5-amino-1mq

small-molecule NNMT inhibitor. reproducible mouse data, zero published human trials, recent community discussion driven primarily by vendor-affiliated commercial promotion.

tier C · weight loss · NNMT inhibitor · research

verdict

small-molecule NNMT inhibitor. reproducible mouse data, zero published human trials, recent community discussion driven primarily by vendor-affiliated commercial promotion.

if you're asking what the human evidence looks like — empty. zero published RCTs. zero peer-reviewed PK data. zero dose-finding work. zero safety dataset. user reports exist but the loud ones come from sources with vendor relationships, and the independent forum signal is mixed. it's not the BPC-157 pattern (a decade of distributed reports across thousands of independent users). it's a recent, shallow, commerce-driven discussion.

if you're asking about the mouse data — reproducible across multiple research groups and across two distinct chemical scaffolds in the broader NNMT-inhibitor class. Neelakantan 2018 reported ~7% body weight reduction in high-fat-diet obese mice over 11 days. follow-ups reported muscle strength and function improvements in aged mice and accelerated muscle regeneration after injury. the mechanism (NNMT inhibition preserves NAD+ and SAM pools) is well-described in the literature.

if you came in via the longevity / weight-loss vendor framing — the compound isn't at the stage where 'does it work in humans' can be answered. it's at the stage where 'is it safe enough to take' is being decided informally by the market rather than formally by the peer-reviewed process. independent voices in the longevity and metabolism research communities have not, as of 2026, published substantive analyses.

based on published evidence and disclosed clinical practice. not medical advice.

why C-tier

C-tier because the mechanism is well-described in the peer-reviewed literature and the preclinical mouse-model evidence is reproducible across multiple research groups, while the human evidence base is still absent (zero registered or completed clinical trials as of 2026). A plausible mechanism with thin data is what C-tier describes. Not D-tier because nothing here has failed: the chemistry and the academic preclinical work are legitimate, and the compound is untested in humans rather than tested and found wanting. Not B-tier because no human trial has confirmed the mouse findings translate, and commercial marketing has run ahead of the published research.

the core tension

5-Amino-1MQ illustrates a recurring pattern: a research-tool small molecule with reproducible preclinical mouse data and a clear mechanism (NNMT inhibition) entering the research-chemical market and accumulating community attention before any human clinical trial has been registered or published. The preclinical case is well-documented: Kraus 2014 (genetic validation in mice, Nature), Neelakantan 2018 (the foundational efficacy paper, Biochemical Pharmacology), Hong 2015 (mechanism via 1-methylnicotinamide / SIRT1, Nature Medicine), Kannt 2018 (independent confirmation with a different scaffold, Scientific Reports). Counter-evidence also exists in the published literature: Brachs et al. (Diabetes 2019) reported that global NNMT-KO mice show only a mild metabolic phenotype, partially contradicting the strong-effect interpretation. Recent community discussion has been driven primarily by vendor-affiliated commercial promotion rather than by the broader independent longevity and metabolism research communities. Independent forum discussion is mixed and lacks the longitudinal distributed-cohort character of well-established peptide community evidence. The published record contains: zero human trials, zero in-vivo methylation-pathway studies in animals at chronic doses, zero peer-reviewed combination studies with GLP-1 receptor agonists. Where research-grade evidence supports the molecule, the report below describes that. Where evidence is absent, the report below names that absence.

what it is

5-Amino-1MQ is a small-molecule selective inhibitor of nicotinamide N-methyltransferase (NNMT), originally synthesized as a research tool to probe NNMT's role in metabolism. Despite being sold alongside peptides by research-chemical vendors, it isn't a peptide: it's a methylated quinolinium derivative, MW ~159 Da as the free cation (~286 Da as the iodide salt). The compound is moderate-potency by today's standards (Ki ~1.6 µM); newer-generation NNMT inhibitors with sub-µM potency exist in the published literature but have not advanced to clinical trials either.

what it does

by inhibiting NNMT, 5-Amino-1MQ preserves cellular NAD+ pools and SAM (S-adenosylmethionine) that NNMT would otherwise consume during nicotinamide methylation. NNMT is upregulated in white adipose tissue and liver in obesity, and inhibition is reported to shift adipocyte metabolism toward thermogenic phenotype in mice. The Neelakantan 2018 paper reported approximately 7% body weight reduction in high-fat-diet obese mice over 11 days. A 2019 follow-up from the same group reported muscle strength and function improvements in aged mice. A 2022 paper from a related group reported accelerated muscle regeneration after injury. The published research base is preclinical; no human RCT evidence exists.

