5-Amino-1MQ
A selective NNMT inhibitor that reduces fat mass by boosting NAD+ and cellular energy expenditure — without affecting appetite. In mice, 11 days of treatment produced 5% weight loss and 35% reduction in white adipose tissue.
5-Amino-1MQ is a small molecule — not a peptide — that blocks NNMT, an enzyme that drains the cell's NAD+ supply. In obese mice it cut body weight about 5% and white fat about 35% in 11 days without the animals eating any less. No human has ever taken it in a clinical trial, so every human dose and safety claim is guesswork scaled from rodents. Two of the three studies that have actually dosed the compound in animals come from one lab whose senior author founded a company developing the drug class.
What is 5-Amino-1MQ?
5-Amino-1MQ is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme that drains the body's NAD+ supply by methylating nicotinamide. NNMT is overexpressed in white adipose tissue of obese individuals, creating a metabolic bottleneck that promotes fat storage. By blocking NNMT, 5-Amino-1MQ preserves cellular NAD+ levels, increases energy expenditure, and shifts metabolism away from fat storage — all without reducing food intake. In diet-induced obese mice, 11 days of treatment produced 5.1% body weight loss and a 35% reduction in white adipose tissue mass with adipocyte volume reduced by over 40%. It is technically not a peptide but a quinolinium derivative, widely discussed in the peptide and metabolic optimization community. The foundational NNMT-obesity connection was published in Nature (2014).
What 5-Amino-1MQ Is Investigated For
5-Amino-1MQ is primarily investigated for fat loss through a non-appetite-suppressing mechanism — NNMT inhibition that preserves cellular NAD+ and increases energy expenditure in adipocytes. The strongest evidence comes from a single 11-day mouse study showing 5% body weight loss, 35% reduction in white adipose tissue, and 30% lower cholesterol without any change in food intake, backed by the foundational 2014 Nature paper establishing NNMT's role in obesity. No human clinical trials have been published — every human dose, safety claim, and outcome expectation is extrapolation from rodent data. Secondary interest centers on NAD+ preservation for longevity and theoretical synergy with NMN or NR, but those combinations are mechanistically rational rather than clinically validated. The honest framing is strong preclinical rationale for a specific obesity mechanism, zero human trial data, and important open questions about the oncological implications of chronic NNMT inhibition.
History & Discovery
5-Amino-1MQ emerged from chemistry programs targeting nicotinamide N-methyltransferase (NNMT), an enzyme whose role in obesity was established by a 2014 Nature paper from the lab of Barbara Kahn at Beth Israel Deaconess. That foundational paper showed that NNMT knockdown protected mice from diet-induced obesity by increasing energy expenditure and shifting cellular metabolism — establishing NNMT inhibition as a credible target for fat loss without appetite suppression. 5-Amino-1-methylquinolinium was characterized in subsequent medicinal chemistry work as a small-molecule, membrane-permeable, selective NNMT inhibitor that increases intracellular NAD+ and SAM levels by blocking nicotinamide methylation. The headline preclinical paper (Neelakantan et al.) showed that 11 days of subcutaneous 5-amino-1MQ in diet-induced obese mice produced 5.1% weight loss, 35% reduction in white adipose tissue mass, and 30% lower cholesterol — without altering food intake. The compound has subsequently moved into the longevity and metabolic-optimization market through compounding pharmacies and research-chemical suppliers, well in advance of any human clinical trial. Note that 5-amino-1MQ is a small molecule (a quinolinium derivative), not a peptide — it is included on this site because it is widely discussed alongside metabolic peptides in the optimization community. Through 2026 the broader NNMT-inhibitor pipeline has continued to diversify well beyond the obesity indication that anchored the class. A J Invest Dermatol 2026 paper (PMID 42716212) reported a bisubstrate NNMT inhibitor that suppresses myofibroblast reprogramming and mitigates skin fibrosis, and a systematic review in Curr Drug Metab (PMID 42260786) mapped NNMT's role as a central metabolic regulator in hepatocellular carcinoma — reinforcing the oncological caveat this file has carried and providing concrete evidence that chronic NNMT modulation carries context-dependent tumor-biology implications. Note that the skin-fibrosis work used a bisubstrate inhibitor designated II559, a different chemotype from 5-amino-1MQ — the class is advancing, but not through this molecule. In October 2026, Nature Metabolism reported that NNMT overexpression in ovarian granulosa cells drives hyperandrogenism by stripping the H3K27me3 histone mark and that pharmacological NNMT inhibition reverses both the metabolic and the hormonal phenotype, extending the enzyme's biology from NAD+ bookkeeping into direct epigenetic control. Two features of 5-amino-1MQ's own evidence base deserve to be stated plainly, because they are easy to miss. First, the compound has a remarkably thin literature: across PubMed and PubMed Central, roughly a dozen papers name it at all, and only three have actually dosed it in a living system or a cell line as the subject of the experiment. Second, both of the in vivo obesity studies come from the same laboratory — Harshini Neelakantan first author and Stanley Watowich senior author on both — and the 2022 paper discloses that Watowich founded Ridgeline Therapeutics, which is commercialising NNMT inhibitors, with the first author a paid employee. The 2018 anchor paper declared no conflict of interest, and nothing here implies misconduct; but a reader weighing the evidence should know that the obesity case for this specific molecule rests on one group with a commercial stake and has not been reproduced elsewhere. The one genuinely independent in vivo result comes from a 2024 Sun Yat-sen University study in bladder cancer, where 5-amino-1-methylquinolinium iodide reduced tumour growth and improved the response to anti-PD-L1 therapy. No first-in-human data has appeared, and no company anywhere has an NNMT inhibitor registered in a clinical trial.
