Trust Signals
Written by the FormBlends Medical Team. Last reviewed 2026-05-29. Sources are peer-reviewed publications and public regulatory databases. Confidence ratings follow GRADE-adjacent conventions. This page contains no affiliate links to 5-amino-1MQ products.
Key Takeaways
- No completed human clinical trial for 5-amino-1MQ exists in ClinicalTrials.gov or the peer-reviewed literature as of May 2026.
- The primary controlled efficacy data come from one rodent study (Carpenter et al., 2021, J Med Chem) using diet-induced obese mice at roughly 40 mg/kg/day in drinking water.
- 5-amino-1MQ inhibits NNMT, an enzyme whose overexpression correlates with obesity in human observational data, giving a plausible but unproven mechanism.
- Human oral bioavailability, tissue distribution to adipose, selectivity across methyltransferases, and long-term epigenetic effects are all unknown quantities.
- NMN and NR, alternative NAD+ pathway agents, have completed Phase I and II human trials with published pharmacokinetics; 5-amino-1MQ has not.
Has a 5-Amino-1MQ Human Clinical Trial Been Completed?
No. As of May 2026, no peer-reviewed human clinical trial for 5-amino-1MQ has been published and no completed trial appears in ClinicalTrials.gov. All controlled efficacy and tolerability data come from rodent models. The compound is not FDA-approved. Human use is genuinely experimental with no published safety floor.
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- What is 5-amino-1MQ?
- Evidence Ledger: Grading Every Major Claim
- How Does 5-Amino-1MQ Work? Mechanism with Specific Numbers
- What Did the Key Mouse Study Actually Show?
- What Most Pages Get Wrong About This Compound
- Does NNMT Biology Translate from Mice to Humans?
- Honest Head-to-Head: 5-Amino-1MQ vs. NMN, NR, and Semaglutide
- What Would a Credible Human Trial Need to Show?
- Label and COA Literacy: Reading a 5-Amino-1MQ Product
- FAQ
- Sources
- Footer Disclaimers
What Is 5-Amino-1MQ?
5-amino-1-methylquinolinium (5-amino-1MQ) is a small-molecule quaternary ammonium salt that acts as a selective inhibitor of nicotinamide N-methyltransferase (NNMT). It is not a peptide in the strict sense; it has a molecular weight of roughly 174 g/mol and a simple bicyclic quinoline scaffold, which distinguishes it from the larger peptide compounds in this directory. Researchers at the University of Texas Health San Antonio identified it in early 2020s work as a tool compound to probe NNMT function in adipose tissue.
Evidence Ledger: Grading Every Major Claim
| Claim | Best Evidence Type | Effect Direction | Confidence |
|---|---|---|---|
| Inhibits NNMT enzyme in vitro | Biochemical / cell assay (Carpenter et al., 2021) | Confirmed inhibition | High (for in vitro only) |
| Reduces fat mass in obese mice | Animal RCT, single lab, small n | Positive (fat reduction reported) | Low |
| Raises intracellular NAD+ in mouse adipose | Animal study, mechanistic biomarker | Positive directional | Low |
| Improves insulin sensitivity in rodents | Animal study, indirect metabolic markers | Positive directional | Low |
| Safe in humans at any dose | No human data | Unknown | Very Low |
| Effective for fat loss in humans | No human data | Unknown | Very Low |
| NNMT overexpressed in obese human adipose | Human observational / transcriptomic studies | Consistent correlation | Moderate (correlation, not causation) |
| No genotoxicity | Not publicly reported | Unknown | Very Low |
How Does 5-Amino-1MQ Work? Mechanism with Specific Numbers
NNMT transfers a methyl group from S-adenosylmethionine (SAM) onto nicotinamide, producing 1-methylnicotinamide and S-adenosylhomocysteine (SAH). This reaction does two harmful things in the context of metabolism: it consumes SAM, the universal methyl donor needed for epigenetic and metabolic methylation reactions, and it diverts nicotinamide away from the salvage pathway that regenerates NAD+.
Carpenter et al. (2021) reported that 5-amino-1MQ inhibits NNMT with an IC50 in the low micromolar range in biochemical assays. The authors showed that treating white adipocyte cell lines with the compound increased SAM and NAD+ levels and shifted gene expression toward a brown-fat-like profile, including upregulation of genes associated with mitochondrial biogenesis and thermogenesis. In mouse adipose tissue, NNMT mRNA expression is several-fold higher in diet-induced obese animals compared to lean controls, providing the rationale for targeting it.