origin

the foundational paper Neelakantan et al. (2018, Biochemical Pharmacology) emerged from an academic NNMT-inhibitor program. The genetic-validation paper that motivated the program is Kraus et al. (2014, Nature), reporting that adipose-specific NNMT knockdown protects mice from diet-induced obesity. Subsequent work in mouse and rat models expanded the preclinical envelope. A 2019 paper (Brachs et al., Diabetes) reported that global NNMT-KO mice show only a mild metabolic phenotype, partially contradicting the original target-validation work. No IND-stage clinical program for 5-Amino-1MQ has been publicly registered as of 2026. Newer-generation NNMT inhibitors (van Haren 2017; Gao 2021) report better potency in the published literature but have also not entered human trials.

why researchers are interested

the mechanism is well-described in the published research. NNMT/NAD+/SAM biology is an active research area in metabolism, and the mouse-model efficacy is reported across multiple research groups (Neelakantan 2018; Kannt 2018 with a different scaffold; Komatsu 2018 in NAFLD). The oral small-molecule framing makes it more accessible than injectable peptides for community-research contexts. Recent community discussion has been driven primarily by vendor-affiliated commercial promotion (peptide-vendor blogs, podcasts produced by individuals with affiliate relationships to vendors selling the compound). Independent voices in the longevity and metabolism research communities have not, as of 2026, published substantive analyses of the compound.

does it work

in mice, yes. the effect is reproducible across multiple research groups and across two distinct chemical scaffolds in the broader NNMT-inhibitor class. in humans, the evidence column is empty: zero published RCTs, zero peer-reviewed PK data, zero dose-finding work, zero safety dataset. user reports exist but most of the loud ones come from sources with vendor relationships, and the independent forum signal is mixed. it's not the BPC-157 pattern (a decade of distributed reports across thousands of independent users) - it's a recent, shallow, commerce-driven discussion. the compound isn't at the stage where 'does it work in humans' can be answered. it's at the stage where 'is it safe enough to take' is being decided informally by the market rather than formally by the peer-reviewed process.

claims vs the data

• produces fat loss by inhibiting NNMT — partially true — Demonstrated in mice across multiple research groups and a second scaffold (Neelakantan 2018; Kannt 2018 with JBSNF-000088). Mouse fat-mass reduction has been reproduced. The mechanism is described in the published literature. Whether it produces a comparable effect in humans is not established - Brachs 2019 reported that global NNMT-KO mice show only a mild metabolic phenotype, which is published counter-evidence to the strong-effect interpretation.
• comparable to GLP-1s for fat loss — weak — No head-to-head data. The mouse effect size (~7% body weight in 11 days under HFD) does not directly translate to human pharmacology. GLP-1 receptor agonists have multi-thousand-patient phase-3 trials with 14-22% body weight reduction at 68-72 weeks. Comparison is not supported by the available evidence.
• stacks well with GLP-1s for synergistic fat loss — unsupported — No peer-reviewed combination studies are published - not in mice, not in any model. The combination is discussed in commercial promotion contexts but has not been characterized for additive efficacy or safety interactions in published research.
• robust user community supports the compound — partially true — user reports exist. the loudest positive ones come from sources with vendor relationships - peptide-vendor blogs, podcasts running affiliate codes for the compound. the independent forum signal is mixed: roughly half the reports describe clear effects, roughly half describe nothing. that's not the BPC-157 pattern of a decade of distributed reports across many independent communities. it's a recent and shallow discussion.
• safe based on rodent studies — weak — Rodent toxicology in the published research was for short-term efficacy testing, not chronic exposure. No long-term toxicology at human-equivalent doses has been published. No in-vivo measurement of homocysteine, SAM:SAH ratio, or DNA methylation marks under chronic 5-Amino-1MQ dosing has been published, even though Pissios 2017 explicitly flagged this pathway concern in the broader NNMT-inhibitor literature. The methylation-pathway question remains unresolved in published research.
• the next-generation fat loss molecule — overreach — A research-tool small molecule with no published human clinical trials does not meet the scientific or regulatory threshold for 'next-generation.' The compounds with that descriptor (retatrutide, orforglipron) are in or past phase-3 trials with thousands of patients enrolled.
• raises NAD+ levels — supported — NNMT inhibition reduces nicotinamide methylation and consequently preserves nicotinamide for NAD+ salvage, increasing NAD+ pools in target tissues in published animal-model research. The mechanism is described in the literature; human-level magnitude of effect has not been characterized in published studies.
• tolerance/effect-fade due to antibody buildup — unsupported — This claim has appeared in some commercial-promotion contexts. Antibody-mediated tolerance is mechanistically uncharacteristic of small molecules under 300 Da, which generally do not elicit antibody responses without protein conjugation. The 'antibody' framing does not appear in the peer-reviewed literature on 5-Amino-1MQ. Effect-fade in research contexts has alternative published explanations including receptor-level adaptations and feedback regulation in metabolic pathways.
• 5-amino-1mq has proven human fat-loss data — contradicted — The published signal is preclinical. Mouse obesity data and NNMT biology are real, but there are no published human RCTs, no human pharmacokinetics, and no dose-finding safety record for the retail compound.