How It Works
Your body has an enzyme called NNMT that breaks down a molecule needed for cellular energy (NAD+). In obese people, NNMT is overactive in fat tissue, draining NAD+ and slowing metabolism. 5-Amino-1MQ blocks this enzyme, preserving NAD+ levels. With more NAD+ available, fat cells burn more energy — leading to fat loss without needing to eat less.
5-Amino-1MQ is a selective, membrane-permeable inhibitor of nicotinamide N-methyltransferase (NNMT). NNMT catalyzes the transfer of a methyl group from S-adenosylmethionine (SAM) to nicotinamide, generating 1-methylnicotinamide (1-MNA) and consuming both SAM and NAD+ precursors. In white adipose tissue, NNMT overexpression in obesity creates a metabolic drain: reduced NAD+ impairs oxidative metabolism, and reduced SAM impairs polyamine flux, both favoring fat storage. 5-Amino-1MQ inhibition reverses this: it increases intracellular NAD+ and SAM, upregulates polyamine metabolism enzymes (ODC, SSAT, PAO), increases GLUT4 transporter expression, and enhances oxygen consumption in adipocytes. In diet-induced obese mice (11 days, 20 mg/kg x3/day SC), it produced 5.1% weight loss (vs 1.4% gain in controls), 35% reduction in epididymal white adipose tissue mass, >40% reduction in adipocyte volume, and 30% lower total cholesterol — all without altering food intake. The compound shows high selectivity, not inhibiting related SAM-dependent methyltransferases or NAD+ salvage pathway enzymes.
Evidence Snapshot
Human Clinical Evidence
None. No human clinical trials have been published for 5-Amino-1MQ. The compound is used off-label through compounding pharmacies but without clinical trial support.
Animal / Preclinical
Moderate, and narrower than it first appears. The key study demonstrated 5.1% weight loss, 35% WAT reduction, and 30% lower cholesterol in 11 days in DIO mice without altering food intake. The foundational Nature paper (2014, Kraus et al. from Barbara Kahn's group at Beth Israel Deaconess) established NNMT knockdown as protective against diet-induced obesity via increased energy expenditure. A companion study reported that NNMT inhibition combined with a switch to low-fat diet produced a distinct caecal microbiome pattern — though that paper found no significant difference in alpha diversity and only minimal differences between lean and obese controls, so it is exploratory rather than evidence of benefit. Importantly, both in vivo obesity studies come from the same laboratory, whose senior author founded Ridgeline Therapeutics to commercialise the compound class (disclosed in the 2022 paper). The only independent in vivo work with 5-amino-1MQ is in cancer models, not obesity.
Mechanistic Rationale
Strong for the target, weaker for this particular molecule. NNMT's role in obesity is well-validated (Nature, 2014), the NAD+/SAM/polyamine cascade is well-characterized, 5-amino-1MQ's selectivity over related SAM-dependent methyltransferases and NAD+ salvage enzymes is confirmed in vitro, and the absence of appetite effects is consistently demonstrated. A 2026 Trends in Pharmacological Sciences review tempers the class picture: it describes the first generation of NNMT inhibitors as having suffered "insufficient target engagement, reduced bioavailability, and unknown safety profiles" that "led to limited preclinical success across diseases," while arguing that newer medicinal-chemistry efforts have produced more drug-like compounds. 5-amino-1MQ belongs to that earlier generation, which bears directly on the unresolved question of whether oral capsules achieve meaningful target engagement in humans.
