Class 10 · Metabolic / longevity · NNMT inhibitor · Quinolinium SMALL MOLECULE · Not a peptide · Oral (research)
5-Amino-1MQthe NNMT-inhibitor small molecule sold beside the peptides
First, the thing that matters most: 5-Amino-1MQ is not a peptide. It's a synthetic small-molecule drug that's sold alongside peptides because it's grouped with metabolic/longevity research compounds. It blocks an enzyme called NNMT, which is linked to how cells use NAD⁺ and how fat cells store fat. The early research — all in cells and mice — is interesting, but it is not an approved weight-loss drug, there is no established human dose, and in 2026 the FDA cited it in a warning letter.
A synthetic quinolinium NNMT inhibitor (not a peptide; no amino-acid sequence) studied preclinically for obesity/metabolic dysfunction. Its proposed relevance centers on nicotinamide methylation, NAD⁺/SAM availability, lipogenesis suppression, and adiposity reduction. The efficacy evidence is animal and in-vitro only — no published human outcome trial, and there is no validated human dosing protocol.
5-amino-1-methylquinolinium (5-AMQ, "NNMTi"; CAS 42464-96-0, iodide salt C₁₀H₁₁IN₂, MW 286.11; free cation C₁₀H₁₁N₂⁺ ~159.21; PubChem CID 66522933 / cation 950107) is a membrane-permeable, substrate-site NNMT inhibitor (IC₅₀ ~1.2 µM). It reduces 1-methylnicotinamide and raises intracellular NAD⁺ and SAM in adipocyte models; in diet-induced obese mice it reduced body weight and fat mass at 20 mg/kg SC three times daily.
Not a peptideQuinolinium small molecule
NNMTEnzyme inhibitor · IC₅₀ ~1.2 µM
Mice onlyNo human efficacy/safety trial
FDA-warnedNot approved · 2026 warning letter
Status
Not FDA-approved · 2026 warning letter · not 503B-eligible
A small molecule with a real mechanism and no human data.
5-Amino-1MQ is unusual in this atlas for two reasons. It isn't a peptide — it's a quinolinium small-molecule NNMT inhibitor, which the identity section makes explicit. And its evidence is entirely preclinical: a credible biochemical rationale (block NNMT → preserve NAD⁺ and SAM → reduce fat-cell lipogenesis) backed by cell studies and short rodent experiments, but with no published human efficacy or safety trial of any kind. In the U.S. it is unapproved, and a 2026 FDA warning letter cited a compounder for making it ineligibly — under conditions that caused documented harm.
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Primary use case
Metabolic research
Studied preclinically as an NNMT inhibitor for obesity/metabolic-dysfunction models — not validated for human fat loss. Grade C.
Animal and in-vitro only for efficacy; no published human outcome trial identified. Grade C.
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Typical "dose"
No human dose
No approved human dose; mouse studies used 20 mg/kg SC three times daily — human commercial protocols are speculative. Grade D/P.
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Identity flag
NOT a peptide
A synthetic quinolinium small molecule with no amino-acid sequence — sold in peptide markets, but chemically not a peptide. Grade D.
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Key risk
Unknown in humans
Unknown human safety; theoretical methylation-cycle, NAD⁺, off-target, pregnancy, and oncology uncertainties. Grade D/P.
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US regulatory
FDA-warned
Not FDA-approved; a 2026 warning letter cited 5-Amino-1MQ as not eligible for 503B compounding exemptions. Grade D.
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Pharmacokinetics
Rat only
Rat PK: oral t½ ~6.9 h, IV t½ ~3.8 h, oral bioavailability 38.4% — human PK not established. Grade C.
02 · Mechanism of action
How blocking one enzyme rewires fat-cell metabolism.
5-Amino-1MQ has a clean, single-target mechanism: it inhibits NNMT (nicotinamide N-methyltransferase), the cytosolic enzyme that methylates nicotinamide to 1-MNA using SAM as the methyl donor. NNMT is overactive in obese fat tissue, where it wastes nicotinamide and burns through methyl donors. Block it, and cells retain more nicotinamide for NAD⁺ salvage and more SAM for methylation — which in adipocyte models shifts metabolism toward less fat storage. The chain is biochemically coherent and well-supported in cells (Grade P); everything downstream of "in mice" is still preclinical (Grade C).
