5-Amino-1MQ, MOTS-c and NAD+ Doses in Published Studies: What Was Reported

People searching for a "5-Amino-1MQ, MOTS-c and NAD+ dosage chart" are usually looking for a single grid of milligrams, frequencies and cycle lengths. This page does not provide one, and the reason is not caution for its own sake: the published literature verified for this page does not contain a validated human dosing schedule for any of these three items. What it contains is mechanistic work, preclinical experiments and a large body of review literature on nicotinamide adenine dinucleotide (NAD⁺) metabolism. Those are different objects. A dose reported inside an experiment is a variable chosen to test a hypothesis in a defined model; a dosing chart is a clinical instruction. Converting the first into the second is the step that the literature itself has not made.

This page is for educational purposes only and is not medical advice; consult a licensed physician about any health decision. Nothing below should be read as a protocol, and no numbers are restated beyond what the cited papers themselves covered.

What the verified literature on this page actually is

Before describing doses, it helps to be precise about study type, because the answer to "what dose did the study administer?" depends entirely on whether a dose was administered at all. Several of the most-cited sources on NAD⁺ are narrative or systematic reviews: they synthesise other people's experiments rather than dosing anything themselves.

That distinction matters for anyone reading a supposed "studied dose" online. A review can describe that a compound was administered in earlier experiments without the review itself being a dosing source, and second-hand summaries frequently strip away the species, route and duration that gave the original number its meaning.

MOTS-c: what researchers reported

The mitochondrial-derived peptide framing

MOTS-c is described in the literature as a mitochondrial-derived peptide — a short peptide encoded within mitochondrial DNA rather than the nuclear genome. Reviewers reported that it has been studied as a regulator of skeletal muscle and fat metabolism, with attention to glucose handling and metabolic homeostasis in laboratory models (PMID 27216708). A later review characterised MOTS-c as a candidate for therapeutic exploitation across metabolic and age-related conditions, while framing that potential as an open research programme rather than a settled clinical application (PMID 36761202).

The oncology experiment

A 2024 experimental study reported that MOTS-c suppressed ovarian cancer progression, and the researchers attributed the effect to attenuation of USP7-mediated deubiquitination of LARS1 (PMID 39321430). That study is mechanistic oncology work in cancer models; the exposure levels it used were selected to interrogate a specific ubiquitin–protease pathway in tumour biology, not to establish a tolerable or effective amount for a healthy person. A reader looking for a "MOTS-c dose" will not find a transferable one there, and the study did not present one.

What was not reported

None of the MOTS-c sources verified for this page reported a standardised human regimen — no established milligram amount, injection schedule, cycle length or duration of administration for people. Reviewers instead reported that translational questions, including delivery and dosing, remain open (PMID 36761202). Any chart circulating online that lists a MOTS-c "weekly protocol" is therefore not tracing back to these papers.

NAD+: what the reviews report about levels, precursors and translation

Why NAD+ is studied at all

NAD⁺ is a central redox cofactor and a substrate for enzymes that consume it, including sirtuins, PARPs and CD38. Reviewers reported that NAD⁺ availability declines in multiple tissues with age and that this decline has been linked to mitochondrial function, DNA repair capacity and metabolic regulation (PMID 33353981, PMID 32694684). The relationship between NAD⁺ and sirtuin activity in ageing and disease has been reviewed at length, with researchers describing NAD⁺ as a limiting factor for sirtuin-dependent signalling (PMID 24786309).

Further reviews reported roles for NAD⁺ metabolism in cellular senescence and ageing biology (PMID 37424179), in stemness, immune responses and cancer (PMID 33384409), and across health and disease states generally (PMID 37848251, PMID 34041853).

Dosing is precisely the unresolved part

The reviews that discuss intervention did so at the level of strategy, not schedule. Researchers described NAD⁺-raising approaches — precursor supply, inhibition of NAD⁺-consuming enzymes, and modulation of salvage pathway flux — and reported that evolving concepts in the field have repeatedly revised assumptions about which precursor reaches which tissue and in what form (PMID 33930322). A 2024 review was explicit that targeting NAD⁺ metabolism carries substantial challenges, including tissue specificity, compartmentalisation and the possibility that raising NAD⁺ is not uniformly desirable in every cell type — a concern that is sharpest in the cancer literature (PMID 39026037, PMID 33384409).

In other words, the field's own reviewers have reported that the dosing question is unsettled. A chart claiming otherwise is claiming more than the reviews do.

5-Amino-1MQ: what the cited literature does and does not cover

5-Amino-1MQ is discussed in online material as a small-molecule inhibitor of nicotinamide N-methyltransferase, an enzyme within nicotinamide handling. Honesty about sourcing matters here: none of the papers verified for this page is a study of 5-Amino-1MQ. No dose, route, species or duration for that compound can be described from this evidence set, and inventing one would be exactly the failure mode this page exists to counter.

What the verified reviews do cover is the broader architecture that such an approach would sit inside — the salvage and consumption arms of NAD⁺ metabolism and the difficulty of manipulating them selectively (PMID 39026037, PMID 33930322). Readers who want to evaluate 5-Amino-1MQ specifically will need primary literature on that molecule; this page will not fill the gap with numbers it cannot source.

