5-Amino-1MQ

5-Amino-1MQ, also written 5-amino-1-methylquinolinium iodide, is a small molecule that inhibits nicotinamide N-methyltransferase (NNMT), an enzyme that methylates nicotinamide and drains NAD+ precursors Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice+1. It is not a peptide; it is a synthetic methylquinolinium analogue developed through medicinal chemistry to be membrane-permeable and selective against related methyltransferases Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice.

Research has focused on metabolic and muscle-related conditions. In diet-induced obese mice, NNMT inhibition reduced body weight, white adipose mass, and adipocyte size without changing food intake Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Adding a reduced-calorie diet normalized body composition and liver adiposity more than diet alone Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition and enhances metabolic benefits in obese mice. In aged mice, NNMT inhibition improved grip strength and muscle stem cell function Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice+1. Early cancer studies also show anti-proliferative effects in cell lines and xenograft models Small molecule inhibitor of nicotinamide N-methyltransferase shows anti-proliferative activity in HeLa cells+2.

NNMT is an enzyme that moves a methyl group from S-adenosylmethionine (SAM) onto nicotinamide, a form of vitamin B3. This reaction creates 1-methylnicotinamide and drains a building block the body could otherwise use to make NAD+, a coenzyme central to energy metabolism Mechanisms and inhibitors of nicotinamide <i>N</i> -methyltransferase. By blocking NNMT, 5-Amino-1MQ preserves nicotinamide and SAM, which raises intracellular NAD+ and lowers S-adenosylhomocysteine, a homocysteine precursor Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice+1.

In fat tissue, NNMT is upregulated in obesity and insulin resistance. Inhibiting it suppresses lipogenesis, the process by which fat cells make new fat Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice+1. In muscle, NNMT inhibition restores the ability of aged muscle stem cells to proliferate and fuse, leading to larger muscle fibers and greater strength in old mice Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice+1. The same pathway may influence cancer-associated fibroblasts and immune responses in tumors Proteomics reveals NNMT as a master metabolic regulator of cancer-associated fibroblasts+1.

Preclinical studies document a consistent metabolic profile. In diet-induced obese mice, 5-Amino-1MQ reduced body weight, white adipose tissue mass, fat-cell size, and plasma total cholesterol without changing total food intake Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Combining NNMT inhibition with a low-fat diet normalized body composition and liver fat to lean-control levels, an effect not seen with diet switch alone Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition and enhances metabolic benefits in obese mice.

Muscle outcomes are also strong in aged mice. NNMT inhibition alone raised grip strength by about 40 percent, while combining it with exercise produced about 60 percent improvement versus sedentary controls Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. In a muscle injury model, 5 and 10 mg/kg NNMT inhibitor increased muscle stem cell proliferation and nearly doubled myofiber cross-sectional area, with peak torque roughly 70 percent higher Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle.

Other documented effects include:

• Cancer cell models: 5-Amino-1MQ inhibited HeLa cervical cancer cell proliferation in a concentration-dependent manner and reduced tumor growth in urothelial bladder cancer models when paired with anti-PD-L1 therapy Small molecule inhibitor of nicotinamide N-methyltransferase shows anti-proliferative activity in HeLa cells+1.
• Insulin sensitivity: NNMT knockdown or inhibition improves glucose tolerance and fasting glucose in rodent models of metabolic syndrome Roles of Nicotinamide N-Methyltransferase in Obesity and Type 2 Diabetes+1.
• NAD+ restoration: NNMT inhibition restores NAD+ levels and improves mitochondrial and cardiac function in models of impaired autophagic flux, though direct cardiac outcomes for 5-Amino-1MQ are not established Control of NAD+ homeostasis by autophagic flux modulates mitochondrial and cardiac function.

All of these findings are preclinical. No human interventional trials have been reported Roles of Nicotinamide N-Methyltransferase in Obesity and Type 2 Diabetes+1.