Grade P/C
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1 · NNMT inhibition / methylation blockade
5-Amino-1MQ blocks an enzyme that normally diverts nicotinamide away from NAD⁺ recycling.
Clinical significance: NNMT inhibition may shift adipocyte metabolism toward higher energy expenditure and lower lipogenesis in preclinical systems. It is the on-target action that defines the compound.
Molecular detail: NNMT catalyzes nicotinamide methylation using SAM to form 1-methylnicotinamide. 5-Amino-1MQ is a membrane-permeable, substrate-site NNMT inhibitor (IC₅₀ ~1.2 µM) that reduced intracellular 1-MNA and increased NAD⁺ and SAM in adipocyte models — without affecting related methyltransferases or NAD⁺-salvage enzymes.
Grade P
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2 · NAD⁺ preservation / salvage support
By blocking nicotinamide "waste" through NNMT, cells may retain more substrate for NAD⁺ biology.
Clinical significance: This is relevant to adipocyte energy metabolism, mitochondrial function, and possibly muscle regeneration — but human benefit is unproven. NNMT is positioned as a tractable metabolic-disease target.
Molecular detail: NNMT inhibition increased intracellular NAD⁺ in adipocyte systems and altered metabolic programming tied to NAD⁺-dependent energetics. The NAD⁺ rise is a mechanistic cell finding, not a validated clinical biomarker response.
Grade P
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3 · SAM / methylation-economy modulation
NNMT consumes methyl donors; blocking it may preserve methylation resources.
Clinical significance: Methylation balance can influence adipocyte gene expression and metabolic phenotype. This links NNMT to broader obesity/T2D biology.
Molecular detail: Every NNMT reaction consumes one SAM as methyl donor. Inhibition raises SAM availability, influencing SAM:SAH-linked methylation reactions — potentially affecting histone methylation and metabolic gene expression. Mechanistic; clinical significance unknown.
Grade P/C
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4 · Lipogenesis suppression in adipocytes
In fat-cell models, NNMT inhibitors reduced fat-making signals.
Clinical significance: This is the main rationale for obesity/metabolic research, but it has not been validated in human weight-loss trials. NNMTi reduced 3T3-L1 lipogenesis (EC₅₀ ~30 µM).
Molecular detail: In differentiating adipocytes, NNMT inhibition suppressed lipogenesis and changed metabolic phenotype, with downstream effects on lipid accumulation and cell size. Cell + mouse evidence only.
Grade C
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5 · Body-weight / adiposity reduction in DIO mice
In obese mice, injected 5-Amino-1MQ reduced body weight and fat mass over a short period.
Clinical significance: The main in-vivo proof-of-concept used diet-induced obese mice at 20 mg/kg SC three times daily for 11 days — not humans, and the dosing was intensive.
Molecular detail: The study linked NNMT inhibition to reduced adiposity, smaller adipocytes, improved metabolic markers, and energy-expenditure changes not explained simply by reduced food intake. Animal in-vivo; the translational bridge to humans is unbuilt.
In old mice, NNMT inhibition improved muscle stem-cell function and strength.
Clinical significance: A separate research line beyond fat loss: in 24-month-old mice, the NNMTi chemotype elevated muscle stem-cell proliferation/fusion and improved regenerative capacity. NNMT is overexpressed in skeletal-muscle aging.
Molecular detail: Reported effects include ~2-fold greater fiber cross-sectional area and ~70% greater peak tibialis-anterior torque versus controls, linked to restored NAD⁺-pathway function. Rodent-only; opens a muscle-aging avenue alongside the adipose work.
