot both describe the same molecule. Another gives a CAS number that resolves to nothing. If a supplier's own datasheet contradicts itself, that tells you something about the rest of their quality system.
How it is said to work
The mechanism is real, it is well described, and the usual one-line version of it skips the step that matters.
"MOTS-c activates AMPK" is a compression of something longer
Here is FDA's own summary of the chain, from its 2026 evaluation, quoted exactly:
"MOTS-c can cause accumulation of the intermediate 5-aminoimidazole-4-carboxamide (AICAR), which is a well-known AMPK activator, that can, in turn stimulate mitochondrial metabolism, fatty acid oxidation, glycolysis, and shunting of glucose to the glucose phosphate pathway."
Read the order of events. MOTS-c is not shown to bind AMPK or switch it on directly. It is proposed to interfere with folate-dependent one-carbon metabolism, which causes a metabolite called AICAR to build up, and AICAR is the thing that activates AMPK. That inference comes from metabolomics in cells and mouse muscle.
So there are two failure points, not one: MOTS-c has to reach the right compartment at a high enough concentration to perturb that pathway, and the resulting AICAR has to accumulate enough to matter. Neither step has been measured in a human. "Activates AMPK" hides both.
Worth knowing: the 2026 WADA Prohibited List files MOTS-c under "Activators of the AMP-activated protein kinase," in the same clause as AICAR itself. Anti-doping classifies it by the mechanism the vendors advertise — which is a nice irony, and not independent evidence that the mechanism operates in people.
Reynolds 2021 — the paper the whole category rests on
Published in Nature Communications, and a good piece of work. In mice given 15 mg/kg a day by intraperitoneal injection for two weeks, the results were striking: all of the young treated mice reached the top sprint speed against one in six of the controls; twenty-two-month-old mice ran roughly twice as long and twice as far. Late-life intermittent treatment improved grip strength, stride length and walking at around thirty months.
Three things that paper did not show, all of which get claimed for it:
- It did not show a lifespan extension. The authors' own words are a "trend towards" increased median and maximum lifespan, at P = 0.05, in roughly eighteen animals per arm, and they wrote that "larger cohorts will be needed to confirm the broader significance." Anyone saying MOTS-c extends lifespan is overstating the paper's own conclusion.
- Its human half administered nothing. Ten sedentary young men rode a bicycle once. Muscle MOTS-c rose 11.9-fold. Nobody was given any MOTS-c.
- It measured no pharmacokinetics.
The 11.9-fold exercise rise is the origin of the "exercise mimetic" framing. Follow the logic though: a molecule going up when you exercise is not evidence that putting it in reproduces exercising. Lactate rises when you exercise too.
Pharmacokinetics
No pharmacokinetic study of MOTS-c exists. Not in a human, not in an animal, by no route. FDA looked in 2026 and said so twice.
"The nominator did not submit, and FDA did not identify clinical studies that provided pharmacokinetic data for MOTS-c-related BDSs."
"The nominator did not submit, and FDA did not identify, published in-vivo nonclinical pharmacokinetic studies."
Which means every half-life you will read is invented
There are three figures circulating, and they disagree with each other by three orders of magnitude. We traced all of them.
| The claim | What is actually behind it |
|---|---|
| "7 to 12 minutes" after IV, in preclinical models | No study, no DOI, no citation anywhere on the page making the claim |
| "1 to 2 hours" | A back-inference from how fast naturally occurring MOTS-c falls after exercise in untreated men. Not a measurement of an injected dose |
| "4 to 5 days, so dose twice weekly" | Cites nothing — and the same article also states the 1 to 2 hour figure a few paragraphs away |
One vendor document contains two of these numbers simultaneously. That is not a disagreement between sources; it is a document nobody read before publishing.
