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5-Amino-1MQSmall moleculeNo amino acid sequence. Icon reflects category theme only.Also known as: 5-Amino-1MQ, 5A1MQ, 5-amino-1-methylquinolinium
Four amino acids short of being a peptide, 5-Amino-1MQ is actually a quinolinium salt weighing just 159.19 g/mol. It blocks nicotinamide N-methyltransferase (NNMT), an enzyme overexpressed in the fat tissue of obese individuals. In diet-induced obese mice, subcutaneous dosing cut fat mass, shrank adipocytes, and improved glucose tolerance without reducing food intake (Babula et al.)[1]. A separate 2024 study flagged a 40% grip strength increase in aged mice (Dimet-Wiley et al.)[2]. Zero human trials exist. The community figured out oral capsules before the science caught up, though Babula 2024 confirmed poor oral bioavailability in rodents. Most users take 100 mg/day for 8 to 12 weeks targeting body composition.
5-Amino-1MQ (5-amino-1-methylquinolinium, MW 159.19 g/mol) is a synthetic NNMT inhibitor taken orally as a capsule. No human clinical trial has been completed. All efficacy data comes from rodent models, and that gap matters. NNMT methylates nicotinamide using S-adenosylmethionine (SAM) as a donor. When the enzyme runs hot in obese fat tissue and liver, it drains two molecules the body needs: NAD+ precursors and SAM. Block NNMT, and both pools recover. NAD+ feeds into sirtuin activation, mitochondrial biogenesis, and fatty acid oxidation. SAM drives a polyamine cycling loop that burns ATP. Think of it as flipping a metabolic switch that makes fat cells waste energy on purpose. Kraus and colleagues first identified NNMT as an obesity target in a 2014 Nature paper [3]. The University of Texas group then screened quinolinium-based inhibitors and landed on 5-Amino-1MQ for its selectivity; it doesn't hit related methyltransferases (Neelakantan et al.)[4]. A 2018 follow-up showed subcutaneous dosing cut body weight and fat mass in obese mice without changing food intake [5]. Babula's 2024 study in Diabetes, Obesity and Metabolism confirmed dose-dependent improvements in glucose tolerance, insulin sensitivity, and hepatic steatosis over 28 days [1]. Community use runs ahead of the science. Most users take 50 to 150 mg/day orally for 8 to 12 weeks, stacking with AOD-9604 or semaglutide. Reports on r/Peptides and AnabolicMinds describe gradual midsection fat loss and improved energy, but a meaningful non-responder rate persists. Babula 2024 confirmed poor oral bioavailability in rodents; the community's preferred route has no preclinical validation. That gap matters.
NNMT sits at the intersection of two metabolic currencies: SAM (the body's primary methyl donor) and nicotinamide (a precursor for NAD+ biosynthesis). In obese individuals, NNMT is overexpressed in white adipose tissue and liver. It catalyzes a methyl transfer from SAM to nicotinamide. The products, 1-methylnicotinamide and S-adenosylhomocysteine, are metabolically inert. The result is a steady drain on both SAM and NAD+ pools. 5-Amino-1MQ blocks this reaction selectively. When NNMT can't methylate nicotinamide, intracellular nicotinamide accumulates. It feeds into the NAD+ salvage pathway via NAMPT. Rising NAD+ levels activate SIRT1 and other sirtuin-dependent pathways that drive mitochondrial biogenesis and fatty acid oxidation. SAM levels rise simultaneously. Raised SAM increases H3K4 histone methylation, which upregulates ornithine decarboxylase (ODC) and SSAT expression. These enzymes drive polyamine flux, an energy-expensive futile cycle that burns ATP and raises total cellular energy expenditure. The net effect is a two-pronged metabolic shift. Fat cells burn more through polyamine cycling and mitochondrial activity. New fat creation (lipogenesis) drops. Across multiple mouse studies, this occurred without changes in food intake. Neelakantan's 2018 study confirmed that subcutaneous 5-Amino-1MQ reduced body weight, white adipose tissue mass, and adipocyte size in diet-induced obese mice [5]. Babula's 2024 study replicated these improvements and added dose-dependent glucose tolerance and hepatic steatosis corrections over 28 days [1].