L3 · Cascade
From NNMT block to thinner fat cells (preclinical)
🧪 NNMT inhibition
IC₅₀ ~1.2 µM
→
🔻 ↓ 1-MNA
on-target marker
→
🔋 ↑ NAD⁺ / SAM
intracellular
→
🫀 ↓ Lipogenesis
adipocyte
→
🐭 ↓ Adiposity
mouse (not human)
L3 · Why a small molecule, not a peptide
Identity check
Property
5-Amino-1MQ
A peptide
Building blocks
Quinolinium ring + amine
Amino acids (peptide bonds)
Sequence
None
Defined residue sequence
MW
~159 (cation) / 286 (salt)
Typically larger
Oral viability
Yes (small molecule)
Usually poor (degraded)
Why in "peptide" markets
Grouped with metabolic/longevity compounds
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L3 · NNMT in disease
Why NNMT is a target
Context
NNMT role
Obese adipose tissue
Overexpressed / hyperactive
NAD⁺ economy
Wastes nicotinamide via methylation
Methyl economy
Consumes SAM
Cancer biology
Implicated — inhibition not universally benign
03 · Dosing models (speculative, research-only)
No approved human dose — only animal anchors and market practice.
There is no established human dose for 5-Amino-1MQ — no human trial has set one. So everything here is a speculative model scaffold built from rodent dosing and commercial-market practice, not medical advice. The compound is a small molecule (working unit: mg, not µg), commonly sold as oral capsules or liquid. Only animal routes have real data behind them; the calculator validates mg arithmetic only. A 2026 FDA warning letter cited 5-Amino-1MQ as not eligible for 503B compounding.
Not a peptide · no approved human dose · FDA-warned (2026)
In a 2026 warning letter (GenoGenix), the FDA cited 5-Amino-1MQ as ineligible for 503B compounding exemptions — it is not on the 503B bulks list — and documented unsanitary manufacturing conditions at the facility. 5-Amino-1MQ is not FDA-approved, not a dietary ingredient with GRAS status, and should not be presented as a peptide therapy. There is no validated human protocol.
Pharmacokinetics (rat only)
A rat LC-MS/MS PK study reported oral Cmax ~2252 ng/mL, terminal half-life ~3.80 h IV and ~6.90 h oral, and oral bioavailability 38.4%. These are rat values and should not be assumed to predict human dosing — human Cmax, Tmax, clearance, and half-life are unestablished.
Oral capsule / liquid — research model
Commercial-practice observation, not a recommendation
Grade D/P
"Starting"
Not clinically established. A cautious placeholder reflecting commercial practice is 25–50 mg/day — an observation, not advice.
Ladder (model)
25 → 50 → 50 mg BID; all D-grade practice-pattern extrapolation, no evidence-based titration.
Cycle
Not established; research-market cycles often 4–8 weeks, evidence D-grade.
PK logic
Rat oral bioavailability 38.4%; oral t½ ~6.9 h (rat).
Monitoring
Weight, waist, BP/HR, fasting glucose/insulin, CMP, lipids — all unvalidated for this compound.
Avoid pregnancy/lactation, active malignancy; caution in liver/kidney disease; anti-doping concern. No approved human dose. Grade D/P.
Dose bands · model only
Global dose-band table (hypothesis engine, not clinical doses)
Band
Oral mg/day
≈ mg/kg/day @ 80 kg
Basis
Low
25 mg
0.31
Conservative commercial placeholder (no trial)
Standard
50 mg
0.63
Common capsule size (no trial)
High
100 mg
1.25
Upper speculative practice range
Mouse anchor
60 mg/kg/day SC
N/A
20 mg/kg SC TID in DIO mice
Weight-band · hypothesis only
Weight interpolation — no human dose-finding study
Body weight
Low 0.3 mg/kg
Std 0.6 mg/kg
High 1.2 mg/kg
55 kg
16.5 mg
33 mg
66 mg
65 kg
19.5 mg
39 mg
78 mg
75 kg
22.5 mg
45 mg
90 mg
85 kg
25.5 mg
51 mg
102 mg
95 kg
28.5 mg
57 mg
114 mg
105 kg
31.5 mg
63 mg
126 mg
Hypothesis interpolation only — not a validated clinical dosing table.
