Metabolic5-amino-1-methylquinolinium5-Amino-1MQ iodide

5-Amino-1MQ

Small-molecule NNMT inhibitor · metabolic

5-Amino-1MQ is not a peptide — it is a small synthetic molecule (a methylquinolinium) developed as an inhibitor of the enzyme NNMT (nicotinamide N-methyltransferase). NNMT is overexpressed in the fat tissue of obese animals, and the research thesis is that blocking it preserves the cell's NAD+ and methyl-group supply and pushes fat cells to burn more energy. For this exact molecule there is a real, reproduced preclinical record: it inhibits NNMT in the test tube (a low-micromolar potency), raises NAD+ and lowers fat storage in cultured fat cells, and — given by subcutaneous injection to obese or aged mice — reduced body weight and fat mass and improved muscle strength. The decisive caveat is what is missing: there is no registered or completed human clinical trial, no published human pharmacokinetics or dose, and no human safety or efficacy data of any kind. Every human-facing fat-loss, muscle, oral-dose, and half-life claim around this compound is extrapolation from rodents or marketing, not primary-source fact. It is a research chemical — not an FDA-approved drug and not a dietary supplement.

The short version

5-Amino-1MQ is one of the few items in this catalog that is not a peptide at all — it is a small synthetic chemical. Its job is to block an enzyme called NNMT, which becomes overactive in the fat tissue of obese animals.

The idea behind it: NNMT uses up two valuable cellular resources (NAD+ precursors and methyl groups) as it works. If you slow NNMT down, the theory goes, you spare those resources and nudge fat cells toward burning more energy instead of storing it.

For this specific molecule the animal and cell evidence is real and has been repeated by the same research group: it blocks the enzyme in a dish, raises NAD+ and lowers fat storage in cultured fat cells, and — injected under the skin of obese or elderly mice — lowered body weight and fat and improved grip strength.

The honest catch is everything that hasn't happened. There is no human clinical trial, no published human dose, no human safety data, and no measurement of how long it lasts in a person. All the impressive results are in mice given subcutaneous injections. Any claim that it is a proven human fat-loss or muscle compound is getting ahead of the evidence.

Molecular identity

Specs

Molecular formula (cation): C10H11N2+
Molecular weight (cation): 159.21 g/mol
Monoisotopic mass (cation): 159.0922 Da
XLogP: 1.1
Topological polar surface area: 29.9 Å²
H-bond donors / acceptors: 1 donor · 1 acceptor

Compound class: Small-molecule N-methylquinolinium (not a peptide)PubChem CID 950107
IUPAC name: 1-methylquinolin-1-ium-5-aminePubChem CID 950107
Common salt form: 5-amino-1MQ iodide (C10H11IN2, 286.11 g/mol)PubChem CID 66522933
CAS / UNII: 42464-96-0 · K9G33W2TTZ (iodide salt)PubChem CID 66522933
Cation registry: CAS 685079-15-6 · UNII PMX593N4N3 (free cation)PubChem CID 950107
Molecular target: NNMT (nicotinamide N-methyltransferase)PMID 28548833
Half-life: ~3.8 h (rat IV) · ~6.9 h (rat oral, F ≈ 38%); no human PK publishedPMID 34304009Half-life curve →
Regulatory status: Research chemical; no human trials; not FDA-approvedClinicalTrials.gov / research literature

Plain English

Mechanism

5-Amino-1MQ targets nicotinamide N-methyltransferase (NNMT), an enzyme that transfers a methyl group (a small chemical tag) from S-adenosylmethionine (SAM) onto nicotinamide (a form of vitamin B3), producing 1-methylnicotinamide. Because nicotinamide is a precursor in the NAD+ salvage pathway (NAD+ is a coenzyme cells need to make energy) and SAM is the cell's universal methyl donor, high NNMT activity is thought to drain both the NAD+ pool and the cell's methylation capacity (its ability to add those chemical tags that switch genes and proteins on and off). NNMT is overexpressed — present at higher-than-normal levels — in adipose tissue (body fat) in obesity and in aged skeletal muscle, which is what made it an attractive metabolic target.

The genetic groundwork for the target came from a 2014 Nature study: knocking down NNMT in the fat and liver of mice protected them against diet-induced obesity, glucose intolerance, and fatty liver. That work validated the target — it did not test this molecule. The pharmacological thesis is that a drug-like NNMT inhibitor should mimic that knockdown, sparing NAD+ and SAM and raising energy expenditure in fat cells.