Research Gaps & Open Questions
What the current literature has not yet settled about 5-Amino-1MQ:
- 01Human pharmacokinetics, oral bioavailability, dosing, and safety are entirely uncharacterized — no published Phase 1 trial exists.
- 02Long-term oncological implications of chronic NNMT inhibition. The direct evidence on this compound currently runs the reassuring way — 5-amino-1MQ was anti-proliferative in HeLa cervical cancer cells without affecting non-cancerous HEK-293 cells, and in bladder cancer mouse models it reduced tumour growth and enhanced anti-PD-L1 response — while a 2026 Curr Drug Metab systematic review positions NNMT as a central regulator in hepatocellular carcinoma metabolism. What is missing is not a safety signal but a chronic-exposure study: every cancer experiment to date is a short tumour model, and nobody has characterised what sustained NNMT inhibition does to histone methylation and cell-cycle control in healthy tissue over months or years.
- 03Independent replication of the obesity result. Both in vivo obesity studies come from a single laboratory whose senior author founded a company developing NNMT inhibitors; the only independent in vivo work with this compound is in oncology models. Until a second group reproduces the adiposity findings, the headline fat-loss numbers rest on one commercially interested research line.
- 04Whether metabolic effects observed in 11-day mouse studies translate to clinically meaningful body composition or metabolic outcomes in humans is unproven.
- 05Combination with NAD+ precursors (NMN, NR) is mechanistically promising but unstudied in any species at clinical scale.
- 06Synergy or interference with GLP-1 receptor agonists for combined fat-loss strategies is entirely speculative.
- 07Effects on related SAM-dependent methyltransferases — selectivity has been demonstrated in vitro, but in vivo selectivity over chronic human dosing is unknown.
Forms & Administration
5-Amino-1MQ is available as an oral capsule through some compounding pharmacies, typically at 50-150 mg daily. In mouse studies, it was administered via subcutaneous injection at 20 mg/kg three times daily. Optimal human dosing is not established. All medications should only be used under the guidance of a qualified healthcare provider.
Dosing & Protocols
The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.
Typical Range
There is no clinically validated human dose because no human clinical trials have been conducted. Compounded oral capsules from US compounding pharmacies typically come in the 50–150 mg daily range, but these doses are extrapolated from mouse pharmacology rather than derived from any human dose-ranging study. The published mouse protocol used 20 mg/kg three times daily subcutaneously — an allometric scaling to humans is fraught and the oral-bioavailability question is itself unresolved.
Frequency
Compounded oral capsules are typically taken once daily, though some protocols split into twice-daily dosing on the assumption of shorter human half-life. The mouse studies dosed three times daily by injection. None of these regimens are evidence-based in humans.
Timing Considerations
No specific timing requirements: can be administered at any time of day, with or without food, and is not tied to exercise timing. Consistency matters more than the specific clock — dose at roughly the same time each day (or same day each week, for weekly protocols) to keep exposure steady.
Cycle Length
Some compounding pharmacy protocols recommend cycles of 8–12 weeks on, 2–4 weeks off, but this cycling pattern reflects general convention applied to longevity compounds rather than NNMT-specific evidence. Long-term safety of chronic NNMT inhibition in humans is unknown — NNMT has roles in cancer biology that warrant caution about indefinite use until those questions are addressed.
Protocol Notes
5-amino-1MQ occupies a particular position in the metabolic-optimization landscape: an unstudied small molecule with promising rodent data, available through legitimate compounding pharmacies with a prescription as well as through research-chemical suppliers, and discussed as a 'fat loss without appetite suppression' option that could complement GLP-1 therapy. The mechanistic premise is real and validated — NNMT's role in adipose metabolism is well-established — but the leap from 11 days of mouse dosing to chronic human use rests on essentially no data. Anyone using 5-amino-1MQ should understand that they are not taking a clinical drug and that the dosing, the safety profile, and the long-term oncological implications of chronic NNMT inhibition are all uncharacterized in humans.
5-amino-1MQ is not FDA-approved for any indication. No human clinical trials have been published. The doses cited reflect compounding-pharmacy convention extrapolated from rodent data, not validated human dosing.
