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5-Amino-1MQ

10mg vial
A$ 141Rp 1.800.000
Bulk buy pricing
3–5 vials
A$ 129
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6–9 vials
A$ 121
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10+ vials
A$ 110
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A small molecule — not a peptide — studied as an inhibitor of the enzyme NNMT, which is overexpressed in fat tissue in obesity. Blocking it raises cellular NAD+ and activates pathways linked to mitochondrial function and fat oxidation. The distinguishing feature in the preclinical work is that fat mass reduces without food intake reducing: it does not suppress appetite.


Compound overview

What it is

5-Amino-1MQ (5-amino-1-methylquinolinium, CAS 42464-96-0) is a small molecule rather than a peptide — worth stating plainly, since it sits alongside peptides in most catalogues. It selectively inhibits nicotinamide N-methyltransferase (NNMT), an enzyme that consumes nicotinamide and is markedly overexpressed in adipose tissue in obesity. Inhibiting NNMT spares nicotinamide for NAD+ synthesis, raising cellular NAD+ levels. Higher NAD+ availability activates the sirtuin pathway (SIRT1), which is associated with mitochondrial biogenesis and increased fat oxidation. The result in preclinical models is reduced adipocyte size and fat mass through altered energy handling rather than through appetite signalling.

The reported response is metabolic rather than appetite-driven. Cellular NAD+ rises, mitochondrial activity in fat and muscle tissue increases, and fat oxidation improves. Because appetite is not suppressed, there is no reduction in food intake to signal that the compound is working — which makes it a poor fit for anyone expecting the felt experience of a GLP-1. This is also why it is more usefully positioned as a stack partner to Retatrutide or Tirzepatide than as an alternative to them. Human data is limited; most of what is known comes from animal and cell studies.

Studied outcomes
  • Reduced fat mass and adipocyte size in diet-induced obese mice without reduced food intake
  • Increased cellular NAD+ and activation of SIRT1-associated pathways
  • Improved metabolic parameters when combined with reduced-calorie feeding in preclinical models
  • NNMT knockdown independently protects against diet-induced obesity — the target itself is well validated
  • Human weight-loss evidence is not yet established — the fat-loss findings above are preclinical

Suitability

Who it's for

  • Metabolic support alongside a GLP-1 or GIP agonist protocol — a different mechanism, not a competing one
  • Clients who want a fat-loss lever that does not act through appetite suppression
  • NAD+-focused metabolic and longevity protocols
  • Clients comfortable with a compound whose human evidence base is still early
Who should avoid it
  • Competing athletes subject to anti-doping testing — see cautions
  • Pregnancy or breastfeeding (no safety data)
  • Clients expecting appetite suppression or GLP-1-comparable weight loss
  • Clients who want an established human evidence base before starting

Dosing guidance

Protocol guidance

Dose
2.5mg per day
Frequency
Once daily. Plasma half-life is approximately 3.8–6.9 hours, so the daily dose is sometimes split into two 1.25mg administrations, morning and evening.
Cycle length
8–12 weeks
Route
Subcutaneous injection
Timing
Morning, or split morning and evening if dosing twice daily

Safety

Contraindications & cautions

  • Supply: at 2.5mg per day a 10mg vial is four days of material. A month requires roughly 7.5 vials. Plan and price the full cycle before starting, and speak to us about bulk pricing — this is not a one-vial compound.
  • WADA-banned under category S0 (unapproved substances) — not permitted for any athlete subject to anti-doping testing
  • Not registered with the FDA or any equivalent regulator
  • Human data is limited; the weight-loss evidence is preclinical, and effect sizes in humans are unknown
  • It is a small molecule, not a peptide — reconstitution and handling guidance differs from the peptides in this catalogue, so follow the guidance supplied with the vial

Stacking

Pairs well with

Both raise cellular NAD+ — 5-Amino-1MQ by reducing its consumption, NAD+ by direct supply. The same pathway approached from both ends.

Mitochondrial signalling and metabolic flexibility alongside NNMT inhibition — complementary metabolic mechanisms

Appetite-driven and non-appetite-driven fat loss run on separate mechanisms — a stack partner rather than an alternative


Evidence base

Research

Neelakantan et al. (2018) — Selective NNMT inhibitors reverse diet-induced obesity in mice, Biochem Pharmacol ↗Kraus et al. (2014) — NNMT knockdown protects against diet-induced obesity, Nature ↗Sampson et al. (2021) — NNMT inhibition with reduced-calorie diet, Sci Rep ↗Ruf et al. (2022) — Small molecule NNMT inhibitors for metabolic disorders, Sci Rep ↗

Not medical advice. Not a substitute for medical care. Consult your licensed practitioner before beginning any protocol. Peptides are sold for research purposes only and are suitable for adults aged 18 years and over.