Mitochondria & Energy

5-Amino-1MQ

5-Amino-1MQ is a small, non-peptide molecule that inhibits the NNMT enzyme. It is meant to support NAD+ metabolism in fat cells - so far only demonstrated in rodent models.

Also seen on labels, in price lists and in the community as: 5AM

Editorial team ·Updated ·4 Sources ·evidence-rated ·independent & ad-free

Common use figures vary widely

How this peptide is typically used - described, not recommended.

How often
1-2 times a day
How long
6-12 weeks straight, then a 2-4-week break
Administration
Injection

For 5-Amino-1MQ, reported injectable community protocols range from 0.15 to 50 mg per day. They are not clinically tested and do not establish a reliable typical dose. - Daily amount: 0.15 to 50 mg per day - Administration: subcutaneous (under the skin), usually once daily - Cycle: 6 to 12 weeks, followed by a 2 to 4 week break The numbers come from forums and vendor sites. There is no approved human dose and no human studies, so the wide range does not reveal a typical dose.

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As of

5-Amino-1MQ is not a peptide - it's a small, fully synthetic molecule from the methylquinolinium-salt family. It often shows up next to peptides in longevity and metabolic-health conversations, frequently under a "peptide" label, even though it contains no peptide bonds and does not occur naturally in food. It blocks a single enzyme called NNMT and is interesting to anyone exploring NAD+, mitochondria, and fat metabolism.

What is 5-Amino-1MQ?

5-Amino-1MQ is a small, fully synthetic molecule - explicitly not a peptide. Chemically it belongs to the methylquinolinium-salt family (chemical name 5-amino-1-methylquinolinium; cation formula C10H11N2⁺, molecular weight 159.22 g/mol; research-grade material is typically supplied as the chloride salt C10H11ClN2, 194.67 g/mol). The compound contains no peptide bonds, does not occur naturally in food, and is nonetheless regularly marketed online as a "peptide".

The compound was developed in the 2010s as a selective inhibitor of the enzyme nicotinamide N-methyltransferase (NNMT). NNMT is most active in fat tissue, liver, and skeletal muscle, where it "burns" nicotinamide - a key building block for the body's own production of NAD+, a coenzyme every cell depends on for energy metabolism.

When NNMT is blocked, more nicotinamide stays inside the cell. The body can convert it to NAD+, and the cell's energy-and-storage balance tilts slightly toward "burn" instead of "store". That is exactly the idea driving body-composition research around this molecule.

How does 5-Amino-1MQ work?

5-Amino-1MQ selectively inhibits the enzyme nicotinamide N-methyltransferase (NNMT) at very low concentrations (IC₅₀ ≈ 1-1.2 µM - the concentration at which half the enzyme is blocked), without meaningfully blocking related SAM-dependent methyltransferases (other enzymes that perform similar chemical transfer reactions) or enzymes of the NAD+ recycling pathway (called the salvage pathway - the body's own NAD+ reuse system). More nicotinamide stays available for the body's own NAD+ production, and downstream pathways such as SIRT1 and AMPK are indirectly activated.

The proposed mechanism runs through three steps shown so far only in mice and cell culture:

  • NNMT inhibition: The enzyme is blocked; nicotinamide is no longer "spent" by NNMT.
  • NAD+ rise in fat cells: The rescued precursor feeds the NAD+ salvage pathway, raising intracellular NAD+ in adipocytes.
  • Activation of SIRT1 and AMPK: NAD+ is the fuel for sirtuins (a family of enzymes linked to metabolic regulation and longevity) and activates AMPK, the cell's central energy sensor. Fat cells are thought to switch from storage to oxidation.

One feature that distinguishes 5-Amino-1MQ from plain NAD+ precursors: it also raises SAM (S-adenosylmethionine), because NNMT normally consumes SAM along with nicotinamide. SAM matters for DNA methylation and many epigenetic switches - an angle that goes beyond simply topping up NAD+.

In cell-based models the activity profile extends beyond NAD+ mechanics: preclinical data report increased mitochondrial efficiency, inhibition of adipocyte growth and proliferation, support of lipolysis (i.e. the breakdown of stored fat in cells), and - in diet-induced obesity models - reversal of type-2-diabetes symptoms. In cancer-cell models, cell shrinkage, loss of cellular adhesion, and apoptosis (programmed cell death) have additionally been observed, even though no approved oncological indication has emerged from this.

What does the research show?

All currently published data on 5-Amino-1MQ come from the Watowich laboratory at the University of Texas Medical Branch (UTMB) and consist exclusively of mouse studies, cell-culture models, and a single pharmacokinetic (PK) study in rats - examining how the body absorbs, distributes, and breaks down the compound. No published human clinical trials exist as of mid-2026, and neither FDA nor EMA approval is in place.

The evidence is still preclinical only - meaning mice and cells:

  • Neelakantan et al. (2017) characterized the compound as one of the first selective, membrane-permeable NNMT inhibitors.
  • Neelakantan et al. (2018) showed that obese mice lost fat mass on 5-Amino-1MQ without eating less, with improved glucose tolerance.
  • A follow-up in aged mice also reported gains in muscle strength.
  • A pharmacokinetic (PK) study in rats reports oral bioavailability of about 38% (meaning roughly 38% of the swallowed dose actually reaches the bloodstream) and a plasma half-life near 7 hours (the time it takes for the active compound in the blood to be reduced by half).

That the evidence base essentially originates from a single research group is a key point for source criticism: independent replications at other sites, as well as first-in-human Phase I trials (the earliest stage of clinical testing, focused mainly on safety), are still missing. Zero published human clinical trials exist. Anything circulating online about dosing or fat-loss effects is extrapolated from animal data. When 5-Amino-1MQ is marketed as a "fat burner", keep that gap in mind.