Titration logic
Titration / safety decision logic
Trigger
Action
Rationale
No adverse effects after 1–2 weeks, goal unmet
Consider one model-band step
Practice-pattern only; no trial basis
GI upset, headache, insomnia, palpitations
De-escalate or hold
Unknown human tolerability
Abnormal ALT/AST, bilirubin, creatinine, eGFR
Hold and reassess
Unknown hepatic/renal handling in humans
Hypoglycemia / unstable glucose
Hold
Potential metabolic interaction
Pregnancy / conceiving / lactation
Hard stop
No reproductive safety data
Active malignancy / unexplained mass
Hard stop, clinician review
NNMT implicated in cancer biology
Biomarker scaffold
Monitoring scaffold (none validated for 5-Amino-1MQ)
Marker
Why
Validated?
Weight / waist
Mouse adiposity endpoint
No
Fasting glucose / insulin
Metabolic context
No
Lipid panel
Metabolic relevance
No
CMP (ALT/AST/Cr/eGFR)
Hepatic/renal safety
No
1-MNA
Closest NNMT-output marker
Not clinically validated
SAM/SAH ratio
Methylation cycle
Not clinically validated
Subcutaneous — animal-study anchor
The route of the key mouse study · not a human protocol
Grade C → D/P
Preclinical anchor
The DIO-mouse study used 20 mg/kg SC three times daily for 11 days.
Human starting dose
None established. Do not derive directly from mouse mg/kg.
HED caution
A raw body-surface conversion from 60 mg/kg/day mouse ≈ 4.9 mg/kg/day human — far above common commercial use, and a hypothesis tool only, not a protocol.
No approved injectable product; sterility, concentration-error, and unknown-safety risks. Grade C (animal route) · D/P (any human extrapolation).
Mouse → human gap
Why the mouse dose isn't a human dose
Step
Value
Mouse dose
20 mg/kg SC × 3/day = 60 mg/kg/day
Raw HED (BSA)
≈ 4.9 mg/kg/day (hypothesis only)
Commercial practice
~0.3–1.2 mg/kg/day oral — far lower
Conclusion
No validated translation exists
Intravenous — rat PK anchor
PK literature only · no human IV use
Grade C → D/P
Literature basis
Rat PK included IV administration with terminal half-life ~3.80 h.
Clinical use
Not established; not a practical protocol — not used in the page calculator as such.
IV use magnifies sterility, excipient, dosing, and acute-reaction risks. Grade C (rat PK) · D/P (human relevance).
Concentration-response curves are not translatable to human dosing. Grade P.
In-vitro potencies
Cell-assay potency values
Readout
Value
NNMT inhibition (IC₅₀)
~1.2 µM
1-MNA reduction (EC₅₀)
~2.3 µM
Lipogenesis (EC₅₀)
~30 µM
Topical / intranasal / transdermal
Not established
Grade D/P
Evidence
No reliable clinical or PK basis for topical, intranasal, or transdermal 5-Amino-1MQ.
Status
Not modeled; not a supported route.
Marked not established. Grade D/P.
Route reality
Where data actually exist
Route
Status
Oral
Commercial practice + rat PK
SC / IV
Animal studies only
Topical / intranasal / transdermal
Not established
L2 · Concentration math (research only)
Reconstitution & Concentration Calculator
For concentration math only — not a dosing recommendation. 5-Amino-1MQ is not a peptide and has no approved human dose (working unit: mg). It's commonly sold as an oral product; injectable use has no approved product and adds sterility/error risk. A 2026 FDA warning letter cited it as not 503B-eligible.
Concentration
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Draw volume
—
Units (U-100)
—
Doses/amount
—
Basis
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04 · Combinations
Combinations — mechanistic ideas, not human data.
The combinations discussed around 5-Amino-1MQ are mechanistic hypotheses and market practice, not studied human regimens. The mouse work paired NNMT inhibition with a diet switch; the rest (exercise, NAD⁺ precursors, GLP-1 agonists) are conceptual pairings that overstate a thin evidence base if presented as validated. Every entry is Grade C or below, and the honest theme is that no human combination has been tested — the diet pairing is the only one with even animal support.
5-Amino-1MQ + Calorie Deficit / Low-Fat Diet
Animal-study context
5-Amino-1MQDiet change
Mouse microbiome/adiposity studies used NNMT inhibition in diet-switch contexts, with NNMTi-plus-low-fat-diet producing microbiome and metabolome profiles distinct from obese controls. Do not imply human weight-loss efficacy — this is the only combination with even animal support. Grade C.