Timeline of Effects
Onset
In the published mouse study, body weight differences from controls emerged within the 11-day dosing window. No human onset data exist. Compounding-pharmacy users typically report subjective changes in metabolic markers (energy, body composition shifts) over weeks to months, but these reports are anecdotal and not validated against placebo or against any objective measure.
Peak Effect
The published mouse data covered 11 days; longer-duration kinetics in any species are not well characterized. Whether the metabolic effects plateau, continue to accumulate, or attenuate with chronic dosing is unknown.
After Discontinuation
No formal washout data exist in mice or humans. Mechanistically, NNMT inhibition would be expected to reverse within days of stopping the compound as enzyme activity returns to baseline; whether the metabolic and body-composition effects persist or revert is undetermined. Anecdotal reports suggest gradual reversion of subjective metabolic effects after cessation, but objective data are absent.
Monitoring & Measurement
Bloodwork & Labs
- •Fasting glucose, fasting insulin (HOMA-IR) and HbA1c — the metabolic axis NNMT inhibition is claimed to move
- •Full lipid panel — the mouse work reported roughly 30% lower total cholesterol, making lipids the most directly comparable readout available to a human user
- •ALT, AST and a basic metabolic panel — baseline organ-function anchors for an unstudied compound with no human pharmacokinetic data
- •CBC — a baseline reference rather than a response marker
Functional & Performance Tests
- •DEXA scan for body composition — the mouse result was a fat-mass effect with no change in food intake, so fat mass rather than scale weight is the endpoint that would actually test the mechanism
- •Waist circumference and body weight recorded on a fixed schedule, since the claimed effect is specifically on white adipose tissue
- •A food diary or intake log — the entire premise is fat loss without appetite suppression, so an unrecorded drop in calorie intake would confound any result
When to Test
Baseline, 8 weeks, 16 weeks.
Interpretation & Notes
There is no validated human biomarker of NNMT inhibition available outside a research laboratory. Urinary or plasma 1-methylnicotinamide is the enzyme's direct product and would be the logical target-engagement assay, but it is not offered as a clinical test, so a user has no way to confirm the compound is reaching its target at all — a particularly sharp problem given that oral bioavailability in humans has never been published and the 2026 class review flags insufficient target engagement as a recurring failure of first-generation NNMT inhibitors. What remains is indirect: body composition by DEXA, a lipid panel, and insulin sensitivity. Interpret cautiously. Any fat loss accompanied by a drop in logged calorie intake tells you nothing about NNMT, because the entire distinguishing claim is that the mechanism works without reducing appetite. Standard metabolic panels and DEXA are widely available direct-to-consumer; neither requires a specialist.
Common Questions
How does 5-Amino-1MQ differ from GLP-1 drugs for weight loss?
Completely different mechanism. GLP-1 drugs reduce appetite — you eat less. 5-Amino-1MQ doesn't affect food intake at all. Instead, it increases cellular energy expenditure by preserving NAD+ levels, essentially making fat cells burn more energy. In mouse studies, treated animals ate the same amount but lost significantly more weight. This makes it a potential complement to GLP-1 therapy, not a competitor.
How does 5-Amino-1MQ relate to NAD+ supplements like NMN?
They're two sides of the same coin. NMN/NR provide raw material to make more NAD+. 5-Amino-1MQ blocks the enzyme (NNMT) that drains NAD+ away. Combining both — increasing NAD+ production while blocking its degradation — is theoretically synergistic, though this hasn't been tested in clinical trials.
Is 5-Amino-1MQ available?
It's available through some compounding pharmacies and research peptide vendors with a prescription. It is not FDA-approved for any indication. No human clinical trials have been completed. Quality varies significantly across sources.
Does 5-Amino-1MQ work in humans?
Unknown — no human clinical trials have been published. Every claim about human fat loss, dosing, or safety is extrapolated from an 11-day study in diet-induced obese mice. The mechanistic rationale (NNMT inhibition raising NAD+ and energy expenditure) is well-validated in adipose biology, but mechanistic plausibility is not the same as clinical evidence. Anecdotal reports from compounding-pharmacy users exist but are not placebo-controlled.
Does blocking NNMT raise or lower cancer risk?
Both directions are argued, and the direct evidence on this specific compound currently points the reassuring way. NNMT is overexpressed in many tumours, and a 2026 systematic review positions it as a central metabolic regulator in hepatocellular carcinoma. Where 5-amino-1MQ itself has been tested in cancer models, it suppressed tumour biology rather than promoting it: it inhibited HeLa cervical cancer cell proliferation without affecting non-cancerous HEK-293 cells, and in bladder cancer mouse models an independent group found it reduced tumour growth and improved the response to anti-PD-L1 immunotherapy. That is not the same as a clean bill of health. NNMT also regulates histone methylation, those studies are short-term tumour experiments rather than chronic-exposure safety studies, and nobody has characterised what years of NNMT inhibition does in a healthy person. The uncertainty is about long-term human exposure, not about a demonstrated cancer signal.