What is actually known is unflattering. MOTS-c does not last long in blood — a doping-control assay found levels in stored plasma samples falling by roughly a quarter over twenty-four hours at 4 °C. That is enzymatic clearance in a protease-rich matrix, and it is a fact about circulation rather than about shelf life; what a reconstituted vial does in a fridge is a different question, answered under Storage. It does not cross the blood-brain barrier. The most recent review of the field is candid that "there is still a great deal of unclarity as to how MOTS-c enters cells without being degraded," and attributes the stalling of clinical development to "the current lack of reliable delivery systems."
What the evidence shows
This is the section that matters, and the distinction it turns on is the single most important thing on this page.
Nearly every human MOTS-c study measured people who were given nothing
There is a substantial human literature: MOTS-c levels in obesity, in type 2 diabetes, in kidney disease, in coronary disease, in sleep apnoea, in COPD, across ageing, after exercise. In every one of those studies the peptide was measured, not administered. They tell you that people with metabolic disease tend to have less circulating MOTS-c. They do not tell you that injecting it does anything, and they were never designed to.
What has actually been given to a human
One trial is enrolling. It is the first ever.
| NCT07505745 | |
|---|---|
| What | MOTS-c for insulin sensitivity in prediabetes with overweight or obesity |
| Design | Phase 2a, randomised, quadruple-blind, placebo-controlled |
| Size and route | 120 participants, subcutaneous, once daily for 12 weeks |
| Dose | Not disclosed in the public record |
| Where | Peking University Shenzhen Hospital |
| Started | February 2026 · first results expected 2027 |
So the honest statement is narrow and precise: no interventional trial of MOTS-c has ever reported. One has begun. Note that it lists immunogenicity as a secondary endpoint — the first time anyone will actually look at whether injecting this peptide provokes an immune response.
The trial people cite instead is a different molecule
CB4211 is described by the company that made it as "a novel and improved analog of MOTS-c." Analog, not MOTS-c. It went through Phase 1a and 1b: sixty-five healthy adults, then twenty obese subjects at 25 mg subcutaneously daily for four weeks. It was well tolerated, with injection-site reactions the main complaint.
Its efficacy result is worth reading properly, because the press release was headlined "Positive Topline Results." Liver fat fell 5.03% on drug against 4.88% on placebo — in roughly ten people per arm. That is a null result inside an optimistic announcement. Clinical development of CB4211 subsequently stopped.
One study that gets cited does not exist
A widely-read dosing guide justifies its protocol with "a 2021 randomised controlled trial, twelve older adults, a single intravenous dose of MOTS-c at 2 mg/kg." We went looking. It appears in no index. FDA, reviewing the compound in 2026, stated that it "did not identify, any clinical studies or human exposure data for MOTS-c via any route of administration." And 2 mg/kg would be about 140 mg in a 70 kg adult — an order of magnitude above anything ever given to a person, even of the analog. If a page cites that trial, stop reading the page.
Reconstitution
A 10 mg vial, against doses commonly quoted in whole milligrams:
| Bacteriostatic water | Concentration | 1 unit (U-100) = | 5 mg draw |
|---|---|---|---|
| 1 mL | 10 mg/mL | 100 mcg | 50 units · 0.50 mL |
| 2 mL | 5 mg/mL | 50 mcg | 100 units · 1.00 mL |
| 3 mL | 3.33 mg/mL | 33.3 mcg | 150 units · 1.50 mL |
At 1 mL a 5 mg dose is half a syringe, which is the comfortable option. At 2 mL it fills a whole 1 mL syringe and at 3 mL it needs two.
Whatever schedule you are on, the vial is unlikely to outlast the 28 days bacteriostatic water's preservative is validated for — at the commonly quoted 5 to 10 mg a week, a 10 mg vial is one to two weeks. That is one of the few things about this compound that is straightforward. The supply planner will do the arithmetic.
One handling note: with MOTS-c the variable that matters is temperature, not elapsed days. The stability work that exists found it essentially intact after a month refrigerated, and losing ground quickly at room temperature. Mix what you are ready to start, keep it cold and dark, and see Storage.