Published animal protocols use systemic injection, often intraperitoneal, at 5 to 10 mg/kg daily. In aged-muscle injury models, 5 and 10 mg/kg daily for one to three weeks improved muscle stem cell proliferation and fiber cross-sectional area Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. In sedentary aged mice, chronic treatment for about eight weeks raised grip strength, especially when combined with exercise Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. Obesity studies combined NNMT inhibition with a reduced-calorie diet over several weeks Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice+1.

Human community and practitioner protocols are not validated by clinical trials. Reported subcutaneous protocols typically start at 2 to 5 mg once daily for one to two weeks, then move to 10 to 20 mg once daily for an 8 to 12 week cycle. There is no human equivalence established; allometric estimates from mouse data are not supported by human pharmacokinetic studies.

5-Amino-1MQ is a water-soluble methylquinolinium salt Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Reconstitution guidance originates from practitioner consensus rather than published human trials.

• Diluent: Bacteriostatic water (0.9% benzyl alcohol) is preferred for multi-dose vials because it contains a preservative; sterile water for injection can also be used.
• Mixing: Swirl the vial gently after adding diluent. Do not shake, which can damage the compound.
• Clarity: Confirm the solution is clear before use. Discard any turbid or discolored solution.
• Storage before reconstitution: Keep lyophilized powder at minus 20 degrees Celsius for long-term storage, or refrigerated at 2 to 8 degrees Celsius for shorter periods. Protect from light and moisture.
• Storage after reconstitution: Refrigerate the solution and use within 30 days. Avoid repeated freeze-thaw cycles; if freezing is necessary, aliquot and thaw only once.

The interactive calculator on this page handles specific volumes and concentrations. Desired doses, vial sizes, and diluent volumes can be entered there.

5-Amino-1MQ has no human drug-interaction studies. All interactions below come from animal data, mechanistic overlap, or practitioner reporting.

Glucose-lowering agents
NNMT inhibition improves insulin sensitivity and glucose tolerance in obese and diabetic mouse models Roles of Nicotinamide N-Methyltransferase in Obesity and Type 2 Diabetes+1. Combining with metformin, GLP-1 receptor agonists, SGLT2 inhibitors, or insulin could amplify glucose lowering. No human data guide dose adjustment.

Cancer therapies
NNMT is overexpressed in cancer-associated fibroblasts and contributes to resistance against PD-L1 immune checkpoint blockade. In mouse bladder cancer models, 5-Amino-1MQ reduced tumor growth and enhanced anti-PD-L1 effects NAD⁺ metabolism enzyme NNMT in cancer-associated fibroblasts drives tumor progression and resistance to immunotherapy by modulating macrophages in urothelial bladder cancer. In HeLa cervical cancer cells, a related methylquinolinium compound inhibited proliferation Small molecule inhibitor of nicotinamide N-methyltransferase shows anti-proliferative activity in HeLa cells. Specialist supervision is needed around active cancer treatment.

NAD+ precursors and methyl donors
Because 5-Amino-1MQ preserves nicotinamide and SAM, adding NAD+ precursors such as niacin, nicotinamide riboside, or NMN, or methyl donors such as SAM-e, could shift NAD+ and methylation balance. These combinations are unstudied in humans Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice+1.

Peptide and supplement combinations

• GLP-1 receptor agonists like semaglutide or tirzepatide are complementary in theory: one suppresses appetite, the other increases energy expenditure Roles of Nicotinamide N-Methyltransferase in Obesity and Type 2 Diabetes+1.
• Growth hormone secretagogues are sometimes stacked for body recomposition, but no direct data exist Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice+1.
• MOTS-c and SS-31 may support mitochondrial function alongside NAD+ elevation, but synergy is unstudied The role of NAD+ metabolism and its modulation of mitochondria in aging and disease.
• BPC-157 and AOD-9604 have no known mechanistic conflict.

Tolerance or desensitization to NNMT inhibition has not been directly studied. In preclinical work, effective doses produced sustained target engagement without reported tachyphylaxis Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice+1. However, because NNMT inhibition changes NAD+, SAM, and homocysteine-related methylation balance, long-term safety is unresolved Mechanisms and inhibitors of nicotinamide <i>N</i> -methyltransferase.