NNMT inhibition reduces fat mass, improves glucose tolerance, and attenuates hepatic steatosis in diet-induced obese mice. A July 2024 study [2] also demonstrated grip strength (~40% increase) and exercise capacity gains in aged mice. No human clinical trials have been conducted.
Babula et al., Diabetes Obes Metab 2024 (PMID 39161060): 28-day diet-induced obese mouse study; dose-dependent reductions in body weight, fat mass, glucose intolerance, and hepatic steatosis via subcutaneous 5-amino-1MQ.
All evidence from rodent models; zero human clinical trials. Babula 2024 confirmed poor oral bioavailability in rodents: subcutaneous administration was required for efficacy. Community primarily uses oral capsules, a route with no animal or human efficacy validation. Allometric scaling from 10 mg/kg SC mouse dose does not produce community flat-dose oral protocols.
Used orally for fat loss, energy enhancement, and body composition over 8-12 weeks. Results are inconsistent; a meaningful non-responder rate is reported at standard doses. Oral bioavailability is increasingly questioned after Babula 2024.
Science validates NNMT inhibition for fat loss and metabolic improvement but exclusively via subcutaneous administration in animal models. Community uses oral capsules: a route that Babula 2024 flagged as having poor bioavailability in rodents. Community flat oral doses (50-200 mg/day) also bear no clear relationship to validated SC mg/kg doses in animals. Route, dose rationale, and mechanism of oral benefit are all unaligned with the scientific evidence base.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 50mg | Daily |
| Moderate | 100mg | Daily |
| Aggressive | 150mg | Daily |
This isn't an injectable. You're taking a capsule. No vials, no bacteriostatic water, no syringes, no reconstitution math. Standard vendor offering is 60 capsules at 50 mg each. Start at 50 mg/day for the first one to two weeks. If you tolerate it, bump to 100 mg (two capsules). That's the most common community dose. Some users go to 150 mg but side effect reports pick up past that point. The estimated half-life sits around 4 to 6 hours. If you notice an energy dip by early afternoon, splitting your dose (50 mg morning, 50 mg around noon) is a common workaround. No data supports or refutes this; it's community logic based on the PK estimate. Source quality matters more than most people realize. Avoid Amazon and Walmart marketplace listings. No COA accountability exists on those platforms. Buy from specialty research vendors who provide current HPLC certificates of analysis with purity at or above 98%. Underdosing in capsule fill weight is the primary reported quality failure. Store at room temperature. Cool, dry, away from sunlight. Shelf life runs 12 to 24 months.
Most community protocols recommend 8-12 weeks on followed by 4-8 weeks off. The absence of long-term human safety data makes cycling a precautionary measure rather than an evidence-based one. Start at the lower dose (50 mg/day) for the first 1-2 weeks before increasing. No more than 3 cycles per year is a common recommendation.
No long-term human safety data exists for 5-Amino-1MQ. Cycling is a precautionary community convention, not evidence-based. NNMT plays roles in SAM metabolism, epigenetic regulation (H3K4 methylation), and liver function. Chronic uninvestigated NNMT inhibition in humans carries unknown risks across these pathways. The 8-12 weeks on / 4-8 weeks off convention allows hepatic and methylation pathway normalization.
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Expected: Gradual, modest body fat reduction (particularly visceral/abdominal) and energy increase. Community reports are variable: do not expect rapid fat loss. Non-responder rate at this dose is notable.
Monitor: Baseline and end-of-cycle fasting glucose and lipid panel recommended. Check ALT/AST if cycling more than twice per year.
Most vendors sell 50 mg capsules. Check the label and the certificate of analysis to verify fill accuracy.
Take one 50 mg capsule by mouth each morning for the first one to two weeks. This is your tolerance window. Take with food if GI discomfort occurs.
After tolerance is established, increase to 100 mg/day (two capsules). Take both in the morning, or split: 50 mg morning, 50 mg around noon.