Reported protocols
The usual complaint about research-peptide dosing is that it scales animal doses up too aggressively. MOTS-c is the opposite case, and it is more interesting.
The circulating convention is 5 to 10 mg a week, subcutaneous, often as a single injection or split over two days, on a twelve-week cycle. Here is the animal work it is supposedly derived from — every systemic study, from FDA's own summary of the literature:
| Study | Dose | Route and frequency |
|---|---|---|
| Lee 2015, weight gain, 8 weeks | 0.5 mg/kg | Intraperitoneal, daily |
| Lee 2015, glucose uptake and ageing | 5 mg/kg | Intraperitoneal, daily |
| Kim 2019 | 2.5 mg/kg | Intraperitoneal, twice daily |
| Lu 2019, 12 weeks | 5 mg/kg | Intraperitoneal, daily |
| Reynolds 2021, the headline results | 5 and 15 mg/kg | Intraperitoneal, daily |
| Wei 2020, rats | 5 mg/kg | Intraperitoneal, daily |
What those doses come to in a person
Converted by body surface area using FDA's own published method, for an 80 kg adult:
| Mouse dose | Human equivalent | Per week |
|---|---|---|
| 0.5 mg/kg/day — the lowest chronic dose | 3.3 mg/day | ~23 mg |
| 5 mg/kg/day — most of the metabolic results | 32.5 mg/day | ~230 mg |
| 15 mg/kg/day — Reynolds' running results | 97.6 mg/day | ~680 mg |
The sold dose is roughly a twentieth of the lowest one that worked in mice
5 to 10 mg a week sits below the human equivalent of the smallest chronic rodent dose, and around a sixtieth of the regimen that produced most of the published metabolic effects. It is also about a twenty-fifth of the only dose ever actually given to humans in a trial — and that was the analog, at 25 mg a day, which came out indistinguishable from placebo on its main endpoint.
So the point is not that the dose is an uncertain extrapolation. It is that the animal results cannot be invoked to support it at all. If MOTS-c worked exactly as the mouse papers describe, 5 mg a week would not reproduce them.
Two more things that do not survive contact with the source material. Every systemic animal study injected into the abdominal cavity, which is not a human route, and nobody has shown that a subcutaneous injection in a person reaches comparable exposure — because nobody has measured exposure in either. And every effective regimen was daily or twice daily. Weekly dosing appears nowhere in the literature. Its justification is the four-to-five-day half-life from the pharmacokinetics section, which cites nothing. On that specific point, splitting a weekly total across three injections sits closer to the frequency every study used than a single weekly bolus does. That is an observation about the shape of the schedule rather than the amount — neither is supported by human data, because none exists.
To its credit, one of the dosing guides says outright that its protocol is "a conservative titration framework based on available research, clinical reasoning, and reported protocols — not a prescription." "Reported protocols" means what other vendors say. That is an honest description of the circular process by which these numbers exist.
Storage
Lyophilised, sealed, cold, dark and dry. The conventions in our storage guide apply.
MOTS-c is one of the few compounds in this library where a real storage measurement exists, and it is considerably more reassuring than the figure usually quoted for it.
Refrigerated, it keeps. High-resolution mass spectrometry on MOTS-c held in water found intact peptide at the highest intensities after thirty days, with methionine oxidation unchanged — at 4 °C, and at 37 °C as well. Separate third-party testing of MOTS-c reconstituted in bacteriostatic water and kept dark found roughly 96% remaining at fifteen days and 89% at thirty-one days refrigerated.
At room temperature it does not. That same third-party testing found about 76% at fifteen days and 17% by thirty-one days at around 24 °C. Ambient storage is where the loss actually happens, and it is what the cold-and-dark advice is for.
Both lines deserve their caveats. The mass-spectrometry work is a conference abstract rather than a peer-reviewed paper, and ran at a far lower concentration than a reconstituted vial. The third-party testing used UV-Vis spectrophotometry, inferring loss from the aromatic-range extinction coefficient, which is a weaker method than HPLC purity. Two independent lines agreeing is worth more than either alone, and neither is a pharmacopoeial stability study.
