About 5-Amino-1MQ
5-Amino-1MQ is a methylated quinoline that inhibits nicotinamide N-methyltransferase (NNMT). Preclinical studies show effects on adipose tissue, muscle mass, and metabolic markers. Limited human data.
Longevity
5-Amino-1MQ
NNMT Inhibitor
A small-molecule NNMT inhibitor studied for metabolic health and longevity. Not a peptide; commonly stocked in peptide vendor catalogs.
PreclinicalResearch use only
Where to buy
Vendor offerings
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Best $/mg
Atomik LabzTestedLIQUID – 5-Amino-1MQ/NADH (50mg/40mg per ml) (20ml)
EVERYDAY25$99.00
$1.98/mg · 50mg
Atomik LabzTested5-Amino-1MQ – 50mg (Lyophilized)
EVERYDAY25$129.00
$2.58/mg · 50mg
Solution PeptidesTested5-Amino-1MQ – 50mg (Lyophilized)
EVERYDAY15$129.00
$2.58/mg · 50mg
Atomik LabzTestedCAPSULES – 5-Amino-1MQ 50mg x 90 Capsules
EVERYDAY25$169.00
$3.38/mg · 50mg
Solution PeptidesTestedCAPSULES – 5-Amino-1MQ 50mg x 90 Capsules
EVERYDAY15$169.00
$3.38/mg · 50mg
Solution PeptidesTestedLIQUID – 5-Amino-1MQ/NADH (20ml)
EVERYDAY15$99.00
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Evidence level
Preclinical only
A small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT). Studied preclinically for fat-loss and lean-mass preservation by preserving cellular NAD+ and SAM. Not technically a peptide, but routinely stocked in peptide catalogs.
Mechanism
Inhibits NNMT to preserve cellular NAD+ and SAM pools.
Researched benefits
Adipocyte size reduction
In diet-induced obese mice, oral 5-Amino-1MQ reduced white adipose tissue mass and adipocyte diameter without changing food intake. The effect is attributed to NNMT inhibition releasing the brake on SAM-dependent methylation flux in fat.
Lean mass preservation
Aged mouse muscle shows elevated NNMT; pharmacological inhibition restored myogenic capacity and grip strength in preclinical models. Suggested as an exercise-adjacent intervention for sarcopenia, though human studies have not been published.
NAD+ and SAM sparing
NNMT consumes SAM and produces 1-methylnicotinamide from nicotinamide, draining methyl donors. Inhibition raises intracellular NAD+ precursors and SAM, with downstream effects on histone methylation and energy metabolism.
Risks & cautions
- high
No human efficacy or safety trials
All efficacy data is rodent. Human pharmacokinetics, chronic-dosing safety, and effective dose ranges are extrapolated. Adverse events at typical research doses are not characterized.
- moderate
Methylation pathway perturbation
Raising SAM globally has unpredictable epigenetic and neurochemical effects (catecholamine methylation, homocysteine balance). The long-term consequences of sustained NNMT inhibition in humans are unknown.
- moderate
Off-target effects unclear
5-Amino-1MQ was developed as a research tool; selectivity in humans across the broader methyltransferase family has not been thoroughly mapped.
Dosing
Commonly reported as 50–150 mg orally once daily, taken with food. Cycled 8–12 weeks on, 4 weeks off in practitioner protocols.
- Conservative
- 50 mg oral, daily
- Standard
- 100 mg oral, daily
- Aggressive
- 150 mg oral, daily (not commonly used)
Vial sizes
100mg
Half-life
~6 hours
Route
oral
Oral bioavailability is reasonable in mice. Take with food to reduce GI upset. No reconstitution required for the freebase capsule form.
Contraindications
- Pregnancy or breastfeeding — no data
- Active malignancy — methylation-pathway modulation is theoretically concerning
- Concurrent methyl-donor supplementation (TMG, SAMe) without monitoring
In depth
Background
5-Amino-1-methylquinolinium (5-Amino-1MQ) is a small-molecule inhibitor of nicotinamide N-methyltransferase, an enzyme that quietly drains the cell's methyl-donor pool. NNMT activity is upregulated in white adipose tissue of obese humans and in aged muscle, and the prevailing hypothesis is that this drain is a node in metabolic dysfunction.
It is not a peptide in the chemical sense — it's a methylated quinoline — but it has been adopted into the "research peptide" supply chain because the audience overlaps with longevity and body-composition users.
Mechanism in depth
NNMT catalyzes the transfer of a methyl group from S-adenosylmethionine (SAM) to nicotinamide, producing 1-methylnicotinamide (1-MNA) and S-adenosylhomocysteine. By doing so it:
- Consumes SAM, the cell's universal methyl donor.
- Sequesters nicotinamide, a precursor in the NAD+ salvage pathway.
- Produces 1-MNA, which has its own (still-debated) signaling roles.
Inhibiting NNMT therefore preserves both NAD+ and SAM. The downstream consequences include:
- Increased histone H3K4 methylation in adipocytes, shifting gene expression away from lipid storage programs.
- Increased NAD+ availability for sirtuins and PARPs.
- Lower 1-MNA, which has been implicated in adipose energy expenditure.
Human evidence
There is essentially none. Search of clinicaltrials.gov returns no completed trials of 5-Amino-1MQ. Human safety, efficacy, and pharmacokinetics are inferred. Practitioner reports are anecdotal.
Preclinical evidence
Several rodent studies converge on the same story:
- Kraus 2014 used antisense knockdown of NNMT in DIO mice and saw resistance to weight gain.
- Neelakantan 2018–2019 developed 5-Amino-1MQ as a tool compound and reproduced the phenotype pharmacologically: reduced adiposity, smaller adipocytes, no effect on lean mass loss under caloric restriction.
- Independent work in aged mouse muscle showed restored regenerative capacity after NNMT inhibition.
The signal is consistent across labs at the rodent level. Translation is the question.
Stack synergy
Frequently combined with:
- NAD+ precursors (NR, NMN) — complementary rather than redundant; NNMT inhibition slows the methylation-mediated drain on these precursors.
- MOTS-c — both target mitochondrial-adjacent metabolic pathways.
- GLP-1 agonists — anecdotal use for muscle-mass preservation during semaglutide weight loss; no controlled data.
Avoid stacking with high-dose nicotinamide if the goal is to maximize NAD+, since unblocked NNMT will methylate it away — but the inhibitor is doing exactly that work, so this is more a theoretical issue than a clinical one.
Open questions
- Does NNMT inhibition lower 1-MNA enough to matter? 1-MNA itself has been described as a beneficial signaling molecule, so the net effect is not obvious.
- What is the human dose-response? Mouse doses scale poorly without proper PK data.
- Are there epigenetic risks from raising SAM chronically?
- Is the muscle-mass effect real in humans, or a rodent-specific phenomenon?
References
- 1.Kraus D. et al. — Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity (Nature, 2014)
- 2.Neelakantan H. et al. — Selective and membrane-permeable small molecule inhibitors of NNMT (Biochemical Pharmacology, 2018)
- 3.Neelakantan H. et al. — Small molecule NNMT inhibitor reduces fat mass and improves metabolic health (Biochemical Pharmacology, 2019)