Is oral 5-Amino-1MQ as effective as the injected form used in mice?
Unresolved. The headline mouse data used subcutaneous injection at 20 mg/kg three times daily, while most human compounded products are oral capsules. Oral bioavailability of 5-amino-1MQ in humans has not been published, and the allometric scaling from rodent injection to human oral dosing is unvalidated. The 50–150 mg daily oral doses commonly offered reflect compounding-pharmacy convention rather than any dose-ranging or bioequivalence study.
Who 5-Amino-1MQ Is NOT For
- •Pregnancy and breastfeeding — no human safety data; NNMT plays roles in epigenetic regulation that warrant strong caution during fetal and infant development.
- •Active or recent-history cancer — not because 5-amino-1MQ has shown a tumour-promoting signal (the published cancer-model work points the other way), but because NNMT sits at the junction of NAD+ metabolism and histone methylation in tumour biology, no chronic-exposure data exist in humans, and anyone with active malignancy should not be adding an unstudied epigenetic modifier to a treatment plan without their oncologist's involvement.
- •Pediatric use — entirely unstudied; no plausible justification for use in a developing population.
- •Significant hepatic impairment — first-pass metabolism, drug clearance, and the consequences of NAD+/SAM modulation in compromised liver tissue are uncharacterized.
- •Concurrent use of methotrexate or other antifolate therapies — theoretical interaction via SAM and one-carbon metabolism perturbation, though magnitude in humans is unknown.
- •Known hypersensitivity to quinolinium compounds or to compounding excipients.
Drug & Supplement Interactions
Documented drug-interaction data for 5-amino-1MQ in humans are essentially absent because no human clinical trials have been performed. Theoretical interactions follow from the mechanism (NNMT inhibition raises intracellular NAD+ and SAM, modulates polyamine metabolism, and alters one-carbon flux). Co-administration with NAD+ precursors (NMN, NR) is mechanistically synergistic — increasing NAD+ supply while blocking its degradation — and is the most commonly discussed combination in the longevity space, though no human data evaluate the safety or magnitude of any synergy. Co-administration with methotrexate or other antifolates could theoretically interact through perturbation of one-carbon metabolism and SAM levels, but the clinical relevance has not been characterized. Effects on drug-metabolizing enzymes (CYPs) have not been systematically studied. Co-administration with other off-label longevity compounds (rapamycin, metformin, GLP-1 agonists) is widely discussed but entirely unstudied. Anyone combining 5-amino-1MQ with chronic medications should disclose use to their prescribing clinician, recognizing that absence of documented interactions reflects absence of study, not safety.
Safety Profile
Common Side Effects
Cautions
- • No human clinical trials have been conducted
- • Not FDA-approved
- • NNMT plays roles beyond fat metabolism (epigenetics, cancer biology) — chronic inhibition effects unknown
- • Highly selective for NNMT (does not inhibit related SAM-dependent methyltransferases), which is favorable for safety
What We Don't Know
Human pharmacokinetics, dosing, and safety are entirely unknown. NNMT has roles in cancer biology (both tumor-promoting and tumor-suppressing depending on context) — whether long-term NNMT inhibition has oncological implications is unstudied. The 11-day mouse study is too short to assess chronic safety.
Legal Status
United States
5-amino-1MQ is not FDA-approved for any indication. It is available through some US compounding pharmacies with a prescription, where the regulatory basis is contested under FDA 503A rules (the bulk drug substance is not on the FDA approved list). Research-chemical suppliers sell 5-amino-1MQ for laboratory research use only; this material is not authorized for human use, and quality and purity vary widely.
International
No regulatory authority in any major jurisdiction has approved 5-amino-1MQ. Availability outside the US is primarily through grey-market and research-chemical channels.
Sports & Competition
5-amino-1MQ is not currently listed by name on the WADA Prohibited List, but it falls under WADA's S0 category (substances not approved by any government regulatory health authority for human therapeutic use). Athletes subject to WADA, USADA, or equivalent codes should treat it as prohibited in and out of competition.
Regulatory status changes over time. Verify current local rules with a qualified professional.
