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    Research Use Only (RUO). For laboratory research only. Not for human or veterinary use.

    Avenor Peptides
    Research Use Only (RUO):Research classification with product and batch documentation where available.
    5-AMINO-1MQ - NAD+ 50 mg + 50 mg - Avenor Peptides

    Body composition

    5-AMINO-1MQ - NAD+

    Strength: 50 mg + 50 mg

    A combination of two substances in a pill: 5-Amino-1MQ, studied around fat burning, and NAD+, which is linked to the energy of cells.

    €135,52€154,00
    -12% off
    In stock
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    Batch documentationShips from Greece

    Free shipping: Greece from €50, Cyprus and Bulgaria from €100, France, Germany, Italy, Belgium, Netherlands and Spain from €200. Details

    This product is intended exclusively for laboratory research use. It is not intended for human consumption, diagnosis, treatment, or prevention of disease.

    Product information

    FormOral form
    Strength50 mg + 50 mg
    SKUAVR-5AMINO1MQNAD-50MG50MG
    Stock statusIn stock
    COA / BatchSee the documentation state below
    StorageRefer to the label and available documentation details.
    Packaging / shippingControlled shipping preparation according to the available SKU variant.

    Documentation on request

    There is no published document for this specific SKU variant at the moment.

    Contact us about documentation

    Research overview

    What it is researched for

    Research focuses on topics such as:

    • fat burning
    • cellular energy
    • body composition

    Areas of research — not a promise of results.

    How this category is positioned

    It is not a peptide — it is a combination of two substances, taken by mouth. 5-Amino-1MQ is also available on its own, as a vial.

    Documentation & COA

    Batch documentation and COA, where available, are linked to the specific product batch and SKU.

    This product is intended exclusively for laboratory research use. It is not intended for human consumption, diagnosis, treatment, or prevention of disease.

    Product profile

    2

    components — one small molecule and one coenzyme; neither is a peptide

    0

    published studies of the COMBINATION — none, anywhere

    2014

    year NNMT was identified as a metabolic target in Nature (Kraus et al.)

    ≥98%

    purity by HPLC

    Research context

    What it is

    It is a pairing of two things that act at the two ends of the same pathway.

    The first part, 5-amino-1MQ, stops an enzyme from wasting a critical cellular fuel.

    The second part feeds that same fuel directly.

    The technical detail

    NAD+ is nicotinamide adenine dinucleotide. 5-amino-1MQ inhibits NNMT, while a precursor molecule (NMN-type) supplies the substrate for NAD+ synthesis.

    How it works

    Picture a tank with a leak and a tap that fills it.

    The target enzyme is the hole where NAD+ drains out. The inhibitor plugs it.

    The precursor is the tap. Together, the tank fills and stays full.

    The technical detail

    NNMT methylates nicotinamide and diverts it away from recycling into NAD+ (Kraus et al., Nature, 2014). Inhibition raises intracellular NAD+ and SAM (Neelakantan et al., 2017).

    Why combine them

    The logic is simple. Adding fuel is not enough if the body spends it faster.

    And plugging the leak is not enough if the tank is already empty.

    The combination does both at once.

    The technical detail

    The pairing of an NNMT inhibitor with an NAD+ precursor has not been tested as such in a clinical trial; each arm has been studied separately.

    What the studies showed

    NAD+ levels fall with age. Clinical studies tested whether replenishing it reverses that decline.

    11

    men, 8 weeks (2024)

    80

    adults, dose-dependent NAD+ rise (2024)

    40–65

    participant ages

    In the larger study, blood NAD+ rose in proportion to the dose, and that rise was linked to better performance on a 6-minute walk test.

    Laboratory use

    Used in a controlled laboratory setting as research material for in vitro studies of NNMT enzyme inhibition, for quantification of intracellular 1-methylnicotinamide, NAD+ and SAM levels by mass spectrometry, for NAD+ salvage pathway flux studies using stable isotope tracers, for gene expression analysis in adipocyte and hepatocyte cell lines, and as a reference standard in analytical chemistry and quantitation method development.

    Research Use Only. For laboratory research exclusively. Neither component is a peptide. 5-amino-1MQ (5A1MQ) is a preclinical research compound with NO approval from the FDA, EMA, the Greek NOM or any other regulatory authority, in any country and for any indication, and with NO clinical trial or human safety data of any kind. The COMBINATION of 5-amino-1MQ with NAD+ has NOT been studied in any published work — not in cells, not in animals, not in humans. The oral bioavailability of intact NAD+ is DISPUTED in the literature. All findings referenced derive from cell culture and laboratory animals and do not transfer to humans. Not intended for human or veterinary use, diagnosis, treatment or disease prevention, nor for consumption in any form. No dosing or administration protocols are provided.