Element
Role
Diet change
The actual intervention
5-Amino-1MQ
NNMT-inhibition add-on (mouse)
5-Amino-1MQ + Exercise / Resistance Training
Mechanistic interest
5-Amino-1MQTraining
Mechanistic interest around NAD⁺, adipose metabolism, and the aged-muscle regeneration findings. NNMT relates to muscle/metabolic biology, but human performance data are absent. A hypothesis, not a protocol. Grade P/D.
Rationale
Status
NAD⁺ / muscle biology
Mouse-level interest
Human performance
No data
5-Amino-1MQ + NAD⁺ Precursor (NR / NMN)
Conceptual NAD⁺ pairing
5-Amino-1MQNR / NMN
A mechanistic idea: NNMT inhibition may preserve the nicotinamide/NAD⁺ pool while a precursor supplies substrate. Both touch NAD⁺ biology, but pairing them risks overstating NAD⁺ effects, and there are no human combination data. Monitor tolerability. Grade P/D.
Agent
NAD⁺ role
5-Amino-1MQ
Preserves nicotinamide (NNMT block)
NR / NMN
Supplies NAD⁺ precursor
5-Amino-1MQ + GLP-1 / GIP Agonist
Market stack · unstudied
5-Amino-1MQGLP-1/GIP
Commercially discussed for fat-loss stacks; mechanistically distinct (appetite/incretin signaling vs adipocyte NNMT metabolism). Additive weight-loss or metabolic effects have not been studied, and clinical oversight would be required. Grade D.
Mechanism
Pathway
GLP-1/GIP
Appetite / incretin
5-Amino-1MQ
Adipocyte NNMT/NAD⁺
Hard-constraint clinical note — Avoid stacking 5-Amino-1MQ in pregnancy/lactation, active malignancy, severe hepatic/renal impairment, uncontrolled diabetes, eating-disorder history, or WADA-governed competition — human safety and interaction data are absent. None of the combinations above is a validated human regimen; the diet pairing alone has animal support, and presenting any of these as proven would overstate a preclinical evidence base.
05 · Safety & contraindications
Human safety is essentially unknown — and the supply chain has bitten.
Published human adverse-event data for 5-Amino-1MQ are essentially absent. Mouse obesity studies didn't report obvious toxicity, but that does not establish human safety. The real risks split three ways: mechanistic (NNMT touches methylation, NAD⁺, and cancer biology, where inhibition may not be universally benign), regulatory/quality (a 2026 FDA warning letter cited a 503B compounder for ineligibly making it under unsanitary conditions — the same inspection documented ER visits tied to a contaminated companion product), and practical (mg-scale injection math and unverified gray-market sourcing). This page does not call 5-Amino-1MQ "safe."
Safety signals & risks
Human adverse-event data absentNo published human safety dataset; mouse studies don't establish human safety. Grade D.
Methylation-cycle disruptionNNMT uses SAM; inhibition may alter SAM/SAH balance. Grade P.
NAD⁺ pathway perturbationIntracellular NAD⁺ changes may have context-specific effects. Grade P.
Cancer-biology uncertaintyNNMT is implicated across cancer/metabolic pathways; inhibition may not be universally benign. Grade P/D.
Quality / sterility risk (documented)FDA cited unsanitary compounding conditions; the same inspection documented ER visits from a contaminated companion product. Grade D.
Hepatic / renal unknownsNo human clearance/safety study. Grade D.
Reproductive toxicity unknownNo pregnancy/lactation safety data. Grade D.
Dosing-error / anti-dopingmg-scale injection math errors; WADA S0 non-approved substance. Grade D.
Practical safety framework
"Unknown," not "safe"
The absence of reported toxicity in short mouse studies is not evidence of human safety. With no human trial, no clearance data, and no validated monitoring, the honest stance is that human safety is unknown — which is itself a reason for caution, not reassurance.
The supply chain is a documented hazard
The 2026 FDA warning letter cited a 503B outsourcing facility for compounding 5-Amino-1MQ ineligibly under unsanitary conditions; the same inspection tied a contaminated companion product to three ER visits. Gray-market quality risk here is concrete, not hypothetical.