key facts

• molecular formula: C10H11N2+ (cation; commonly sold as iodide salt, C10H11IN2)
• molecular weight: 159.21 Da (free cation); ~286 Da as the iodide salt form most commonly sold
• amino acids: not a peptide; methylated quinolinium derivative
• half-life: not characterized in humans; mouse oral bioavailability adequate in published animal studies
• type: small-molecule NNMT (nicotinamide N-methyltransferase) inhibitor; not a peptide despite being marketed alongside them
• CAS: 1346599-49-2 (5-amino-1-methylquinolinium iodide)
• 0 registered human clinical trials
• 33K monthly Google searches as of 2026
• ~7% body weight reduction in mice (Neelakantan 2018, 11 days, HFD-obese model)
• NNMT the enzyme it inhibits

frequently asked questions

What is 5-Amino-1MQ?

5-Amino-1MQ is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), developed as a research tool to study NNMT's role in obesity and metabolic disease. It is not a peptide despite being grouped with research peptides by some vendors. The compound preserves NAD+ and SAM pools that NNMT would otherwise consume, with effects on fat mass demonstrated in mouse models.

What does 5-Amino-1MQ do?

In high-fat-diet obese mice, 5-Amino-1MQ has been reported to reduce fat mass, decrease adipocyte size, and shift adipocyte metabolism toward thermogenic phenotype, with the foundational Neelakantan 2018 study reporting approximately 7% body weight reduction over 11 days in that model. In humans, no clinical trials have been completed, so the translation of these findings to human metabolism, body composition, or weight loss has not been established.

How is 5-Amino-1MQ studied?

Oral dosing is the standard administration route in published animal research settings. No human dosing standard exists. 5-Amino-1MQ remains a research-tool small molecule with mouse efficacy data and no clinical dosing record.

What are the side effects of 5-Amino-1MQ?

Side effects in humans have not been formally characterized because no human clinical trials have been published. Mouse and rat studies have not reported significant toxicity at the doses used for efficacy testing, but rodent safety data does not extend reliably to chronic human use. NNMT is involved in broader methyl-donor metabolism, so concerns about long-term effects on methylation pathways have been raised in the published literature but have not been resolved by clinical data.

Is 5-Amino-1MQ FDA approved?

No. 5-Amino-1MQ has no FDA approval for any therapeutic indication. U.S. products are generally sold under research-chemical labeling, not under an approved drug or dietary-supplement pathway.

How much does 5-Amino-1MQ cost?

Research-grade 5-Amino-1MQ from research-chemical vendors typically retails in a wide price range depending on purity and supplier. There is no clinical retail price because the compound is not an approved medication.

related peptides

• aod 9604 — other 'fat loss' compound that ran out of evidence at the human stage
• tirzepatide — the GLP-1 with actual human fat-loss efficacy data, for the comparison
• mots-c — other mitochondrial/metabolic peptide with strong preclinical and weak human evidence
• NAD+ — NAD+ pathway connection, both target the same metabolic regulator from different angles

reptides grades the research record and cites the literature behind every call. research reference only; not medical advice.