5-amino-1MQ

5-amino-1MQ is studied in lab research for its effects on fat metabolism and body composition — it works by blocking an enzyme called NNMT, which helps regulate how cells store fat. It's a small molecule, not a peptide, and it's included in this library because it's commonly used alongside peptide protocols. It is not FDA-approved and has never been studied in a published human clinical trial; the evidence is limited to animal and cell studies, and it's sold only as a research compound.

5-Amino-1MQ has been studied as a fat-loss compound (an NNMT enzyme blocker), but the published evidence is exclusively preclinical. A foundational mouse study reported reduced body weight and fat mass in diet-induced obese mice without changing food intake. There is no published human pharmacokinetic, efficacy, or safety data — research-community use operates across a large gap between animal data and humans.

Not FDA-approved for any indication. 5-amino-1MQ has never been studied in human clinical trials in published literature. The published evidence base is exclusively preclinical (cell culture and mouse models). Available exclusively as a research compound through unregulated research-supply chains. Not DEA-scheduled. WADA status: not explicitly named on the 2026 Prohibited List as of last review; the broader NNMT-inhibitor / methylquinolinium class is not currently a WADA-targeted category, though this may change if metabolic-modulator pharmacotherapy expands. Users in regulated sport should verify directly. Research-community use of 5-amino-1MQ in humans operates on a substantial preclinical-to-clinical translation gap — comparable in evidence-base honesty framing to AICAR in the library.

5-amino-1MQ is not FDA-approved and has not been studied in humans in published trials, so its safety in people is unknown. It is not named on the WADA Prohibited List. VialWise is a research and educational reference, not medical advice — consult a licensed professional.

⚠️ For research and educational purposes only. 5-amino-1MQ is not FDA-approved for any indication and has never been studied in human clinical trials in published literature. The published evidence base is exclusively preclinical (cell culture and mouse models). 5-amino-1MQ is available exclusively as a research compound through unregulated research-supply chains. Information in this entry is informational, not medical advice. Always confirm dose calculations with the in-app calculator and consult appropriate professional guidance before any protocol decisions.

⚠️ 5-amino-1MQ is a small-molecule NNMT inhibitor, not a peptide. Unlike the majority of the Vialwise library, 5-amino-1MQ is a methylquinolinium-class small molecule (MW ~157 Da for the free amine; iodide salt ~285 Da) that inhibits the cytosolic methyltransferase enzyme nicotinamide N-methyltransferase (NNMT). This places 5-amino-1MQ mechanistically and pharmacologically distinct from peptide-axis compounds in the library — the cluster context is metabolic-modulator small molecules (AICAR, 5-amino-1MQ) plus the exercise-mimetic peptides (SLU-PP-332, MOTS-c), not the GHS-axis or HPG-axis peptide clusters.

⚠️ The published evidence base for 5-amino-1MQ is exclusively preclinical (mouse) — the foundational Neelakantan 2017 study demonstrated body-weight and white-adipose-mass reduction in diet-induced obese mice, but NO published human trial has been conducted. The Neelakantan 2017 *Biochemical Pharmacology* paper from the University of Texas Watowich group established the methylquinolinium-class NNMT inhibitors as selective, membrane-permeable small molecules that reduce body weight, white adipose mass, adipocyte size, and plasma cholesterol in diet-induced obese mice without affecting total food intake — suggesting the effect operates through enhanced energy expenditure rather than appetite suppression.[²] The mouse-to-human translation gap is substantial: (a) the mouse doses used in Neelakantan 2017 are not directly translatable to human SC/oral dosing; (b) NNMT expression patterns differ between mouse and human white adipose tissue; (c) no published human PK/PD data exist; (d) no published human efficacy or safety data exist. Research-community use of 5-amino-1MQ in humans operates on this preclinical-to-clinical translation gap — analogous to AICAR's preclinical-to-clinical gap on the AMPK-pathway.

⚠️ 5-amino-1MQ dosing in research-community use is poorly anchored to published evidence. Reported research-community doses range widely from sub-mg per administration with oral, SC, or IV routes. The Neelakantan 2017 mouse data used systemic administration (the paper does not specify a single mg/kg human-translation dose); body-surface-area scaling produces a wide range of theoretical human-equivalent doses depending on the specific mouse-dose assumption. No safe dose has been established in human use because no human pharmacokinetic or safety studies have been published. Research-community protocols extrapolate without published evidence base. All doses below should be read as informational, not as recommendations.