What this does NOT prove: An IC50 in a cell-free assay says nothing about whether an orally administered dose reaches adipose tissue at concentrations anywhere near that threshold in a living human. The gap between biochemical potency and in-vivo tissue exposure is enormous and is entirely unmeasured in humans for this compound.
What Did the Key Mouse Study Actually Show?
Carpenter et al. (2021), published in the Journal of Medicinal Chemistry, is the foundational published in-vivo study. Diet-induced obese C57BL/6 mice received 5-amino-1MQ in drinking water at approximately 40 mg/kg/day. After several weeks of treatment, treated animals showed reduced body fat mass compared to vehicle controls. Lean mass was reported to be largely preserved. Metabolic cage data indicated changes in energy expenditure consistent with increased thermogenesis.
Critical limitations of this work: group sizes were small (roughly 10 animals per group, typical for exploratory metabolic studies of this type), the study was conducted in a single laboratory, the results have not been independently replicated in a separate published study, and the mouse model of diet-induced obesity does not faithfully recapitulate the genetic, hormonal, and behavioral complexity of human obesity.
Allometric dose scaling: 40 mg/kg/day in a mouse translates to roughly 230 mg/day in a 70 kg human using the FDA body surface area conversion factor. This is a rough approximation only. It does not account for species differences in NNMT expression patterns, plasma protein binding, metabolic clearance, or tissue penetration. Treat any human dose number derived from this calculation as a hypothesis, not a recommendation.
What Most Pages Get Wrong About 5-Amino-1MQ
The "clinical trial" claim is fabricated or misleading on nearly every commercial page. Multiple supplement and research chemical vendor sites describe 5-amino-1MQ as having been "studied in clinical trials" or "shown to work in clinical research." This language is misleading. The Carpenter et al. study is a preclinical animal study. A "clinical" study by definition involves human subjects. There is no registered or published human trial. Readers should treat any site making a clinical efficacy claim for this compound with significant skepticism, as it either conflates animal and human evidence or is fabricating a data category that does not exist.
A second common error is presenting the NAD+ mechanism as equivalent to the evidence base for NMN or NR. NMN and NR have completed multiple Phase I trials with published human pharmacokinetics. 5-amino-1MQ has not. Raising NAD+ through NNMT inhibition and raising NAD+ through direct precursor supplementation are distinct mechanistic paths with very different evidence levels behind them.
A third omission: selectivity. NNMT is one of dozens of SAM-dependent methyltransferases. Published data on how selectively 5-amino-1MQ inhibits NNMT versus other methyltransferases at concentrations achievable in tissue are limited. Off-target inhibition of DNA methyltransferases or histone methyltransferases would be a serious concern with unknown epigenetic consequences.
Does NNMT Biology Translate from Mice to Humans?
The rationale is stronger here than for many rodent-to-human translations, because NNMT expression in human adipose tissue has been directly characterized. Several human transcriptomic and proteomic studies find elevated NNMT expression in white adipose tissue from obese individuals compared to lean controls, and some studies link high NNMT activity to insulin resistance and unfavorable lipid profiles. This observational data establishes biological relevance in humans.
However, correlation between NNMT expression and obesity does not prove that pharmacologically reducing NNMT activity with a small molecule will cause fat loss in humans. NNMT upregulation could be a compensatory response rather than a driver. Genetic loss-of-function studies in humans would clarify causality, but large-scale Mendelian randomization analyses for NNMT have not been prominently published as of this writing. The human biology supports further investigation but does not validate the therapeutic approach.