If moving to 150 mg/day (intermediate protocol), add a third capsule. Split as 100 mg morning plus 50 mg afternoon. Watch for fatigue or dizziness at this dose.
Morning dosing aligns with daily metabolic activity.
Store capsules at room temperature (15 to 25 degrees Celsius) in a dry place away from sunlight. Shelf life is 12 to 24 months.
Maximum three cycles per year.
Get bloodwork (fasting glucose, lipids, ALT/AST) at baseline and end of cycle.
No injection equipment, reconstitution, or syringe calculations needed. This is an oral compound. For those using the subcutaneous route (the only one validated in animal studies): community SC doses range from 150 to 500 mcg/day. Reconstitute lyophilized powder with bacteriostatic water. Inject subcutaneously in abdominal fat using a 29 to 31 gauge insulin syringe. Rotate sites.
50-200 mg/day flat dose; no relationship to validated SC mg/kg animal doses
Poor oral bioavailability confirmed in rodent model (Babula 2024). All animal efficacy studies exclusively used subcutaneous delivery. Community continues oral use based on convenience and vendor availability. Any benefit from oral dosing is mechanistically unclear.
Community SC use: 150-500 mcg/day; animal efficacy studies: ~10 mg/kg/day SC
The only route with preclinical efficacy data. Requires reconstitution (bacteriostatic water). Less common in community due to injection burden given widely available oral capsules. Community SC doses remain substantially below animal efficacy doses on a mg/kg basis: no bridging data exists.
Complementary fat loss mechanisms: AOD-9604 stimulates lipolysis via beta-3 adrenergic receptor while 5-Amino-1MQ increases adipocyte energy expenditure via NNMT inhibition. Most commonly paired fat-loss combination in community protocols.
GLP-1 receptor agonist reduces caloric intake; 5-Amino-1MQ targets expenditure side. Community pairs them for combined appetite suppression + metabolic rate increase. No clinical data on this combination.
MOTS-c activates AMPK and improves mitochondrial function; 5-Amino-1MQ raises NAD+ via NNMT inhibition. Community uses them as complementary metabolic modulators. No data on combined use.
AMPK activator that enhances fatty acid oxidation. Community pairs with 5-Amino-1MQ for metabolic pathway synergy. No clinical data; both compounds work through distinct but theoretically complementary mechanisms.
NNMT inhibition alters SAM (S-adenosylmethionine) availability. Methotrexate inhibits dihydrofolate reductase and affects the one-carbon methylation cycle. Combined disruption of SAM/methylation balance is unpredictable and potentially harmful.
Do not combineNNMT inhibition improves insulin sensitivity in preclinical models. Combined use with exogenous insulin or insulin secretagogues could produce additive glucose-lowering and hypoglycemia risk.
Pricing updated 2026-04-09
No human safety data exists for 5-Amino-1MQ. Zero clinical trials. Zero formal adverse event reports. Everything below comes from mouse studies and fewer than 100 trackable community posts across Reddit and AnabolicMinds. The most serious theoretical concern is methylation pathway disruption. NNMT plays a direct role in SAM metabolism, and SAM is the methyl donor for DNA methylation, histone modification, and neurotransmitter synthesis. Inhibiting NNMT raises SAM levels, which sounds positive in isolation. But chronically altering SAM/NAD+ balance could have downstream effects on epigenetic regulation, liver function, and hormonal pathways that no one has measured in humans. Babula's 2024 study ran for 28 days in mice [1]. What happens at 6 months or 12 months? The data doesn't exist. NNMT is also implicated in tumor biology. Its role is context-dependent: inhibition could theoretically promote or suppress tumor growth depending on the cancer type. Anyone with active cancer or a history of cancer should treat this as a hard stop. Not a "consult your doctor" situation. Liver effects are a valid concern. NNMT is highly expressed in hepatic tissue. The Babula study showed ALT/AST reductions in obese mice, but the effects of NNMT inhibition in human livers (healthy, fatty, or otherwise) are completely uncharacterized. Monitoring liver enzymes (ALT, AST) at baseline and mid-cycle is a reasonable precaution. In preclinical mouse studies at standard research doses, no observable adverse effects were reported (Neelakantan et al.,; Babula et al.)