Community protocols commonly cycle 5-Amino-1MQ. Reported patterns include:

• Conservative: 5 mg subcutaneous once daily for 6 weeks, followed by 4 weeks off.
• Standard: 10 mg once daily for 8 weeks, followed by 4 to 6 weeks off.
• Aggressive: 20 mg once daily for up to 12 weeks, followed by 6 weeks off.

These cycles are not based on human trials. They exist because no chronic-exposure data are available, and cycling allows re-assessment of whether metabolic changes persist off treatment Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice+1.

5-Amino-1MQ appears in research stacks for metabolic health and body recomposition. No multi-compound human trials exist, but component mechanisms point to complementary actions.

• GLP-1 receptor agonists (semaglutide, tirzepatide): These lower appetite and food intake, while 5-Amino-1MQ may raise energy expenditure and improve insulin sensitivity Roles of Nicotinamide N-Methyltransferase in Obesity and Type 2 Diabetes+1. The combination is theoretically additive; blood glucose should be monitored.
• Growth hormone secretagogues (CJC-1295, ipamorelin, MK-677): These may support lean mass, and NNMT inhibition improved lean-mass-to-body-weight ratio in mouse models Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. No direct data in combination.
• BPC-157: No known mechanism overlap, so risk appears low.
• AOD-9604: Both have lipolytic-relevant pathways; no known conflict.
• MOTS-c and SS-31: Mitochondrial support from NAD+ elevation could theoretically pair well, but this is unstudied The role of NAD+ metabolism and its modulation of mitochondria in aging and disease.
• Exercise: The strongest evidence-supported combination is resistance training. In aged mice, NNMT inhibition plus exercise produced additive gains in grip strength and muscle fiber size Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice.

5-Amino-1MQ is not FDA-approved for any indication, and no human clinical trials have been reported as of 2024 Roles of Nicotinamide N-Methyltransferase in Obesity and Type 2 Diabetes+1. It is sold as a research chemical, not as an approved drug or dietary supplement.

In the United States, 5-Amino-1MQ is not listed in any Controlled Substances Act schedule. It is not eligible for 503A compounding as a bulk drug substance, and no USP or NF monograph exists. No specific FDA enforcement action is documented.

For competitive athletes, 5-Amino-1MQ falls under WADA category S0, which covers non-approved substances. This category applies at all times and means use by athletes carries anti-doping risk even if the compound is not explicitly named on the list.

No country-specific bans are documented in the source material, but personal import rules vary and shipments may be detained.

No human safety data exist for 5-Amino-1MQ. Short-term mouse studies reported no observable adverse effects at doses that reduced body weight and fat mass, with no change in food intake Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice+1. Aged mice treated for about eight weeks also showed no reported adverse events Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice.

The theoretical risks come from NNMT's role in methylation and NAD+ homeostasis:

• Methylation balance: NNMT consumes SAM and produces S-adenosylhomocysteine, a homocysteine precursor. Long-term inhibition could shift methyl-donor balance in tissue-specific ways Mechanisms and inhibitors of nicotinamide <i>N</i> -methyltransferase.
• Tumor biology: NNMT in cancer-associated fibroblasts can drive tumor progression in some models, while inhibition reduced tumor growth in others. The net effect in human cancer is not understood Proteomics reveals NNMT as a master metabolic regulator of cancer-associated fibroblasts+1.
• Microbiome: NNMT inhibition combined with a low-fat diet changed the cecal microbiome in mice, with unknown clinical significance Reduced calorie diet combined with NNMT inhibition establishes a distinct microbiome in DIO mice.
• Liver and kidney: NNMT is expressed in liver and kidney, and preclinical work suggests possible protective or disease-relevant roles Nicotinamide N-methyltransferase and liver diseases+1.

Pregnancy, lactation, pediatric use, and severe liver or kidney impairment have no safety data. Research protocols should include liver enzymes, glucose, lipids, and renal function at baseline and during treatment, though no human monitoring guidelines are validated.