Independent · non-commercial · publishes on a quarterly cycle|Current cycle 2026 Q3
Compound Evidence InstituteEvidence synthesis · established 2023Graded assessments of compounds, trials, methods and supply
Document set current to 30 July 2026
Compound monograph · §2

5-amino-1MQ — pharmacology

Molecular targets, mechanism of action, pharmacokinetics and interactions as characterised in humans.

Document identifier
CEI-MN-047/2
Series
Compound monograph
Version
4.0
Published
07 Jul 2025
Last reviewed
07 Dec 2025
Next review
07 Dec 2027
Identifier
10.71829/cei.mono.47
Certainty
Very low
Cycle
2025 Q3

§2Pharmacology

§2.1Molecular targets

Table 2. Molecular targets recorded for 5-amino-1MQ, with the character of the interaction and the potency where the Institute holds it.

TargetInteractionNote
Nicotinamide N-methyltransferase (NNMT)InhibitorCompetitive with the nicotinamide substrate; reported IC₅₀ in the low micromolar range

§2.2Mechanism of action

NNMT methylates nicotinamide, diverting it from NAD+ salvage and generating 1-methylnicotinamide. Inhibiting NNMT is proposed to raise cellular NAD+ and to reduce adipocyte lipogenesis. In diet-induced obese mice, 5-amino-1MQ reduced fat mass without affecting food intake. The Institute notes that the compound is a permanently charged quaternary cation and that its intracellular access to a cytosolic enzyme target is not well characterised.[1,2]

§2.3Pharmacokinetics

No human pharmacokinetic characterisation of 5-amino-1MQ has been identified. In the absence of a half-life, a volume of distribution and a clearance estimate, no dosing interval used in practice can be related to any exposure that produced an effect in any study, and the Institute records this as a first-order gap rather than a detail.

§2.4Interactions

  • Not characterised

References cited on this page

References are numbered in order of first citation in this document. Each superscript in the text links to its entry below.

  1. Lee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, Cohen P. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism 2015;21(3):443–454. doi:10.1016/j.cmet.2015.02.009 · PMID 25738459
  2. International Council for Harmonisation of Technical Requirements for Pharmaceuticals for Human Use. ICH Q3C(R9) Impurities: Guideline for Residual Solvents. ICH Harmonised Guideline 2024;Step 4 version. identifier not held by the Institute

Identifiers are reproduced only where the Institute holds them. Where a digital object identifier or PubMed identifier is not shown, the Institute has recorded the journal and year and has not constructed an identifier.

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