⚠️ NNMT inhibition has theoretical safety considerations distinct from the peptide-axis library entries. Three load-bearing pharmacological concerns: - NAD+ pathway interactions: NNMT inhibition increases intracellular NAD+ levels. NAD+ pathway interactions with metformin, niacin (B3), nicotinamide riboside, NMN, sirtuin-pathway compounds, and PARP-axis chemotherapy are theoretical concerns. The pharmacology is not well-characterized in humans. - SAM pathway interactions: NNMT inhibition increases intracellular S-adenosyl-L-methionine (SAM). SAM is the methyl donor for hundreds of methyltransferase reactions including DNA methylation, histone methylation, neurotransmitter methylation, and one-carbon metabolism. Increased SAM availability has broad pharmacological consequences across cellular methylation — the published evidence does not characterize which downstream methylation pathways are perturbed by chronic NNMT inhibition. - NNMT is expressed in multiple tissues beyond adipose — including liver, kidney, brain, and several cancers. Off-target effects of systemic NNMT inhibition in non-adipose tissues are not characterized in published preclinical-to-human data.

According to PubMed-indexed research, 5-amino-1MQ is a small-molecule selective inhibitor of nicotinamide N-methyltransferase (NNMT) — the cytosolic methyltransferase enzyme that catalyzes the transfer of a methyl group from S-adenosyl-L-methionine (SAM) to nicotinamide, producing 1-methylnicotinamide (1-MNA).[²] NNMT was originally characterized as a hepatic enzyme involved in nicotinamide metabolism; subsequent research identified strong NNMT expression in white adipose tissue and characterized NNMT as a target for obesity and type 2 diabetes therapeutics through its role in cellular methylation balance and adipocyte metabolism. 5-amino-1MQ was developed by the Watowich/Hommel/McHardy research collaboration at the University of Texas Medical Branch (Galveston) and University of Texas at San Antonio as part of a methylquinolinium-class NNMT inhibitor program; Neelakantan 2017 *Biochemical Pharmacology* is the foundational publication establishing the class as selective, membrane-permeable NNMT inhibitors that reverse diet-induced obesity in mice.[²]

Mechanism. Based on articles retrieved from PubMed, 5-amino-1MQ inhibits NNMT activity at the NNMT enzymatic site.[²] The pharmacological consequences are: (a) Decreased 1-MNA production — the canonical NNMT enzymatic product 1-methylnicotinamide is reduced; (b) Increased intracellular NAD+ — nicotinamide that would otherwise be methylated to 1-MNA remains available for the NAD+ salvage pathway; (c) Increased intracellular SAM — SAM that would otherwise be consumed in the NNMT methylation reaction remains available for other methyltransferase reactions; (d) Suppressed adipocyte lipogenesis — demonstrated by Neelakantan 2017 in cultured adipocytes;[²] (e) In diet-induced obese mice: reduced body weight, white adipose mass, adipocyte size, and plasma cholesterol — without affecting total food intake — suggesting the effect operates through enhanced energy expenditure rather than appetite suppression.[²] The mechanism is mechanistically novel compared to existing FDA-approved obesity pharmacotherapy which acts via appetite suppression (GLP-1 ra family) or peripheral fat-absorption inhibition (orlistat).

Neelakantan 2017 foundational study (Biochem Pharmacol).[²] The Neelakantan 2017 *Biochemical Pharmacology* paper from the UTMB/UTSA Watowich/Hommel/McHardy collaboration is the foundational publication for the methylquinolinium-class NNMT inhibitors including 5-amino-1MQ. Key findings: (a) Membrane permeability: methylquinolinium scaffolds with primary amine substitutions displayed high permeability from passive and active transport across membranes via parallel artificial membrane permeability assays (PAMPA) and Caco-2 cell assays; (b) Selectivity: methylquinolinium analogs displayed high selectivity, not inhibiting structurally-related SAM-dependent methyltransferases or enzymes in the NAD+ salvage pathway; (c) Mechanism validation in cell culture: NNMT inhibitors reduced intracellular 1-MNA, increased intracellular NAD+ and SAM, and suppressed lipogenesis in cultured adipocytes; (d) In vivo efficacy in diet-induced obese mice: systemic administration of a potent NNMT inhibitor significantly reduced body weight and white adipose mass, decreased adipocyte size, and lowered plasma total cholesterol levels — without affecting total food intake and without producing observable adverse effects in the mouse model.[²] This is the foundational and currently the only widely-cited primary preclinical efficacy publication for the 5-amino-1MQ class.