[5]. That's reassuring but limited. Mice aren't people, and research doses aren't community doses. Community-reported side effects at 50 to 150 mg/day oral: GI discomfort is the most common complaint. Nausea and loose stools show up in week one for a visible fraction of users. Taking capsules with food typically helps. Headaches during initiation appear in early reports too, alongside mild fatigue. Both tend to clear by end of week one. At doses above 150 mg/day, users report dizziness and more persistent fatigue. The compound's estimated half-life of 4 to 6 hours means a single morning dose may not sustain levels. Energy crashes mid-afternoon are a reported pattern. Splitting the dose is the common workaround. Pregnancy and breastfeeding are absolute contraindications. No reproductive safety data exists. The same applies to anyone under 18 and anyone taking methotrexate or folate antagonists, where NNMT inhibition could unpredictably alter SAM availability. If GI symptoms persist beyond two weeks, stop. If liver enzyme readings climb on mid-cycle bloodwork, stop. If fatigue doesn't resolve after the first week despite dose reduction, stop. This is a research chemical with zero human trial safety data; conservative decision-making isn't optional.
Verify 5-Amino-1MQ dosing and safety with a second opinion
Research chemical with no pharmaceutical-grade manufacturing standards. Now sold openly on Amazon and Walmart alongside specialty research vendors, introducing significant variability in purity and capsule fill accuracy. FDA confirmed 503B ineligibility in 2025 (cannot be legally compounded at scale by outsourcing facilities). No standardized COA requirements exist for this compound class.
| Test | When | Target |
|---|---|---|
| Fasting glucose + fasting insulin | Baseline before cycle start; end of cycle | Fasting glucose 70-100 mg/dL; fasting insulin 2-20 µIU/mL |
| Lipid panel (total cholesterol, LDL, HDL, triglycerides) | Baseline and end of cycle | — |
| Liver enzymes (ALT, AST) | Baseline, week 6, end of cycle | ALT <40 U/L; AST <40 U/L |
NNMT inhibition improves insulin sensitivity in preclinical models; combined use with hypoglycemic agents carries hypoglycemia risk. Establishes metabolic baseline.
Preclinical data demonstrates significant cholesterol and triglyceride reductions in mice. Human lipid response is unstudied: monitor for unexpected shifts in either direction.
NNMT is highly expressed in liver tissue. Babula 2024 showed ALT/AST reductions in DIO mice, but hepatic effects of NNMT inhibition in healthy or metabolically varied humans are unknown. Chronic use risk is uncharacterized.
No visible changes expected. The compound begins inhibiting NNMT at the cellular level, increasing intracellular NAD+ and SAM. Some users report a subtle uptick in energy or slight GI adjustment. This is a calibration period: assess tolerance before increasing dose.
Metabolic shifts are underway but still largely subclinical. Polyamine cycling and enhanced fatty acid oxidation should be active. Some users report improved energy levels and slightly better workout recovery. Body weight changes are typically minimal at this stage.
This is where animal studies show measurable reductions in adipose tissue mass and adipocyte size. Users may begin noticing changes in body composition: particularly around the midsection. Improvements in fasting glucose and lipid panels may become detectable on bloodwork.
Cumulative effects should be at their peak. In the 28-day mouse study, dose-dependent reductions in body weight, fat mass, and liver triglycerides were well-established by this equivalent timepoint. Users often report the most noticeable body composition changes during this window.
Discontinue use and allow NNMT activity to normalize. Metabolic benefits may persist for 1-2 weeks after the last dose as NAD+ and SAM levels gradually return to baseline. Maintain dietary and exercise habits established during the cycle. Wait 4-8 weeks before starting another round.