A correction, 23 September 2026
This page previously stated that a published measurement found a quarter of MOTS-c gone after a day at 4 °C, and treated it as a shelf-life figure. It is not one. It comes from a WADA doping-control assay validation, where it describes how fast MOTS-c disappears from stored blood plasma samples — a protease-rich matrix — and it was quoted in a review explaining why plasma assays disagree with one another. We applied it to a vial of bacteriostatic water, which it does not describe. The secondary source we took it from carried the water-storage figure as well, two paragraphs further on, and we did not print it. That was our mistake, and this is the correction.
Do not freeze a reconstituted solution. At sixteen residues with two methionines, this peptide has more routes to degradation on paper than most — methionine oxidises readily — though the mass-spectrometry work above found that oxidation did not in fact advance over thirty days in water. Whatever does happen, none of it changes how the vial looks.
Reported effects
There is no human safety dataset for MOTS-c. Not a thin one. None.
Four independent bodies have looked and said the same thing in different words. FDA, in its 2026 evaluation: "FDA lacks important information regarding any safety issues raised by MOTs-C, including whether it would cause harm if administered to humans." USADA: "it is unknown under what conditions (if any) it is safe to use MOTS-c because there are no completed human clinical trials."
The toxicology package is empty in every domain
FDA searched for and could not find acute toxicity studies, repeat-dose toxicity studies, genotoxicity studies, developmental and reproductive toxicity studies, or carcinogenicity studies — for either the free base or the acetate. That is all five standard categories, with nothing in any of them.
Zero adverse event reports is not a safety record
FDA searched the US adverse event database twice, through March 2025. Verbatim: "The searches retrieved no reports."
Read that correctly. That database collects reports about marketed drug products. A research chemical has no route into it — there is no manufacturer obliged to report, no prescriber, no pharmacy. Zero reports on a substance with no approved product is the expected result whether it is perfectly safe or not. It is evidence that nobody is reporting, and nothing more.
What people who use it say
Reviews of the compound list the same cluster from self-experimenter reports: raised heart rate or palpitations, injection site irritation, insomnia, local or generalised immune reactions, and fever. Uncontrolled, unverified, no denominator. We are including it because it is the only signal that exists and leaving it out would be dishonest.
The concern a regulator actually named
FDA's specific worry, stated twice, is immunogenicity: a sixteen-residue peptide given by injection, with potential for aggregation and peptide-related impurities, and nothing measuring either. That is also the reason its assessment kept returning to characterisation — it concluded MOTS-c is not well characterised, citing inconsistent naming and missing data on impurities, aggregates, microbial burden and endotoxin.
One interaction worth knowing. If the AMPK mechanism operates as described, MOTS-c would be expected to interact with other drugs that activate AMPK — metformin above all. That is a mechanistic prediction, not an observation, and nobody has tested it.
Regulatory status
Approval. MOTS-c is not a component of any approved drug product, anywhere, for anything.
United States
MOTS-c sits on FDA's bulk drug substances page in the table of substances nominated but withdrawn — entries previously in category 2 of the interim policies, withdrawn by the nominators. Not, as it is often described, in category 2 itself. The entry reads, verbatim:
"Compounded drugs containing MOTs-C may pose significant risk for immunogenicity for certain routes of administration and may have complexities with regard to peptide-related impurities and API characterization. FDA has not identified any human exposure data on drug products containing MOTs-C administered via any route of administration. FDA lacks important information regarding any safety issues raised by MOTs-C, including whether it would cause harm if administered to humans."