NNMT as obesity / type 2 diabetes target. NNMT was identified as a candidate obesity target in the early 2010s when expression analysis of adipose tissue from obese vs lean humans showed differential NNMT expression patterns. Subsequent preclinical work (Kraus et al. and others) established NNMT knockdown effects on lipogenesis and adipogenesis pathways. The broader NNMT-as-obesity-target framework anchors 5-amino-1MQ's research-community use case — but the specific human translation has not been published.

5-amino-1MQ in research-community use. Despite the absence of published human clinical-trial evidence, 5-amino-1MQ has emerged in research-community use as a putative metabolic-modulator / fat-loss agent. Research-community protocols typically: - Use oral or SC administration daily ranges (no published evidence base for these specific doses) - Cycle the compound in 4–8 week cycles followed by 4+ week off-cycles - Combine with other research-community metabolic-modulators (AICAR, SLU-PP-332, MOTS-c, exercise) - Report subjective body-composition effects within 2–4 weeks

None of these research-community use patterns are supported by published human clinical-trial evidence. The published evidence base remains exclusively preclinical (Neelakantan 2017 mouse data and supporting cell-culture work).

Regulatory status (US — current). 5-amino-1MQ is not FDA-approved for any indication and has never been the subject of a published human clinical trial. The compound is available exclusively as a research compound through unregulated research-supply chains; not legally compoundable through US 503A pharmacies (the compound is not on the 503A bulks list and would be unlikely to qualify given the absent human clinical-trial evidence base). Not DEA-scheduled.

Regulatory status (sport — WADA). 5-amino-1MQ is not explicitly named on the 2026 WADA Prohibited List as of last review. The broader NNMT-inhibitor / methylquinolinium class is not currently a WADA-targeted category. However: the WADA S4.4 (Metabolic Modulators) subsection that captures AICAR and GW1516 could plausibly be extended to encompass NNMT inhibitors as metabolic modulators in future Prohibited Lists. Users in regulated sport should verify the current WADA status directly via the WADA Prohibited List and their National Anti-Doping Organization before any use.

Common research interests. Despite the absent human clinical-trial evidence base, 5-amino-1MQ is used in research-community contexts for: - Putative fat-loss / body-composition effects — the dominant research-community use case, extrapolating from the Neelakantan 2017 mouse data without published human evidence.[²] - Combined with exercise / dietary intervention — research-community use typically pairs 5-amino-1MQ with caloric restriction or exercise protocols, paralleling how AICAR is used in the exercise-mimetic context. - Adjunct to existing GLP-1 ra therapy — some research-community use reports adding 5-amino-1MQ to existing semaglutide or tirzepatide regimens for putative additive fat-loss effect. The combined mechanism (NNMT inhibition + GLP-1 receptor agonism) is mechanistically plausible but no published evidence supports the combination. - Adjunct to other metabolic-modulator compounds — combined with AICAR, SLU-PP-332, MOTS-c, or NAD+ in research-community body-composition / longevity protocols.

Commonly reported

• Injection-site reactions — at SC injection sites; mild
• Mild GI symptoms (nausea, mild bloating) — uncommon; reported in research-community use particularly with oral administration
• Subjective energy / metabolic changes — reported in some research-community use; not characterized in published human evidence
• Sleep changes — uncommon; mixed reports
• Mild headache — uncommon
• The published evidence base for 5-amino-1MQ is exclusively preclinical (mouse). No human safety data exist. Any research-community use operates on the substantial preclinical-to-clinical translation gap.
• NAD+ and SAM pathway perturbations are broad pharmacological effects — increased SAM availability has consequences across hundreds of methyltransferase reactions in cellular methylation. The downstream consequences in chronic human use are not characterized in published evidence.
• NNMT expression in tissues beyond adipose (liver, kidney, brain, cancers) means systemic NNMT inhibition produces off-target effects in non-adipose tissues. The clinical significance of these off-target effects in chronic human use is not characterized.
• Long-term safety in humans is essentially unknown. No published human use data exist beyond research-community anecdote.