    Structural data

    Component 1 — class
    5-amino-1-methylquinolinium (5A1MQ, marketed as "5-amino-1MQ"): a synthetic small molecule built on a quinolinium scaffold. NOT a peptide, with no amino acid chain of any kind
    Component 1 — molecular target
    An inhibitor of the enzyme NNMT (nicotinamide N-methyltransferase), a cytosolic SAM-dependent enzyme
    Component 1 — selectivity
    Does not inhibit structurally related SAM-dependent methyltransferases nor the enzymes of the NAD+ salvage pathway (Neelakantan et al., 2017)
    Component 1 — membrane permeability
    Characterized as permeable in PAMPA and Caco-2 cell assays — both passive and active transport (Neelakantan et al., 2017)
    Component 2 — class
    NAD+ (nicotinamide adenine dinucleotide): a naturally occurring coenzyme, a dinucleotide. NOT a peptide and NOT a drug — it is an endogenous molecule present in every cell
    Component 2 — biochemical role
    Hydrogen carrier in redox reactions and substrate for signalling enzymes — sirtuins, PARPs and CD38 (Rajman et al., 2018)
    Component 2 — biosynthesis
    Produced by the salvage pathway from the precursor nicotinamide, and de novo from tryptophan — the de novo route operating selectively in the liver in laboratory animals (Liu et al., 2018)
    Shared basis of the two components
    Both concern the same metabolic pathway: NNMT consumes nicotinamide, which is the precursor of NAD+
    Study of the combination
    None. A PubMed search for the two substances combined returns zero publications
    Human data
    No clinical trial of 5A1MQ in humans. All published data derive from cell culture and mice
    Oral bioavailability of NAD+
    Disputed in the literature. No publication was found documenting absorption of intact oral NAD+ in humans; this is why precursors (NR, NMN) are the ones being studied
    Regulatory status
    5A1MQ holds no approval from the FDA, EMA, the Greek NOM or any other authority, for any indication
    Product form
    Oral capsule
    Purity
    ≥98% (HPLC) — supplied with CoA

    Comparison

    Feature comparison

    Feature5-AMINO-1MQ + NAD+ (this product)5-amino-1MQ aloneMOTS-c
    What it isA combination of two substances: a small molecule and a coenzyme — neither of them a peptideA single synthetic small molecule — not a peptideA 16-amino-acid peptide encoded by mitochondrial DNA
    Point of action on the pathwayTwo points: blocking consumption of the precursor + supplying the coenzyme itselfOne point: inhibition of the NNMT enzymeDoes not target the NAD+ pathway; acts on broader metabolic signalling
    Molecular targetNNMT (via 5A1MQ); NAD+ has no "target" — it is a substrate for dozens of enzymesNNMTNo single identified receptor target
    Studies of the combination/molecule itselfNo published study of the combinationSeveral preclinical papers in cells and mice (2017-2024)A larger body of preclinical literature
    Human dataZeroZeroLimited human investigation
    FormOral capsuleCapsule or powderLyophilized powder

    Storage & handling

    • Capsules are stored at room temperature in a sealed container, away from light and moisture.
    • NAD+ is moisture-sensitive — reseal the container immediately after use and do not leave it open.
    • Avoid storage in areas with temperature swings or high relative humidity (bathrooms, near heat sources).
    • Avoid exposure to direct sunlight.
    • Keep in the original packaging with any desiccant supplied until the point of laboratory use.
    • Handle using standard laboratory practice and appropriate personal protective equipment; 5A1MQ is a compound with no human toxicology data and should be treated accordingly.
    • Keep away from children and out of food preparation areas.

    Documentation

    • Certificate of Analysis (CoA) per batch, with date and lot number.
    • Purity analysis by HPLC — specification ≥98%.
    • Identity confirmation by mass spectrometry for each component separately.
    • Research Use Only (RUO) declaration on the packaging.
    • Documents available on request for the specific batch you received.

    References

    References & documentation

    1. 1.Kraus D. et al. (2014). Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature, 508(7495), 258-262.
    2. 2.Camacho-Pereira J. et al. (2016). CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism. Cell Metab, 23(6), 1127-1139.
    3. 3.Trammell S.A.J. et al. (2016). Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nat Commun, 7, 12948.
    4. 4.Neelakantan H. et al. (2017). Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol, 147, 141-152.
    5. 5.Rajman L., Chwalek K., Sinclair D.A. (2018). Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. Cell Metab, 27(3), 529-547.
    6. 6.Liu L. et al. (2018). Quantitative Analysis of NAD Synthesis-Breakdown Fluxes. Cell Metab, 27(5), 1067-1080.e5.
    7. 7.Brachs S. et al. (2019). Genetic Nicotinamide N-Methyltransferase (Nnmt) Deficiency in Male Mice Improves Insulin Sensitivity in Diet-Induced Obesity but Does Not Affect Glucose Tolerance. Diabetes, 68(3), 527-542.
    8. 8.Yoshino M. et al. (2021). Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women. Science, 372(6547), 1224-1229.
    9. 9.Dimet-Wiley A. et al. (2022). Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice. Sci Rep, 12(1), 484.
    10. 10.Babula J.J. et al. (2024). Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. Diabetes Obes Metab, 26(11), 5272-5282.