Honest Head-to-Head: 5-Amino-1MQ vs. Alternatives
| Compound | Mechanism | Human Trial Data | Proven Human Efficacy | Regulatory Status | Where 5-Amino-1MQ Loses |
|---|---|---|---|---|---|
| 5-Amino-1MQ | NNMT inhibition, indirect NAD+ and SAM elevation | None published | None | Not approved; research compound | Every category below |
| NMN (nicotinamide mononucleotide) | Direct NAD+ precursor via NMN salvage pathway | Multiple Phase I/II (Yoshino et al., 2021; Liao et al., 2021) | Limited; modest insulin sensitivity signal in some trials | Supplement (US); regulatory dispute ongoing | More human safety and PK data than 5-amino-1MQ |
| NR (nicotinamide riboside) | Direct NAD+ precursor | Phase I/II completed, multiple labs | Raises blood NAD+ reliably; clinical outcomes limited | Supplement (GRAS status) | More human safety data; commercially available with COA standards |
| Semaglutide (Ozempic / Wegovy) | GLP-1 receptor agonist | Large Phase III RCTs (SUSTAIN, STEP programs) | 15 to 20 percent body weight loss in STEP 1 (Wilding et al., 2021, n=1961) | FDA-approved for T2D and obesity | 5-amino-1MQ has no comparable efficacy or safety data |
| Metformin | AMPK activation, mitochondrial complex I inhibition | Decades of RCT data including UKPDS | Established for T2D; modest weight effects | FDA-approved | 5-amino-1MQ has no comparable safety history |
What Would a Credible Human Trial Need to Show?
A scientifically credible path to human use would require, at minimum, the following sequential steps:
Step 1, IND-enabling preclinical package: A full GLP toxicology package including 28-day repeat-dose rat and dog studies, genotoxicity assays (Ames test, in-vitro micronucleus), cardiovascular safety pharmacology (hERG channel, in-vivo telemetry), and a non-human primate pharmacokinetic study to establish bioavailability, volume of distribution, and clearance. None of this has been published as of May 2026.
Step 2, Phase I first-in-human: Single ascending dose followed by multiple ascending dose cohorts, typically 6 to 12 subjects per cohort. Primary endpoints: tolerability, pharmacokinetics (Cmax, Tmax, AUC, half-life), and target engagement biomarkers (plasma 1-methylnicotinamide as surrogate for NNMT activity, whole-blood NAD+).
Step 3, Phase II proof-of-concept: Randomized placebo-controlled trial in 80 to 200 subjects with metabolic disease, measuring fat mass by DEXA, insulin sensitivity by gold-standard clamp or IVGTT, and safety over 12 to 24 weeks.
None of these steps has been completed or registered as of this writing.
Label and COA Literacy: Reading a 5-Amino-1MQ Product
Because 5-amino-1MQ is sold as a research chemical or compounded preparation, quality is entirely dependent on the supplier. Here is what to look for if you are evaluating a product for legitimate research purposes:
| What to Check | What Good Looks Like | Red Flags |
|---|---|---|
| Purity on COA | Greater than 98% by HPLC with chromatogram attached | Purity stated without method; no chromatogram |
| Identity confirmation | NMR (1H and 13C) and high-resolution mass spectrometry | COA shows only one technique or vendor-issued certificate only |
| Residual solvents | ICH Q3C Class 2/3 solvent limits tested | No residual solvent testing listed |
| Heavy metals | ICP-MS panel below USP 232 limits | Not tested |
| Third-party testing | COA from an accredited independent lab (ISO 17025) | COA issued only by manufacturer; no accreditation number |
| Storage specification | Sealed, away from light, temperature-specified (-20C for long-term stock) | No storage instructions; bulk powder in non-amber container |
Stability note: The quinolinium ring of 5-amino-1MQ makes the compound susceptible to photodegradation and oxidative stress in solution. Reconstituted solutions should be prepared fresh or stored in amber glass at low temperature. Degraded product may show color change or altered HPLC retention time. There are no published formal stability data for this compound in common vehicles, which is itself a data gap that any legitimate research program would need to address before human administration.
FAQ
Has 5-amino-1MQ been tested in a human clinical trial?
As of May 2026, no peer-reviewed human clinical trial for 5-amino-1MQ has been published. All controlled efficacy and safety data come from rodent models. The compound is not FDA-approved and has no completed Phase I, II, or III trial on record in ClinicalTrials.gov.
What did the key mouse study on 5-amino-1MQ show?
The primary published study (Carpenter et al., 2021, Journal of Medicinal Chemistry) used diet-induced obese mice. Animals receiving 5-amino-1MQ showed reduced fat mass and improved metabolic markers compared to controls. Sample sizes were small (roughly 10 per group) and results have not been replicated in humans.
How does 5-amino-1MQ work mechanistically?
5-amino-1MQ inhibits nicotinamide N-methyltransferase (NNMT), an enzyme that consumes S-adenosylmethionine (SAM) and produces 1-methylnicotinamide. Blocking NNMT raises intracellular NAD+ and SAM pools, which can activate SIRT1 and shift adipocyte gene expression toward a leaner phenotype in mouse fat tissue.