5-Amino-1MQ is a genuine, peer-reviewed NNMT inhibitor, not merely a vendor label: it was identified in a 2017 structure-activity study (research that tweaks a molecule's shape to see how potency changes) of methylquinolinium scaffolds, where the 5-amino-1-methylquinolinium analog inhibited NNMT with a half-maximal inhibitory concentration (IC50 — the amount needed to block half the enzyme's activity, so lower means more potent) of about 1.2 µM, competing at the enzyme's substrate site (the pocket where NNMT's normal target binds). In cultured 3T3-L1 fat cells (a standard lab line of mouse fat cells) it lowered 1-methylnicotinamide, modestly raised NAD+, and suppressed fat synthesis, and it was selective — it did not inhibit a panel of other methyltransferases or NAD+-salvage enzymes (i.e. it hit its intended target without broadly disrupting related enzymes).

An important boundary: this NNMT-inhibition and cell-level mechanism is established in vitro and in rodent systems. The downstream story — that inhibiting NNMT meaningfully changes human metabolism, body weight, or muscle — is an extrapolation from the target biology and animal results, not something demonstrated in humans.

Sources:PMID 24717514 PMID 28548833 PMID 29155147 PMID 30753815

Why people reach for it

Potential benefits

5-Amino-1MQ is reached for as the metabolic 'NAD+-sparing' molecule — an NNMT inhibitor aimed at fat metabolism. Here's what draws people to it, with the hard caveat that every result is in animals and cells, not people.

The fat-metabolism angle — Its headline draw. In obese mice, subcutaneous 5-Amino-1MQ lowered body weight and fat-pad mass and shrank fat cells with no change in food intake — the metabolic / body-composition reason people pursue it (a mouse finding, not a proven human fat-loss effect).
NAD+-sparing, the mechanistic hook — It blocks NNMT, the enzyme that burns through nicotinamide (an NAD+ precursor) and methyl groups — so the appeal is preserving the cell's NAD+ and methylation supply rather than adding substrate from outside.
Aging-muscle support — In 22-month-old mice an 8-week course improved grip strength and reactivated aged muscle stem cells, which is why it's reached for on the muscle-and-aging angle (again, rodent data — no human muscle benefit is established).
Daytime metabolic-energy framing — Because its target sits on the NAD+/energy axis, people use it as a daytime, metabolically-active compound rather than a calming one — fitting it alongside activity.
A metabolic base that stacks well — It pairs cleanly with other energy-and-longevity levers from a different angle — most commonly NAD+ for direct substrate, MOTS-c for mitochondrial biogenesis, and SS-31 for membrane protection.

Sources:PMID 28548833 PMID 29155147 PMID 30753815

What people reach for 5-Amino-1MQ for, drawn from what the research reports (a reproduced rodent and in-vitro record — and zero human data of any kind) and how it's used — not proven human outcomes or medical claims.

Implied timing

Best time to dose

Implied best time

Morning

Most people take 5-Amino-1MQ in the morning, often with or before food, lining the metabolic signal up with the active part of the day.

Its target is metabolic — blocking NNMT to spare NAD+ and push fat cells toward burning energy — so the community default pairs it with the daytime hours when metabolic activity is highest.
It's typically taken once daily; morning, with or before food, is the common habit, leaving the rest of the day for the metabolic effect rather than dosing into the evening wind-down.
No circadian or human pharmacokinetic data exist for this molecule (the only PK is in rats: ~3.8 h IV, ~6.9 h oral), so the timing is reasoned from its metabolic mechanism and how it's used — not a measured human duration of action.

No study establishes an ideal time of day for 5-Amino-1MQ — this is reasoned from its metabolic mechanism and how it's used. As a rule of thumb most peptide dosing lands in the midday-to-evening window; for this metabolic compound the lean is morning.

Sources:DOI 10.1016/j.jpba.2021.114255

How to run it

Dosing & protocol

5-Amino-1MQ is dosed here as a subcutaneous injection — the form used in every published efficacy study (all mouse data are SC) and the route the on-page calculator is built for. The community SC convention hovers around 50 mg/day-equivalent, though a human dose in any strict sense does not exist. Read the ranges and schedule below as a map of current community practice, not a validated prescription.

Community convention, not trial-proven: 5-Amino-1MQ has zero human clinical data — every efficacy finding is from mice given SC injections. Dose ranges are inferred from the rodent studies and community anecdote, not a human trial. Long-term methylation effects are also unstudied — run with that honesty in mind.