Then July 2026 happened. FDA re-evaluated MOTS-c and published a briefing document ahead of its Pharmacy Compounding Advisory Committee, which heard it on 23 July 2026 alongside BPC-157, KPV and TB-500, under docket FDA-2025-N-6895. The nominated use was injection, subcutaneous, for insulin resistance, obesity, osteoporosis, vascular calcification, muscle and fat metabolism and longevity. FDA's conclusion, verbatim:
"On balance, the physicochemical characterization, information on historical use, lack of any safety and effectiveness information in humans for both MOTS-c (free base) and MOTS-c acetate weigh against their being added to the 503A Bulks List."
The committee voted 7 to 5, with two abstentions, to recommend adding it anyway — against FDA's own scientific review team. A committee recommendation is advice. FDA is not bound by it, no rulemaking has followed, and nothing about the legal status of this compound has changed, in the United States or here.
Canada
Health Canada's public advisory of 9 April 2026 names MOTS-C among fourteen peptides given as "examples of unauthorized injectable peptide drugs seized by Health Canada." The advisory states that peptides function as prescription drugs in Canada, and that research-use-only labelling "does not make these products legal or exempt from regulatory requirements."
Sport — and here there is no ambiguity at all
Unlike most compounds in this library, MOTS-c is named on the 2026 WADA Prohibited List. It appears in section S4.4.1, prohibited at all times, in and out of competition. Verbatim:
"Activators of the AMP-activated protein kinase (AMPK), e.g. 5-N,6-N-bis(2- fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine (BAM15), AICAR, mitochondrial open reading frame of the 12S rRNA-c (MOTS-c);"
There is no S0 argument to have here and no reading of the text that helps. If you are tested, this one is explicitly prohibited by name.
Sentient Biogenix supplies MOTS-c for laboratory research use only. It is not for human or veterinary use.
Questions we actually get
Doesn't MOTS-c go up when you exercise?
Yes, and that is a real finding — muscle levels rose nearly twelve-fold in ten young men after a single bicycle session. But nobody in that study was given any MOTS-c. A molecule rising when you exercise is not evidence that injecting it substitutes for exercising.
Have there been human trials?
None that have reported. One Phase 2a trial in China began in February 2026, with 120 participants on daily subcutaneous injection for twelve weeks; first results are expected in 2027. Before that, the entire human literature measured the peptide people already had.
What about the CohBar trial?
That was CB4211, described by its own maker as an analog of MOTS-c — a different molecule. It was safe at 25 mg a day for four weeks, and on its main endpoint it reduced liver fat by 5.03% against placebo's 4.88%. Development stopped.
What's the half-life?
Unknown. No pharmacokinetic study of MOTS-c exists in any species. The three figures in circulation — twelve minutes, two hours, five days — disagree with each other by three orders of magnitude, and one vendor article manages to print two of them.
Is 5 to 10 mg a week the right dose?
It is the common one. It is also about a twentieth of the human equivalent of the lowest dose that produced results in mice, and every one of those mouse studies dosed daily, not weekly. We cannot tell you the right dose because nobody knows it, but we can tell you that number is not derived from the animal work people cite for it.
Is it banned in sport?
Yes, by name, section S4.4.1 of the 2026 Prohibited List, at all times. No ambiguity.
References
- US Food and Drug Administration. FDA Briefing Document, Pharmacy Compounding Advisory Committee — MOTS-c-related bulk drug substances, July 2026. fda.gov — the molecular formula and weight, the mechanism summary, the complete animal dosing table, the absence of human exposure data and pharmacokinetics, the five empty toxicology domains, the adverse-event database searches, and the conclusion against listing.
- US Food and Drug Administration. Presentation slides, Pharmacy Compounding Advisory Committee, 23 July 2026. fda.gov — the characterisation findings and the absence of published nonclinical pharmacokinetics.
- US Food and Drug Administration. Certain bulk drug substances for use in compounding that may present significant safety risks — the nominated-but-withdrawn table. fda.gov
- Reynolds JC, Lai RW, Woodhead JST, et al. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nature Communications 2021;12:470. PMID 33473109. nature.com — the 15 mg/kg intraperitoneal mouse results, the lifespan "trend" the authors themselves declined to call a finding, and the ten-man exercise study in which nothing was administered.