Serious

• Severe hepatic symptoms (jaundice, dark urine, severe right-upper-quadrant pain) — given the absent human safety data and NNMT's hepatic expression, any hepatic-symptom presentation warrants immediate discontinuation and medical evaluation
• Severe allergic / hypersensitivity reaction — extremely rare but warrants immediate medical evaluation
• Severe metabolic dysregulation (severe hypoglycemia, severe lipid panel changes) — given the absent human safety data, monitor closely and discontinue at the first sign of unusual lab abnormality
• Cardiovascular symptoms (palpitations, chest pain, irregular heart rhythm) — given the absent human cardiovascular-safety data, warrants medical evaluation
• Severe disordered-eating presentation triggered by metabolic-modulator effects — warrants immediate discontinuation and mental-health evaluation

Pregnancy and lactation — no human data; default to contraindicated

Pediatric use — no clinical-trial evidence base; default to contraindicated

Active hepatic disease — NNMT is highly expressed in liver; effects of NNMT inhibition in hepatic disease are not characterized

Active cancer (especially methylation-pathway-sensitive cancers including breast, prostate, hepatocellular) — SAM pathway changes from NNMT inhibition may affect cancer-cell methylation patterns; default to contraindicated absent clinical evidence

Concurrent NAD+ precursor megadosing (NMN, nicotinamide riboside, niacin) — additive NAD+ pathway perturbation

Concurrent methotrexate or other folate/one-carbon-metabolism-affecting drugs — SAM pathway interaction

Active diabetic ketoacidosis or severe metabolic decompensation — caution; metabolic-modulator effects are not characterized in this population

Regulatory note (US): 5-amino-1MQ is not FDA-approved for any indication and is not legally compoundable through US 503A pharmacies.

Regulatory note (sport): Not explicitly named on the 2026 WADA Prohibited List as of last review. The broader metabolic-modulator class (S4.4) captures AICAR and GW1516; future Prohibited Lists may extend to NNMT inhibitors. Verify directly.

Not DEA-scheduled.

Critical: No human clinical trials of 5-amino-1MQ have been published. Research-community use operates on the substantial preclinical-to-clinical translation gap. The published evidence base is exclusively the Neelakantan 2017 mouse study + supporting cell-culture work.[²]

Small molecule

A low-molecular-weight chemical compound, distinct from peptides and proteins.

NNMT

Nicotinamide N-methyltransferase, an enzyme involved in cellular methylation and energy metabolism; blocking it is being studied for fat- loss effects.

Preclinical

Research done in cells or animals, before human clinical trials. Promising preclinical results don't always hold up in people.

Subcutaneous

An injection into the fatty layer just under the skin, rather than into a muscle or vein.

Investigational

Still being studied and not yet approved by regulators for general use.

1. Aksoy S, Szumlanski CL, Weinshilboum RM. (1994). Human liver nicotinamide N-methyltransferase. cDNA cloning, expression, and biochemical characterization. Journal of Biological Chemistry, 269(20):14835–14840 (May 20, 1994).(PMID 8182091)
2. Neelakantan H, Vance V, Wetzel MD, Wang HL, McHardy SF, Finnerty CC, Hommel JD, Watowich SJ. (2017). Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochemical Pharmacology, 147:141–152 (November 15, 2017).(PMID 29155147)
3. Kraus D, Yang Q, Kong D, Banks AS, Zhang L, Rodgers JT, Pirinen E, Pulinilkunnil TC, Gong F, Wang YC, Cen Y, Sauve AA, Asara JM, Peroni OD, Monia BP, Bhanot S, Alhonen L, Puigserver P, Kahn BB. (2014). Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature, 508(7495):258–262 (April 10, 2014).(PMID 24717514)

• AICAR — discussed together in this entry's stacks section
• SLU-PP-332 — discussed together in this entry's stacks section
• MOTS-c — discussed together in this entry's stacks section
• ACE-031 — same mechanism class
• Adipotide — shared research area
• Amycretin — shared research area