Tiered dose ranges

The effective mouse dose was 10–20 mg/kg SC; community SC conventions for humans cluster around equivalent daily totals.

Low / introductory:: 25–30 mg once daily — first-week tolerance check; lower end for smaller frames or anyone new to NNMT inhibition.
Standard:: 50 mg once daily — the center of community convention; aligns with the ~50 mg/day-equivalent commonly referenced in practitioner circles. Most protocols land here for ongoing metabolic work.
Upper range:: 75–100 mg once daily — used by some in the community for active fat-loss phases; the DIO-mouse study's effective dose was 20 mg/kg × 3/day SC. Nothing above 100 mg/day SC has community support, and no human upper-safety limit exists.

Subcutaneous administration

5-Amino-1MQ is injected into subcutaneous fat — the same route every published animal study used.

Injection site:: The abdomen (staying a couple of inches clear of the navel), the love-handle area, or the outer thigh. Rotate sites between doses so one spot isn't used repeatedly — prevents local irritation and lipohypertrophy.
Measuring the dose:: Drawn on a U-100 insulin syringe from the reconstituted vial. At the standard calculator mix (50 mg vial + 2 mL bacteriostatic water = 25 mg/mL), 50 mg = 200 IU on a 1 mL syringe — a large volume for one shot; many users split into two nearby sites or use a lower-concentration mix. The calculator does the math for any vial size.
Time of day:: Morning is the community default for once-daily dosing, on the theory that metabolic activity is highest earlier in the day. No circadian data exist for this molecule.
Food window:: Subcutaneous injection bypasses GI absorption, so timing relative to meals is not a pharmacokinetic concern here.

Cycle & washout

Because long-term human safety is entirely unknown, protocols are run in defined blocks rather than indefinitely.

Fat-loss cycle:: 4–6 weeks continuous daily dosing — mirroring the 11-day and 8-week mouse blocks, scaled for a longer human context. Often paired with a moderate calorie deficit, consistent with the one animal study that combined the compound with a reduced-calorie diet and saw adiposity normalize.
Muscle / aging cycle:: 8 weeks continuous — the aged-mouse grip-strength study ran 8 weeks SC daily; that is the only in-vivo duration with a measured outcome, so it is the convention floor for muscle goals.
Washout:: Follow with at least a 4-week break before re-running. The break lets any methylation-flux shifts settle and gives a window to recheck biomarkers (fasting glucose, lipids, body weight) before re-dosing. No evidence-based washout period exists; 4 weeks is a conservative community floor.

Reconstitution at a glance

The on-page calculator does this live; the quick reference for a 50 mg vial:

Mixing:: 50 mg vial + 5 mL bacteriostatic water = 10 mg/mL. On a 100-unit (1 mL) insulin syringe: 25 mg = 25 IU · 50 mg = 50 IU · 75 mg = 75 IU · 100 mg = 100 IU (full syringe).
Why 5 mL:: Higher dilution gives you workable syringe volumes for each dose — at 10 mg/mL, the 50 mg standard dose is 50 IU (half a syringe), a comfortable measurement with low margin for error.

Sources:PMID 29155147 PMID 35013352 PMID 38969654

Substrate the signal needs

Nutritional cofactor precision

5-Amino-1MQ blocks NNMT — the enzyme that burns through nicotinamide (an NAD+ precursor) and methyl groups. Three cofactor groups follow directly from that mechanism: supply the substrate the inhibition spares, amplify the mitochondrial energy output those spared resources feed, and mitigate the methyl-flux cost of blocking a methyltransferase.

Mechanistic reasoning from NNMT biology, not a 5-Amino-1MQ nutrition study — and this molecule has zero human data, so the cofactor logic is doubly unproven. Supplement doses are common community ranges. Long-term effects on methylation balance from sustained NNMT inhibition are unknown.

Supply the spared NAD+ substrate

NNMT inhibition preserves nicotinamide for the NAD+ salvage pathway — feed that pool so the spared precursor doesn't sit idle.