Mechanism cuts both ways
NNMT sits at the crossroads of methylation, NAD⁺, and cancer biology. The same target that looks favorable in obese adipose tissue is implicated in tumor biology, so "inhibit NNMT" is not automatically benign across contexts — a key reason active malignancy is a contraindication.
Contraindications & cautions
Condition / scenario
Concern
Severity
Pregnancy
No embryo-fetal safety data
High
Lactation
Unknown transfer/exposure
High
Active cancer
NNMT/cancer biology uncertainty
High
Severe liver disease
Unknown hepatic handling
High
Severe renal disease
Unknown renal handling/excretion
High
Eating disorder / underweight
Fat-loss framing could worsen risk
High
Children / adolescents
No developmental safety data
High
Competitive athlete
WADA S0 non-approved substance
High
Use from unregulated source
Impurity, sterility, mislabeling (FDA-documented)
High
Uncontrolled diabetes
Metabolic shifts could complicate glycemic control
Moderate–High
Polypharmacy with metabolic drugs
No interaction studies
Moderate–High
Any human self-administration
No approved dose; unknown safety
Avoid
06 · Evidence base
Credible biology — zero human outcome data.
The evidentiary picture is easy to state honestly: a credible biochemical rationale, solid cell data, and a handful of short rodent studies — and no published human efficacy or safety trial of any kind. The defining work (Neelakantan et al. 2017) characterized 5-Amino-1MQ as a membrane-permeable NNMT inhibitor and showed fat loss in diet-induced obese mice; a 2019 study extended the chemotype to aged-muscle regeneration; a 2021 rat study established PK; a 2022 study looked at microbiome shifts. All preclinical. The honest grade is C for the preclinical biology and D/P for any human protocol.
Human trials
None
No published human efficacy or safety dataset identified for 5-Amino-1MQ. Grade D.
DIO mice · 2017/18
↓ fat mass
NNMTi reversed HFD-induced obesity; 20 mg/kg SC TID × 11 d. Grade C.
Aged muscle · 2019
~70% torque
NNMTi improved aged-muscle stem-cell function and peak torque in old mice. Grade C.
Neelakantan et al. (2017/18) — NNMT inhibitors reverse HFD obesity in mice
The defining study: characterized 5-Amino-1MQ as a selective, membrane-permeable NNMT inhibitor that reduced intracellular 1-MNA and raised NAD⁺/SAM, suppressed adipocyte lipogenesis, and reduced body weight and fat mass in diet-induced obese mice (20 mg/kg SC three times daily for 11 days) — without attributing the effect to reduced food intake. The membrane permeability was the key advance over earlier NNMT inhibitors.
Neelakantan et al. (2019) — NNMT inhibition & aged-muscle regeneration
Extended the NNMTi chemotype (5 and 10 mg/kg) to 24-month-old mice, finding elevated muscle stem-cell proliferation and fusion (~2-fold greater fiber cross-sectional area) and ~70% greater peak tibialis-anterior torque versus controls — opening a muscle-aging/regeneration research avenue alongside the adipose work. Rodent only.
Awosemo et al. (2021) — rat PK & oral bioavailability
Developed and validated an LC-MS/MS assay for 5-Amino-1MQ in rat plasma/urine and characterized pharmacokinetics: oral Cmax ~2252 ng/mL, terminal half-life ~3.8 h IV and ~6.9 h oral, and oral bioavailability 38.4% — the closest thing to defined PK, but in rats, not humans.
Dimet-Wiley et al. (2022) — NNMTi + diet & microbiome
In diet-induced obese mice, NNMT inhibition combined with a low-fat-diet switch produced cecal microbiome profiles distinct from high-fat-diet obese controls and related to adiposity/metabolome shifts — a secondary-endpoint study suggesting host-metabolism effects rather than a direct microbiome drug action.
NNMT in metabolic disease and beyond (2024 review)
Reviews NNMT as a therapeutic target across metabolic disease, positioning small-molecule inhibitors like 5-Amino-1MQ as tools to interrogate adipose, hepatic, and NAD⁺-linked biology — useful mechanistic context, but a review, not human efficacy evidence.