Week 1 (Tolerance establishment): NNMT inhibition kicks in at the cellular level. NAD+ and SAM concentrations begin shifting inside adipocytes. Don't expect anything visible yet. Some users pick up a subtle energy bump within the first few days. GI adjustment is common: mild nausea, loose stools, headache. These typically clear by day seven. This is the calibration window before increasing dose. Weeks 2 to 3 (Metabolic shift initiation): Polyamine cycling and fatty acid oxidation should be running based on mouse PK timelines. Changes are subclinical. Users commonly report improved energy and better workout recovery. Scale weight probably hasn't moved. The internal machinery is working, but the mirror won't show it yet. Weeks 4 to 6 (Early body composition changes): Animal studies show measurable reductions in fat mass and adipocyte size in this window. Users may start noticing midsection changes. Fasting glucose and lipid panels may move on bloodwork. Babula's 2024 DIO mouse data showed clear metabolic marker improvements in this equivalent timeframe [1]. Some community users plateau or report no change; that non-responder pattern is real. Weeks 7 to 10 (Peak cumulative effect): The Babula 28-day study showed dose-dependent reductions in body weight, fat mass, and liver triglycerides by this equivalent timepoint. Most users who respond report their best body composition changes here. If you haven't seen movement by week 8, increasing dose or switching routes (oral to subcutaneous) is the community's go-to adjustment. No data validates either change in humans. Post-cycle, weeks off (NNMT normalization): Stop dosing. NNMT activity returns to baseline. NAD+ and SAM levels normalize over one to two weeks. No rebound fat gain was documented in animal models after discontinuation. Keeping the diet and exercise habits you built during the cycle matters most for holding results. Wait 4 to 8 weeks before starting another round.
NNMT inhibition begins intracellularly. NAD+ and SAM levels start to shift. No measurable fat loss expected at this stage.
Subtle energy increase noted by some users within days. GI adjustment (mild nausea, loose stools) is common. No visible body composition changes.
Polyamine cycling and enhanced fatty acid oxidation should be active based on mouse PK data. Adipocyte-level changes are occurring but not yet clinically measurable.
Improved energy and workout recovery reported. Some users notice mild performance improvements. Scale weight changes still minimal.
Animal studies show measurable reductions in adipose tissue mass and adipocyte size in this window. Glucose and lipid improvements detectable on bloodwork in DIO mouse models.
Most users begin noticing body composition changes, particularly around the midsection. Some report improvements in fasting glucose on labs. A subset report plateau or no change.
Babula 2024 28-day DIO mouse study showed dose-dependent fat mass, liver triglyceride reductions, and metabolic marker normalization well-established by this equivalent timepoint.
Most noticeable body composition changes reported in this window. Some users plateau without additional dietary adjustment. Continued energy and recovery benefits.
NNMT activity returns to baseline. NAD+ and SAM levels normalize over 1-2 weeks. No rebound fat gain documented in animal models after discontinuation.
Users report metabolic benefits persisting for 1-2 weeks after last dose. Maintaining diet and exercise habits during the off period is the primary determinant of sustaining results.
Source: Estimated from the 2024 pharmacokinetic characterization study in DIO mice (PMID 39161060). No human PK data exists. The compound showed adequate oral bioavailability in mice with tissue distribution to adipose and liver compartments.
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5-Amino-1MQ is classified as a research chemical. It has no FDA approval for any indication. No Investigational New Drug application has been filed publicly. The FDA confirmed in 2025 that 5-Amino-1MQ is ineligible for 503B compounding, meaning outsourcing facilities cannot legally produce it at scale. It is not a controlled substance in the United States. Purchase and possession for research purposes is legal. It's now sold openly on Amazon and Walmart alongside specialty research vendors, though marketplace listings carry no standardized COA requirements. WADA has not specifically addressed 5-Amino-1MQ on the 2026 prohibited list. Athletes subject to anti-doping testing should exercise caution; the open-ended metabolic modulator category could theoretically apply. This content is for educational and research purposes only. 5-Amino-1MQ is not approved for human consumption. Consult a licensed healthcare provider before using any research compound. Peptide Schedule does not sell, distribute, or endorse the use of research chemicals.
Peptide Schedule Research TeamReviewed Apr 20266 Citations