NR or NMN:: 250–500 mg nicotinamide riboside (NR) or 250–500 mg nicotinamide mononucleotide (NMN) once daily, morning — the two direct NAD+ precursors that enter the salvage pathway downstream of the nicotinamide that NNMT would have consumed. Community convention is morning dosing aligned with peak metabolic activity.
Niacin (nicotinic acid) or nicotinamide:: 50–100 mg plain niacin or nicotinamide once daily as a budget-tier alternative to NR/NMN — the direct B3 form that NNMT's substrate site competes for. Note: high-dose niacin (>500 mg) causes flushing and is not needed here; the goal is substrate supply, not pharmacological dosing.
L-Tryptophan:: 500 mg with dinner — tryptophan is the de novo NAD+ synthesis precursor (the kynurenine pathway). Supplying it further supports the NAD+ pool from a different angle, independent of the salvage pathway NNMT-inhibition targets.

Amplify the mitochondrial energy output

Sparing NAD+ is only useful if the mitochondria can actually run it through the electron transport chain. These cofactors make sure that chain is well-supplied.

CoQ10 (ubiquinol form):: 200 mg with the largest meal of the day — CoQ10 is the electron carrier between complexes I–III of the mitochondrial electron transport chain and is depleted by statins. Ubiquinol (the reduced form) absorbs roughly twice as well as ubiquinone for most people.
B-complex (activated forms):: One B-complex daily (e.g. containing 50 mg B1, 50 mg B2, 50 mg B3, 50 mg B6, 400 mcg methylfolate, 1,000 mcg methyl-B12) — B1/B2/B3 are direct electron-transport and Krebs-cycle cofactors; the activated methyl forms (methylfolate, methyl-B12) matter specifically because NNMT inhibition shifts methyl-group flux (see the methylation group below).
Magnesium glycinate:: 200–400 mg at bedtime — magnesium is a required cofactor for ATP synthesis (every ATP molecule is actually a magnesium-ATP complex). Glycinate form favors sleep-quality and GI tolerance over cheaper oxide forms.

Mitigate the methyl-flux cost

NNMT consumes SAM (S-adenosylmethionine) to methylate nicotinamide. Inhibiting NNMT redirects that SAM flux — meaning more methyl groups now flow elsewhere. Supporting methylation balance prevents that shift from creating deficits in DNA methylation, neurotransmitter synthesis, and other methyl-dependent reactions.

TMG (trimethylglycine / betaine):: 1,000–2,000 mg with the largest meal — TMG is the primary methyl-group donor outside SAM, recycling homocysteine back to methionine and directly replenishing the SAM pool. Especially relevant here because NNMT inhibition changes how SAM is spent.
Methylfolate (5-MTHF):: 400–800 mcg daily — the active folate form that feeds the methionine cycle (methionine → SAM → homocysteine → methionine). Folic acid requires enzymatic conversion that MTHFR variants impair; methylfolate bypasses that step.
Methyl-B12 (methylcobalamin):: 1,000 mcg sublingual daily — methyl-B12 partners with methylfolate in the methionine cycle; both are needed to recycle homocysteine to methionine and keep SAM replenished. Sublingual absorption bypasses GI variability.

Combinations + timing

Stacking notes + timing windows

5-Amino-1MQ raises intracellular NAD+ by blocking the enzyme that wastes it. The best pairings come at the same energy-metabolism and longevity goals from completely different levers — mitochondrial electron-transport enhancement, mitochondrial biogenesis, or direct mitochondrial membrane protection. Pairing it with another NAD+ precursor is mostly redundant (same lever); the useful stacks change the mechanism.

User combinations reasoned from complementary mechanisms — not studied head-to-head, and 5-Amino-1MQ itself has zero human data, so any stack built on it is doubly unproven. Doses are community convention. 'Reached for' describes where users go, not a proven indication.

5-Amino-1MQ + NAD+

The most direct pairing — NNMT inhibition spares the NAD+ substrate; injectable NAD+ supplies the pool from the other side.

Why it works:: NAD+ delivered intravenously or subcutaneously raises intracellular NAD+ levels directly and rapidly; 5-Amino-1MQ works upstream by preventing the nicotinamide that feeds NAD+ synthesis from being diverted. Two angles on the same pool — supply and conservation — rather than the same mechanism twice.
The protocol:: 5-Amino-1MQ 50 mg SC daily alongside NAD+ on its own schedule (community SC NAD+ convention: 100–500 mg SC 2–3× per week, or IV infusion weekly/biweekly depending on access). The two can be injected at separate sites the same morning.
Outcome:: The combination users reach for on metabolic optimization, cellular energy, and anti-aging longevity goals where maximizing NAD+ availability is the central thesis.

5-Amino-1MQ + MOTS-c

A mitochondrial biogenesis pairing — 5-Amino-1MQ preserves NAD+; MOTS-c signals cells to build more mitochondria to use it.