- Lee C, Zeng J, Drew BG, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism 2015;21(3):443–454. PMID 25738459. pubmed.ncbi.nlm.nih.gov — the founding paper. We read it through FDA's summary rather than directly; the publisher blocks automated access.
- ClinicalTrials.gov. NCT07505745 — MOTS-c for improving insulin sensitivity in adults with prediabetes and overweight or obesity. Phase 2a, 120 participants, subcutaneous daily for 12 weeks, Peking University Shenzhen Hospital; started February 2026. clinicaltrials.gov
- CohBar Inc. Topline results from the Phase 1a/1b study of CB4211, 10 August 2021 — the analog trial, 25 mg subcutaneously daily for four weeks in twenty obese subjects, and the 5.03% against 4.88% liver-fat result. globenewswire.com
- Alzheimer's Drug Discovery Foundation, Cognitive Vitality. MOTS-c, 17 September 2025. alzdiscovery.org — the best independent inventory of the observational human literature, both stability figures (the plasma one and the water one), the self-experimenter adverse effects, and the metformin interaction prediction.
- Merry TL, Chan A, Woodhead JST, et al. Mitochondrial-derived peptides in energy metabolism. Frontiers in Endocrinology 2023;14:1120533. frontiersin.org — cytoplasmic translation of the mitochondrially encoded ORF, and the unresolved question of cellular entry.
- World Anti-Doping Agency. The 2026 Prohibited List, in force 1 January 2026, section S4.4.1. Read via the Austrian Federal Law Gazette's official reproduction (BGBl. III Nr. 219/2025) because WADA blocks automated access to its own copy.
- United States Anti-Doping Agency. What is the MOTS-c peptide? usada.org
- Health Canada. Think twice before injecting peptides bought online: unauthorized products can seriously harm you. Public advisory, 9 April 2026. recalls-rappels.canada.ca
- Knoop A, Thomas A, Thevis M. Development of a mass spectrometry based detection method for the mitochondrion-derived peptide MOTS-c in plasma samples for doping control purposes. Rapid Communications in Mass Spectrometry 2019;33:371–380. PMID 30394592. doi.org/10.1002/rcm.8337 — a WADA assay validation in human plasma. This is the origin of the widely repeated twenty-four-hour figure, and it measures plasma sample stability, not vial storage.
- Mohtashami Z, Ozgul M, Katz B, et al. Analysis of 1-month-old MOTS-c in H₂O; using high resolution mass spectrometry. Investigative Ophthalmology & Visual Science 2022;63:474–A0011. iovs.arvojournals.org — the thirty-day stability in water at 4 °C and 37 °C. An ARVO meeting abstract rather than a peer-reviewed paper, and not indexed in PubMed; we have flagged that where the figure is used.
- Analytical Formulations Inc. Third-party peptide degradation and storage testing, published at peptidecritic.com — the refrigerated and ambient retention figures for MOTS-c in bacteriostatic water. Measured by UV-Vis spectrophotometry rather than HPLC purity; the method caveat is stated where the figures are used.
Publishers blocked automated access to several primary papers, so the following are reported through FDA's briefing document or the Cognitive Vitality review rather than read directly: Lee 2015, and Kim 2018 and 2019. Each is a real, indexed paper; we have not printed any figure from them that those secondary sources did not state. Knoop 2019 was previously on that list and is no longer. Its record was read at source on 23 September 2026, and the figure we had taken from it turned out to describe something it does not measure — see the correction under Storage. Reporting a figure faithfully from a secondary source is not the same as checking what the figure means. We also could not open the trial registry's own page for NCT07505745 — that record is reconstructed from three independent registry mirrors which agree with one another.
For laboratory research use only. Not for human or veterinary use. Nothing on this page is dosing guidance, and no figure here should be read as a recommendation.