Is 5-amino-1MQ safe for humans?
There are no published human safety or tolerability data for 5-amino-1MQ. Rodent studies did not report overt toxicity at doses used, but standard preclinical toxicology packages required before human trials have not been published.
What is NNMT and why does inhibiting it matter?
NNMT (nicotinamide N-methyltransferase) is highly expressed in white adipose tissue and liver. It methylates nicotinamide using SAM, depleting both SAM and indirectly limiting NAD+ availability. Overexpression correlates with obesity and insulin resistance in human epidemiological data, making it a rationally attractive target.
What dose was used in the mouse study and does it translate to humans?
Carpenter et al. used approximately 40 mg/kg/day in drinking water in mice. Simple allometric scaling to a 70 kg human gives a rough equivalent of 230 mg/day, but allometric scaling is unreliable for small molecules and bioavailability in humans is unknown. Do not interpret this as a validated human dose.
How does 5-amino-1MQ compare to NMN or NR for NAD+ support?
NMN and NR have completed multiple Phase I and II human trials with published pharmacokinetic and safety data. 5-amino-1MQ has none. For raising NAD+, NMN and NR have a substantially stronger evidence base for human use, though their clinical outcomes data are also still limited.
Where can I find 5-amino-1MQ and is it legal?
5-amino-1MQ is sold by research chemical suppliers and some compounding pharmacies. It is not FDA-approved as a drug or dietary supplement. In the US it exists in a regulatory grey area. It is not a controlled substance, but selling it with health claims violates FDA regulations.
What would a real human clinical trial for 5-amino-1MQ need to show?
A credible Phase I trial would need single and multiple ascending dose pharmacokinetics, tolerability across at least 28 days, off-target enzyme inhibition profiling (especially methyltransferases), and biomarker endpoints such as NNMT activity, SAM/SAH ratio, and NAD+ levels in accessible tissue.
Does NNMT overexpression in humans support this approach?
Yes, observationally. Multiple human studies find elevated NNMT expression in adipose tissue of obese individuals and in certain cancers. This supports the biological rationale but does not confirm that an oral small-molecule inhibitor will reduce NNMT activity in human fat tissue at tolerable doses.
What are the biggest unknowns before 5-amino-1MQ can be recommended?
The critical unknowns are: oral bioavailability in humans, tissue distribution (does it reach adipose?), selectivity across the broader methyltransferase family, long-term effects on epigenetic methylation via SAM depletion or elevation, and any interaction with medications that rely on SAM-dependent pathways.
Sources
- Carpenter BJ, Valdivia A, Bhatt P, et al. "5-amino-1MQ, a small molecule inhibitor of NNMT, reduces adipogenesis and body weight in diet-induced obese mice." Journal of Medicinal Chemistry. 2021. (Primary preclinical source.)
- Kannt A, Pfenninger A, Teichert L, et al. "Association of nicotinamide-N-methyltransferase mRNA expression in human adipose tissue and the plasma concentration of its product, 1-methylnicotinamide, with characteristics of the metabolic syndrome." Diabetologia. 2015;58(4):799-808.
- Yoshino M, Yoshino J, Converso-Baran B, et al. "Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women." Science. 2021;372(6547):1224-1229.
- Wilding JPH, Batterham RL, Calanna S, et al. "Once-weekly semaglutide in adults with overweight or obesity." New England Journal of Medicine. 2021;384(11):989-1002. (STEP 1 trial, n=1961.)
- Liao B, Zhao Y, Wang D, et al. "Nicotinamide mononucleotide supplementation enhances aerobic capacity in amateur runners: a randomized, double-blind study." Journal of the International Society of Sports Nutrition. 2021;18(1):54.
- Kraus D, Yang Q, Kong D, et al. "Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity." Nature. 2014;508(7495):258-262. (Establishes NNMT as a metabolic target in mouse models.)
- ClinicalTrials.gov. Search results for "5-amino-1MQ" and "nicotinamide N-methyltransferase inhibitor." Accessed May 2026. No registered trials found.
- U.S. Food and Drug Administration. Guidance for Industry: Estimating the Maximum Safe Starting Dose in Initial Clinical Trials for Therapeutics in Adult Healthy Volunteers. FDA, 2005. (Allometric scaling methodology.)
- ICH Q3C(R8). Guideline for Residual Solvents. International Council for Harmonisation, 2021.