Why a dose in a paper is not a dose for a person

Even where an experiment reports a clean number, several layers sit between that number and a human recommendation.

• Species and scaling. Amounts administered to mice are not converted to people by multiplying body weight. Metabolic rate, clearance and receptor distribution all differ, and the mitochondrial-derived peptide literature has been developed largely in rodent and cell systems (PMID 27216708).
• Route and formulation. Intraperitoneal, intravenous, oral and subcutaneous exposure produce different concentration profiles from the same nominal amount. Reviewers of NAD⁺ precursors reported that where a molecule is absorbed and how it is converted changes which tissue actually sees it (PMID 33930322).
• Endpoint mismatch. A dose chosen to suppress tumour growth in a cancer model was chosen for that endpoint (PMID 39321430). It carries no information about what would be appropriate for an unrelated goal in a healthy adult.
• Direction of effect is context-dependent. Reviewers reported that NAD⁺ metabolism intersects with immune function and cancer biology in ways that make "more is better" an unsafe assumption (PMID 33384409, PMID 39026037).
• Purity and identity. Research-grade material is not a pharmaceutical product with assured content, and no study in this set evaluated unregulated preparations.

Combination or "blend" dosing: what the evidence base looks like

Search demand for this page is driven partly by blended products combining NAD⁺ precursors, MOTS-c and 5-Amino-1MQ. The verified literature contains no combination study of these three agents. Each body of work stands alone: MOTS-c has been studied as a peptide in metabolic and oncologic models (PMID 36761202, PMID 39321430), and NAD⁺ biology has been reviewed as a metabolic and ageing question (PMID 37848251, PMID 37424179). Combining agents introduces interaction questions — additive effects, opposing effects, shared metabolic bottlenecks — that were not tested in any source cited here. A blend chart is therefore an extrapolation on top of an extrapolation.

Adverse Events and Tolerability: What Studies Report

The verified sources on this page are mechanistic studies and reviews rather than safety trials, so they do not provide adverse-event tables, dropout rates or tolerability profiles for human administration. What researchers did report are theoretical and biological cautions. Reviews of NAD⁺ metabolism noted that NAD⁺-consuming enzymes and precursor pathways are active in proliferating and immune cells, making the consequences of manipulating them context-dependent and not uniformly benign (PMID 33384409). A 2024 review framed selectivity, tissue targeting and off-target metabolic consequences as central challenges for any therapeutic strategy aimed at NAD⁺ (PMID 39026037). For MOTS-c, reviewers reported that translational development — including safety characterisation — remains ongoing rather than complete (PMID 36761202). Absence of reported harm in mechanistic papers is not evidence of safety; it reflects that those papers were not designed to detect harm.

Regulatory framing

MOTS-c and 5-Amino-1MQ are not approved drug products. Material sold under research-use-only labelling is intended for laboratory investigation and is not evaluated for human administration, quality or content. Certain NAD⁺ precursors are marketed as dietary supplements in some jurisdictions, a category that does not require the pre-market efficacy evidence expected of drugs. These are regulatory facts, not guidance, and they are separate from the scientific question of what the studies showed.

How to read dosing claims critically

1. Ask what the source is. If a number traces back to a review rather than an experiment, the review is quoting someone else's design.
2. Ask for species, route and duration together. A milligram figure without those three is uninterpretable.
3. Ask what the endpoint was. Tumour suppression, insulin sensitivity and lifespan are different questions with different exposures (PMID 39321430, PMID 27216708).
4. Ask whether human data exist at all. For much of this space, reviewers reported that they largely do not (PMID 36761202, PMID 39026037).

The honest summary is that the study literature on MOTS-c and NAD⁺ is scientifically rich and clinically immature, and that the 5-Amino-1MQ literature is absent from this verified set entirely. Decisions about any of these belong with a licensed clinician who can assess an individual's circumstances.

References

• Mitochondrial-Derived Peptide MOTS-c Suppresses Ovarian Cancer Progression by Attenuating USP7-Mediated LARS1 Deubiquitination (Advanced Science, 2024)
• MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation (Frontiers in Endocrinology, 2023)
• MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism (Free Radical Biology & Medicine, 2016)
• NAD+ metabolism and its roles in cellular processes during ageing (Nature Reviews Molecular Cell Biology, 2021)
• Regulation of and challenges in targeting NAD+ metabolism (Nature Reviews Molecular Cell Biology, 2024)
• Evolving concepts in NAD+ metabolism (Cell Metabolism, 2021)
• NAD+ homeostasis in health and disease (Nature Metabolism, 2020)
• NAD+ homeostasis in human health and disease (EMBO Molecular Medicine, 2021)
• NAD+ and sirtuins in aging and disease (Trends in Cell Biology, 2014)
• NAD metabolism: Role in senescence regulation and aging (Aging Cell, 2024)
• NAD+ metabolism, stemness, the immune response, and cancer (Signal Transduction and Targeted Therapy, 2021)
• Roles of NAD+ in Health and Aging (Cold Spring Harbor Perspectives in Medicine, 2024)