    Product information

    Frequently asked questions

    Are these peptides?
    No, neither of them. 5-amino-1MQ (5A1MQ) is a synthetic small molecule on a quinolinium scaffold, with no amino acid chain whatsoever. NAD+ is a dinucleotide — a naturally occurring coenzyme already present in every cell. Neither belongs to the peptide class, even though the product sits in a research peptide catalogue.
    Why together rather than separately?
    Because the two components intervene at two different points on the same metabolic pathway. 5A1MQ acts upstream: it inhibits the NNMT enzyme, which consumes nicotinamide — the precursor from which the cell rebuilds NAD+ via the salvage pathway. NAD+ is supplied downstream: it is the finished coenzyme itself. One approach protects the raw material, the other adds the end product. It must be stressed, however, that this is biochemical reasoning and not an experimentally verified finding — see the next question.
    Has the combination been studied?
    No. No published work has examined co-administration of 5A1MQ and NAD+. A PubMed search for the two substances together returns zero results — not in cells, not in animals, not in humans. Everything known concerns each component separately. The rationale for the combination is coherent; it is not documented.
    Is NAD+ absorbed orally?
    This is the most disputed point and deserves an honest answer. NAD+ is a large, charged dinucleotide, and no publication was found documenting absorption of intact oral NAD+ in humans. This is precisely why the literature studies smaller precursors: nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN). Liu and colleagues (2018, Cell Metabolism) in fact showed that even NR and NMN, when given orally, are metabolized to nicotinamide in the liver, whereas intravenously they reach tissues intact. The route of administration materially changes the picture.
    What exactly does the NNMT enzyme do?
    It takes nicotinamide (vitamin B3) and adds a methyl group to it, producing 1-methylnicotinamide. The methyl group comes from S-adenosylmethionine (SAM), the cell's universal methyl donor. NNMT therefore consumes two things at once: the precursor of NAD+ and methylation units. Inhibiting it in cultured adipocytes was accompanied by reduced 1-methylnicotinamide and increased intracellular NAD+ and SAM (Neelakantan et al., 2017).
    Is there human data for 5-amino-1MQ?
    No. No clinical trial in humans, at any stage. There is no Phase I study, no tolerability study and no human safety data. Every published finding comes from cell culture and mice.
    What did the animal studies show?
    Kraus and colleagues (2014, Nature) showed that knocking down Nnmt in mouse white adipose tissue and liver protected against diet-induced weight gain, with increased adipose SAM and NAD+ levels. Neelakantan and colleagues (2017), using 5A1MQ in obese mice, recorded reduced body weight and white adipose mass, smaller adipocytes and lower total cholesterol, with no change in food intake. Babula and colleagues (2024), over 28 days of dosing, reported improved glucose tolerance and attenuated hepatic steatosis. These are strictly animal findings and do not transfer to humans.
    Do all the data point the same way?
    No, and that matters. Brachs and colleagues (2019, Diabetes) studied mice with full genetic deletion of NNMT and found sex- and diet-dependent results: improved insulin sensitivity in males on a high-fat diet and reduced weight gain in females on a Western diet, but no improvement in glucose tolerance in any group. The field is not settled.
    Why does NAD+ decline with age?
    The review by Rajman, Chwalek and Sinclair (2018, Cell Metabolism) records the steady decline of NAD+ levels with age as a central finding of the field. As to mechanism, Camacho-Pereira and colleagues (2016, Cell Metabolism) showed that expression and activity of the NADase CD38 increase with ageing and are required for the age-related NAD+ decline, through a SIRT3-dependent mechanism.
    Has it been approved anywhere?
    5A1MQ holds no approval from the FDA, EMA, the Greek NOM or any other regulatory authority, for any indication in any country. It is not a medicine and not a drug candidate in clinical trials. NAD+ is an endogenous molecule, not an approved therapeutic product. The product as a whole is research material.
    Can it be used by humans or animals?
    No. The product is supplied exclusively for laboratory research. It is not intended for human or veterinary use, nor for consumption in any form, nor for in vivo application outside a controlled laboratory setting. No administration or dosing guidance is provided.