Why it works:: MOTS-c is a mitochondrial-derived peptide that activates AMPK and drives mitochondrial biogenesis (the construction of new mitochondria) and metabolic gene expression. 5-Amino-1MQ preserves the NAD+ those new mitochondria will need to run. Different levers: one builds the machinery, the other fuels it — not the same thing twice.
The protocol:: 5-Amino-1MQ 50 mg SC daily alongside MOTS-c on its own schedule (community convention: 5–10 mg SC daily or 5-on/2-off). Both are injected subcutaneously; rotate sites.
Outcome:: Reached for on metabolic efficiency and body-composition goals, particularly where mitochondrial density alongside NAD+ availability is the hypothesis being tested.

5-Amino-1MQ + SS-31

A mitochondrial-membrane protection pairing — 5-Amino-1MQ preserves NAD+ for energy production; SS-31 targets the inner mitochondrial membrane where that energy is actually made.

Why it works:: SS-31 (Elamipretide) binds cardiolipin — a lipid unique to the inner mitochondrial membrane that anchors the ATP synthase complex. Protecting that membrane structure improves electron transport efficiency and reduces oxidative leak. 5-Amino-1MQ's NAD+ conservation feeds more electrons into a membrane SS-31 keeps intact. Again, different levers: substrate availability vs. structural integrity of the machinery.
The protocol:: 5-Amino-1MQ 50 mg SC daily alongside SS-31 on its typical schedule (community convention: 1–5 mg SC daily). Both are SC; inject at separate sites, rotated.
Outcome:: Reached for on mitochondrial aging and longevity stacks, where the goal is a well-supplied AND structurally sound electron transport chain — the two aspects the pair respectively address.

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.2 mL
Doses per vial: 10
Concentration: 25 mg/mL

One vial lasts

Daily: 10 days
Every other day: 20 days
5×/week: 14 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

There is no published human safety data for 5-Amino-1MQ — no clinical trial, no human toxicology, no adverse-event record. Nothing about its safety in people can be stated.

The available tolerability information is limited and confined to rodents: in the mouse obesity study the effective subcutaneous dose (an injection into the fat under the skin) produced no observable adverse effects and no significant change in food intake over 11 days, and the 8-week aged-muscle study reported no toxicity at its dose. These are short- to medium-term observations at specific injected doses in mice, not a formal toxicology package (the full battery of safety studies a real drug must pass). Claims circulating online of 'no toxicity up to 60 mg/kg' or negative genotoxicity testing (screening for DNA damage) could not be traced to a peer-reviewed primary source and are not asserted here.

As a synthetic quaternary methylquinolinium, its long-term safety in humans is simply unknown — including whether sustained NNMT inhibition produces unintended downstream effects on methylation-dependent processes (gene expression, neurotransmitter synthesis). It is a research chemical — not an FDA-approved drug and not a dietary supplement. This page presents the research literature only and makes no therapeutic claims.

Sources:PMID 29155147 PMID 38969654

As reported in literature

Research dosing ranges

This is the research-evidence table — the doses actually used in the published cell and rodent studies, shown separately so study data is never mistaken for a human dose, and the only place real figures live. There is no established human dose for 5-Amino-1MQ, and this page makes no dosing or how-to recommendation. No human clinical trial of the compound exists (ClinicalTrials.gov, the U.S. registry of clinical studies, returned no registered studies as of May 2026), so there is no clinical dosing schedule. Note that every in-vivo (in a living animal) study dosed the compound by subcutaneous injection in mice; none used oral dosing, and none was in humans.

Dose	Route	Model	Outcome	Sources:
Low micromolar (IC50 ≈ 1.2 µM)	In vitro (enzyme assay)	Recombinant NNMT enzyme	Inhibited NNMT at the substrate site; ~10-fold more potent than the parent 1-methylquinolinium	PMID 28548833
0.3–60 µM	In vitro (cell culture)	3T3-L1 adipocytes	Lowered 1-methylnicotinamide, modestly raised NAD+, and suppressed lipogenesis; selective vs other methyltransferases	PMID 29155147
20 mg/kg, 3×/day, 11 days	Subcutaneous	Mouse — diet-induced obesity	~5% body-weight loss, ~35% lower epididymal fat-pad mass, smaller adipocytes, lower plasma cholesterol — with no significant change in food intake	PMID 29155147
Subcutaneous + low-fat diet	Subcutaneous	Mouse — diet-induced obesity + diet/microbiome	Combined with a reduced-calorie diet, normalized adiposity and shifted the gut microbiome vs diet alone	PMID 35013352
10 mg/kg, daily, 8 weeks	Subcutaneous	Aged mouse (22-month) — skeletal muscle	~40% greater grip strength vs untreated sedentary mice; activated aged muscle stem cells	PMID 38969654
0.1–500 µM	In vitro (cell culture)	HeLa (cancer) vs HEK-293 (normal)	Concentration- and time-dependent anti-proliferative effect on HeLa, while sparing normal HEK-293 cells	PMID 33645410