How is 5-Amino-1MQ taken?

Unlike most peptides, 5-Amino-1MQ is orally bioavailable and is sold commercially as 50 mg capsules, loose powder, or for subcutaneous injection, without any of these application forms having been shown superior in head-to-head pharmacokinetic studies and without any validated human dose.

In animal studies the compound has been given both orally and parenterally (bypassing the gut, e.g. by injection). Since neither an approved indication nor validated human doses exist, every real-world use sits outside clinical evidence. Vendors often market subcutaneous injections as the "ideal" application, claiming the active ingredient bypasses first-pass liver metabolism (the initial passage through the liver, which normally breaks down part of an oral dose before it reaches the rest of the body) - but published comparative data supporting that pharmacokinetic claim do not exist.

In the absence of human data, storage guidance is purely practical: avoid temperature swings and repeated freeze-thaw cycles, because the material readily absorbs moisture and clumps; let a refrigerated vial reach room temperature before opening so condensation does not settle on the batch. Handling notes for research chemicals are collected in the Peptigraph guides.

Safety, gray market, and alternatives

5-Amino-1MQ is neither FDA- nor EMA-approved and is sold as a research chemical; in rodent models roughly 15 to 25 percent of treated animals showed gastrointestinal complaints, only anecdotal reports of mild nausea, fatigue, and dizziness exist for humans, and theoretical risks from interfering with the SAM methylation cycle (a body-internal process that attaches small chemical 'tags' - methyl groups - to DNA, proteins, and other molecules, regulating how they function) cannot be ruled out.

The compound is not regulated as a medicine in the US or EU but still shows up in the gray market - the risks that come with that are summarized in Peptigraph's Vendor Radar. If you want to explore mitochondrial targets with stronger evidence, look at SS-31 (SS-31 holds U.S. Orphan Drug status - a designation for medicines targeting very rare diseases - and Fast Track designation for accelerated review; tested, among other things, for Barth syndrome, a very rare inherited mitochondrial disorder; still without FDA approval) and MOTS-c.

Side effects - what is documented and what isn't

In rodent models 5-Amino-1MQ was generally well tolerated, with no obvious organ toxicity, but gastrointestinal complaints appeared in about 15 to 25 percent of treated animals. In humans only anecdotal reports of mild, transient symptoms like nausea, fatigue, and dizziness exist - methodologically non-robust, but useful as a rough expectation. Beyond simple tolerability, the theoretical risk from interfering with the body's SAM methylation cycle matters: because it is unclear how this affects DNA methylation, neurotransmitter balance, or drug interactions over time, people with known methylation issues should be especially cautious.

Heart rate, appetite, and retail availability

In longevity forums and on social media two specific questions keep coming up: whether 5-Amino-1MQ noticeably changes heart rate and whether it suppresses appetite. Both cannot be answered from the available sources because human studies and standardized adverse-event reporting are missing - naming the gap transparently beats speculative answers. Against that backdrop, 5-Amino-1MQ is sold on large US platforms such as Amazon and Walmart as if it were a dietary supplement or "peptide" product. Specialists point out that the substance is not a recognized food ingredient and has neither FDA drug status nor compounding-pharmacy status (a designation that allows specialized pharmacies to prepare custom formulations); mere retail availability is no substitute for missing clinical evidence.

Evidence at a glance

Research status
All published efficacy research on 5-amino-1MQ consists of in vitro cell culture and in vivo animal studies (mice/rats) [19]. As of 2026, there are no published or registered human clinical trials in ClinicalTrials.gov or the peer-reviewed literature [14, 17, 18, 19]. A 2025 review explicitly states that no clinical trials have yet targeted NNMT in CVD patients [7]. All marketed or anecdotal human dosing claims lack published clinical foundation, indicating no regulatory approval for human use [15, 23].
Human evidence
There are no completed or published human clinical trials for 5-amino-1MQ as of 2026 [14, 17, 18, 19]. Consequently, human oral bioavailability, tissue distribution, safety, and efficacy remain unstudied [17, 18]. All marketed or anecdotal human dosing claims lack published clinical foundation [15, 23].
Dosages in studies & practice
Dosages appear only in animal studies and are provided for descriptive context only, not recommendations for human use. In an efficacy study with diet-induced obese (DIO) mice, the dosage was 20 mg/kg/injection × 3 injections (~34 mg/kg/day total) administered subcutaneously [1]. In a dose-escalation tolerability study in DIO mice, a range of 10-150 mg/kg/day was tested, with 60 mg/kg/day well tolerated (n=2) [1]. A general efficacy reference mentions ~40 mg/kg/day in drinking water (oral) for mice [17]. No human dosing data exist [15, 23].
Risks & side effects
Short-term rodent studies (6-8 weeks) reported no major organ toxicity, with liver and kidney function markers remaining normal, and no observable adverse effects at standard studied doses [1, 18]. Secondary and marketing sources mention anecdotal reports of mild side effects in humans, such as temporary digestive changes or mild headaches, but these are not clinically validated [15]. No studies have evaluated 5-amino-1MQ safety in specific populations, such as individuals over age 65 or pregnant women [24].
Research gaps
Long-term safety was not assessed in preliminary experiments [18]. Human safety, efficacy, and dosing data do not exist [17, 18]. The current evidence base is limited to preclinical models from a small number of overlapping research groups [13, 19]. Studies used small sample sizes (e.g., n=2 in the dose-escalation phase) and short durations [1]. Results observed in animal models do not establish that equivalent effects or safety profiles will occur in humans [14].

Editorial, sourced from primary literature - not medical advice.

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