Summarizes NNMT's implication in obesity, T2D, metabolic syndrome, and liver/adipose biology — the disease rationale behind targeting the enzyme, again as background context rather than 5-Amino-1MQ-specific clinical proof.
NNMT as metabolic regulator & emerging target (2025)
Discusses NNMT's roles spanning metabolism and cancer biology — important for the safety framing, since the same enzyme implicated favorably in obese adipose tissue is also implicated in tumor pathways, so inhibition is not assumed universally benign.
5-amino-1-methylquinolinium iodide — chemical identity
Chemical records (PubChem, supplier standards) document the identity: CAS 42464-96-0, formula C₁₀H₁₁IN₂ (iodide salt), MW 286.11, a quinolinium small molecule with no amino-acid sequence — the basis for the "not a peptide" classification supplier standard.
FDA cited a 503B outsourcing facility for compounding 5-Amino-1MQ and NAD⁺, both ineligible for 503B exemptions (not on the bulks list), under unsanitary conditions; the same inspection documented three ER visits tied to a contaminated companion product — the central US compliance and real-world-harm anchor.
The 503B bulks-list framework determines which bulk substances outsourcing facilities may compound; 5-Amino-1MQ's absence from that list is the basis for the ineligibility finding — context for why the compounding in the warning letter was unlawful. 503B bulks framework.
GRADE summary — Overall evidence strength is low for human use. The strongest evidence is mechanistic cell work and short-duration rodent studies — credible biochemical rationale as an NNMT inhibitor, with fat-loss and aged-muscle signals in mice. But there is no established human dose, no approved indication, no validated monitoring protocol, and no published human outcome trial. Honest grade: C for the preclinical biology, D/P for any human protocol. Positioning: "a real small-molecule NNMT inhibitor with promising rodent metabolic and muscle data — not a peptide, not a proven human therapy, and FDA-warned in the U.S."
07 · Compare & contrast
5-Amino-1MQ among the metabolic compounds.
5-Amino-1MQ is grouped with metabolic/fat-loss research compounds — but it's the odd one out twice over: it's a small molecule (the others below are peptides), and its mechanism (NNMT enzyme inhibition) is distinct from the GH-fragment, mitochondrial-peptide, and GHRH-analog mechanisms it sits beside in the market. The table keeps both the class distinction and the (very different) regulatory status honest — only Tesamorelin is actually approved, and for a narrow indication.
L1 · Consumer — 5-Amino-1MQ is often marketed beside peptides, but it's actually a small molecule studied for how it blocks NNMT — an enzyme linked to NAD⁺ use and fat-cell metabolism. The early research is interesting, but it's all in cells and mice: it is not an approved weight-loss drug, there's no established human dose, and the FDA cited it in a 2026 warning letter. It is not a peptide.
L2 · Clinical — 5-Amino-1MQ is a synthetic quinolinium NNMT inhibitor with preclinical evidence in adipocyte systems and diet-induced obese mice (plus an aged-muscle regeneration line). Its proposed relevance centers on nicotinamide methylation, NAD⁺/SAM availability, lipogenesis suppression, and adiposity reduction — but current evidence does not support validated human protocols, and human safety is unknown.
L3 · Research — 5-amino-1-methylquinolinium acts as a membrane-permeable, substrate-site NNMT inhibitor (IC₅₀ ~1.2 µM) that reduces nicotinamide methylation to 1-MNA while increasing intracellular NAD⁺ and SAM in adipocyte models. In-vivo rodent work suggests NNMT inhibition can remodel adipose metabolic phenotype, improve aged-muscle regeneration, and shift diet-associated microbiome/metabolome signatures — but the translational bridge to human pharmacology remains unbuilt, with rat-only PK and no human trial.
08 · References & evidence
Source register.
Evidence grades reflect the strength of support for the specific claim cited, not the prestige of the journal. For 5-Amino-1MQ the strongest sources are the rodent proof-of-concept and PK studies (Grade C) and the mechanistic cell/review work (Grade P); there is no human clinical source to grade A or B, which is the central fact about this compound. Regulatory and identity records (Grade D) anchor the "not a peptide / not approved / FDA-warned" framing. The grade ceiling here is C — and that is the honest signal.