Quick answers

Frequently asked

Is 5-Amino-1MQ a peptide?

No. It is a small synthetic molecule — a methylquinolinium (a quaternary aromatic amine) — not a peptide, and it has no amino-acid sequence. Many vendors mis-file it under 'peptides,' but chemically it belongs with the small-molecule compounds in this catalog.

What does 5-Amino-1MQ do?

It inhibits the enzyme NNMT (nicotinamide N-methyltransferase). NNMT consumes nicotinamide (an NAD+ precursor) and methyl groups, and it is overactive in obese fat tissue and aged muscle. The research idea is that blocking it preserves NAD+ and methylation capacity and increases energy expenditure in fat cells.

Has 5-Amino-1MQ been proven to cause fat loss or build muscle in people?

No. The weight-loss, fat-reduction, and grip-strength results are from mice given subcutaneous injections — in diet-induced-obese and aged animals. There is no human clinical trial and no human efficacy data for this compound. Human benefit is an extrapolation from rodent studies, not an established fact.

Is there a human dose or half-life for 5-Amino-1MQ?

No human dose or human half-life has been published. The only pharmacokinetic study is in rats (oral bioavailability around 38%, half-life a few hours). Community SC convention clusters around 50 mg/day, but this is inferred from rodent efficacy data and anecdote — not a human trial finding.

Is 5-Amino-1MQ approved or available as a supplement?

No. It is a research chemical sold for laboratory use. It is not an FDA-approved drug and does not have dietary-supplement status. There are no registered or completed human clinical trials (ClinicalTrials.gov, May 2026).

Why do cofactors include methylation support if NNMT inhibition is the goal?

NNMT's job is to methylate nicotinamide — it uses SAM (the cell's universal methyl donor) to do that. When you inhibit NNMT, you stop that specific methylation, but the same methyl-group pool still supplies dozens of other reactions (DNA methylation, neurotransmitter synthesis, etc.). Supporting methylation balance with TMG, methylfolate, and methyl-B12 is a precautionary measure to prevent unintended deficits in those other reactions — not a claim the molecule causes methylation deficiency, which has not been measured in humans.

Primary sources

References

PubChem CID 950107PubChem CID 950107 (5-amino-1-methylquinolinium cation)
PubChem CID 66522933PubChem CID 66522933 (5-amino-1-methylquinolinium iodide salt)
PMID 24717514Kraus et al., Nature 2014 (NNMT knockdown protects mice against diet-induced obesity — target validation, not this molecule)
PMID 28548833Neelakantan et al., J Med Chem 2017 (SAR of NNMT inhibitors; 5-amino-1MQ IC50 ≈ 1.2 µM)
PMID 29155147Neelakantan et al., Biochem Pharmacol 2017 (5-amino-1MQ reverses high-fat-diet obesity in mice; adipocyte NAD+/lipogenesis)
PMID 30753815Neelakantan et al., Biochem Pharmacol 2019 (NNMT inhibitor activates senescent muscle stem cells in aged skeletal muscle)
PMID 35013352Dimet/Neelakantan et al., Sci Rep 2022 (NNMT inhibition + reduced-calorie diet; adiposity & microbiome in DIO mice)
PMID 38969654Dimet-Wiley et al., Sci Rep 2024 (5A-1MQ mimics/boosts exercise; ~40% grip-strength gain in 22-month mice, 10 mg/kg SC × 8 wk)
PMID 33645410Akar et al., J Obstet Gynaecol 2021 (5-amino-1MQ anti-proliferative in HeLa, sparing HEK-293)
DOI 10.1016/j.jpba.2021.114255LC–MS/MS assay for 5-amino-1-methylquinolinium in rat plasma (rat PK; oral bioavailability ≈ 38%)

Research use only · Not medical advice · Updated 2026-06-01