Myths & Misconceptions
Myth
5-amino-1MQ is a peptide.
Reality
5-amino-1MQ is a small-molecule quinolinium derivative, not a peptide. It is included on this site because it is widely discussed alongside metabolic peptides in the longevity and optimization community, but the molecule, mechanism, and class are entirely distinct from peptide hormone analogs.
Myth
Because 5-amino-1MQ doesn't suppress appetite, it has no side effects.
Reality
The absence of appetite effects is a mechanistic feature, not a safety claim. The actual safety profile in humans is uncharacterized because no human clinical trials have been performed. The mouse studies were 11 days long, which is far too short to assess chronic safety in any species, and tells us nothing about long-term oncological, hepatic, or metabolic consequences of NNMT inhibition.
Myth
5-amino-1MQ is FDA-approved for weight loss because it's available through compounding pharmacies.
Reality
5-amino-1MQ is not FDA-approved for any indication. Its availability through some US compounding pharmacies rests on a contested regulatory basis under FDA 503A rules; the active ingredient is not on the FDA approved bulk drug substances list. Compounded availability is not the same as FDA approval.
Myth
5-amino-1MQ is the NNMT inhibitor.
Reality
'NNMT inhibitor' is a drug class, not a synonym for this molecule. Several structurally unrelated NNMT inhibitors exist in the literature — including the bisubstrate compound II559 used in 2026 skin-fibrosis work and NNMTi'960 from a University of Chicago and NIH patent application — and findings reported for one chemotype do not transfer to another. 5-amino-1MQ is an early, relatively simple quinolinium inhibitor, and a 2026 review of the class describes that first generation as having struggled with target engagement and bioavailability.
Myth
Combining 5-amino-1MQ with NMN or NR is proven synergistic for longevity.
Reality
The combination is mechanistically rational — NMN/NR raise NAD+ supply, 5-amino-1MQ blocks its degradation — but the synergy is theoretical. No published human studies evaluate the combination, and no clinical outcome data support the longevity claim. Mechanistic plausibility is not the same as clinical evidence.
Published Research
11 studiesNNMT enhances hyperandrogenism in polyendocrine metabolic ovarian syndrome through epigenetic remodelling.
Nature Metabolism 2026 — NNMT overexpression in granulosa cells lowers H3K27me3 and drives a RARB-androgen feedforward loop; pharmacological NNMT inhibition restored the methylation mark and improved both metabolic and hormonal phenotypes. The clearest demonstration to date that NNMT inhibition acts through histone methylation as well as NAD+ supply.
A Bisubstrate Inhibitor of NNMT Suppresses Myofibroblast Reprogramming to Mitigate Skin Fibrosis.
Nicotinamide N-Methyltransferase (NNMT): A Central Regulator in Hepatocellular Carcinoma Metabolism and Therapeutic Targeting - A Systematic Review.
Emerging opportunities for nicotinamide N-methyltransferase (NNMT) inhibitor clinical translation.
Exploring NNMT: from metabolic pathways to therapeutic targets.
NAD(+) metabolism enzyme NNMT in cancer-associated fibroblasts drives tumor progression and resistance to immunotherapy by modulating macrophages in urothelial bladder cancer.
The only published in vivo study of 5-amino-1MQ from a group independent of the compound's originating laboratory. Targeting NNMT with 5-amino-1-methylquinolinium iodide reduced tumour growth and enhanced the effect of anti-PD-L1 antibody in bladder cancer mouse models — direct evidence that bears on this page's central open question about what chronic NNMT inhibition does to cancer biology.
Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice.
Small molecule inhibitor of nicotinamide N-methyltransferase shows anti-proliferative activity in HeLa cells.
Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity.
Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice.
The Neelakantan et al. foundational paper — demonstrated that 11 days of 5-amino-1MQ in diet-induced obese mice produced 5.1% weight loss and 35% reduction in white adipose tissue without altering food intake. The anchor preclinical study driving 5-amino-1MQ's metabolic positioning.
Roles of Nicotinamide N-Methyltransferase in Obesity and Type 2 Diabetes.
Popular Stacks Including 5-Amino-1MQ
Quick Facts
- Class
- Metabolic Modulator
- Tier
- D
- Evidence
- Preliminary
- Safety
- Limited Data
- Updated
- Oct 2026
- Citations
- 11PubMed
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Evidence Score
Clinical Trials
View Clinical TrialsLinks to ClinicalTrials.gov for reference. Listing does not imply endorsement.