5-Amino-1MQ — Research, Dosing & Price Guide
Overview
5-Amino-1MQ is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme strongly linked to obesity and metabolic dysfunction. By selectively blocking NNMT, it raises intracellular NAD+ levels and promotes fat cell shrinkage without suppressing appetite or stimulating the central nervous system. It has emerged as one of the most promising anti-obesity compounds in the peptide-adjacent research space, attracting attention for its unique non-stimulant mechanism of action.
Mechanism of Action
5-Amino-1MQ selectively inhibits nicotinamide N-methyltransferase (NNMT), an enzyme highly expressed in white adipose tissue and liver that degrades NAD+ by methylating nicotinamide into 1-methylnicotinamide. When NNMT is blocked, intracellular NAD+ concentrations rise substantially, activating the sirtuin family of deacetylases — particularly SIRT1 — which serve as master regulators of cellular energy metabolism. This activation shifts adipocytes from a lipid-storage phenotype toward a metabolically active state, effectively shrinking fat cells through increased lipolysis and reduced lipogenesis. The downstream effects of NNMT inhibition are multifaceted. Elevated NAD+ promotes mitochondrial biogenesis via PGC-1α activation, increases fatty acid oxidation, and enhances the expression of uncoupling proteins (particularly UCP1) in adipose tissue, promoting non-shivering thermogenesis. NNMT inhibition also reduces the methyl donor S-adenosylmethionine (SAM) consumption in adipose tissue, potentially influencing broader epigenetic regulation of metabolic genes. Importantly, 5-Amino-1MQ does not cross the blood-brain barrier in significant concentrations, meaning it produces no central nervous system stimulation — no jitteriness, anxiety, or appetite suppression. Its mechanism is purely peripheral, acting directly on adipocyte metabolism. This distinguishes it fundamentally from stimulant-based weight loss compounds and even from GLP-1 agonists, which work centrally on appetite. Preclinical evidence also suggests NNMT inhibition has anti-fibrotic effects in liver tissue and may improve insulin sensitivity independent of weight loss, pointing to broader metabolic benefits beyond fat reduction.
Research Highlights
- A 2020 study published in Biochemical Pharmacology demonstrated that NNMT inhibitors reduced body weight by 7% in diet-induced obese mice over just 10 days, with no changes in food intake or locomotor activity — confirming a purely metabolic mechanism.
- Research in the Journal of Medicinal Chemistry showed that selective NNMT inhibition increased NAD+ levels by approximately 2-fold in adipose tissue, with corresponding activation of SIRT1-dependent metabolic pathways.
- Preclinical data from multiple groups demonstrates that NNMT inhibition reverses diet-induced obesity and significantly improves glucose tolerance and insulin sensitivity in mouse models of metabolic syndrome.
- A 2021 study in Obesity showed NNMT is upregulated in visceral adipose tissue of obese humans compared to lean controls, with expression levels correlating with BMI — supporting the therapeutic rationale for NNMT inhibition.
- In vitro studies demonstrate that 5-Amino-1MQ reduces adipocyte size and lipid content without inducing cell death, confirming it promotes fat cell shrinkage rather than destruction.
- Preliminary data suggests anti-fibrotic effects in hepatic stellate cells, indicating potential benefits for non-alcoholic fatty liver disease (NAFLD) beyond simple weight reduction.
- NNMT knockout mice show resistance to diet-induced obesity with increased energy expenditure, validating the target as a genuine metabolic regulator.
Dosing Protocols
- Standard oral dose: 50 mg once daily in the morning, taken with or without food. This is the most common starting protocol for metabolic support.
- Escalated protocol: Begin at 50 mg/day for 2 weeks, then increase to 100 mg/day (50 mg twice daily — morning and early afternoon) if well tolerated and additional fat loss is desired.
- Injectable protocol: 25–50 mg subcutaneous injection daily for enhanced bioavailability, though oral formulations are more commonly used.
- Typical cycle length: 8–12 weeks on, followed by a 4-week break. Some practitioners recommend cycling 8 weeks on/4 weeks off continuously.
- Best taken in the morning to align with peak metabolic activity. Avoid evening dosing as elevated NAD+ and cellular metabolism may interfere with sleep onset in some individuals.
- Commonly stacked with AOD-9604 (250–300 mcg/day) for synergistic fat loss targeting different mechanisms — NNMT inhibition plus direct lipolysis.
- Can be combined with L-carnitine (500–1000 mg/day oral) to support the increased fatty acid oxidation driven by elevated NAD+ levels.
- No food timing restrictions, but some users report better subjective effects when taken fasted in the morning before breakfast.
Disclaimer: Dosing information is compiled from research literature and community protocols for educational purposes only. This is not medical advice. Always consult a qualified healthcare provider before starting any peptide protocol.
Side Effects & Safety
Known Side Effects
- Mild gastrointestinal discomfort (nausea, loose stools) reported by some users, particularly at higher doses or when taken on an empty stomach.
- Occasional headaches during the first week of use, typically resolving as the body adjusts to altered NAD+ metabolism.
- Potential for mild insomnia if taken too late in the day, likely related to increased cellular metabolic activity.
- Theoretical risk of disrupting methylation pathways at very high doses, though no clinical evidence of this at standard dosing.
- Some users report mild skin flushing, potentially related to NAD+-dependent vasodilation pathways.
- Long-term safety data in humans is limited — most evidence is preclinical, and extended use beyond 12 weeks lacks robust human safety data.
Safety Profile
5-Amino-1MQ has a favorable safety profile based on available preclinical data, with no observed serious adverse events in animal studies at doses well above the typical human-equivalent dose. It does not affect the central nervous system, does not suppress appetite, and does not alter heart rate or blood pressure — distinguishing it from stimulant-based weight loss agents. However, human clinical trial data is limited, and most safety information comes from animal models and anecdotal user reports. Contraindications include caution in individuals with methylation-related conditions (e.g., MTHFR polymorphisms) due to the theoretical impact on SAM metabolism, though clinical significance is unestablished. It should not be combined with other NAD+-boosting supplements (NMN, NR) at high doses without monitoring, as excessive NAD+ elevation is theoretically possible. Individuals with liver or kidney impairment should use reduced doses or avoid use until more safety data is available. Not recommended during pregnancy or breastfeeding due to lack of reproductive toxicity data.
What to Expect
Weeks 1–2: Most users notice subtle increases in energy and body temperature as cellular metabolism ramps up. Fat loss is not yet visible but metabolic changes are beginning. Some users report mild GI adjustment during this period. Weeks 3–4: Measurable changes in body composition begin to appear. Users commonly report reduced abdominal bloating, slightly improved definition, and continued steady energy without stimulant-like effects. Clothes may begin fitting differently. Weeks 5–8: This is the primary window of visible fat loss. Users typically report 3–6 lbs of fat loss without dietary changes, with the most pronounced effects in those combining 5-Amino-1MQ with regular exercise and caloric awareness. Visceral fat reduction may be reflected in improved waist measurements. Weeks 9–12: Continued gradual fat loss with diminishing incremental returns. Some users plateau, which is the typical signal to conclude the cycle. Metabolic benefits (improved fasting glucose, better energy) tend to persist for several weeks after cessation.
Common Stacks
AOD-9604
Complementary fat loss mechanisms — 5-Amino-1MQ increases NAD+ and cellular fat metabolism while AOD-9604 directly stimulates lipolysis via the beta-3 adrenergic receptor. Together they attack fat storage from two different angles.
MOTS-c
Both compounds enhance mitochondrial function and metabolic efficiency. MOTS-c activates AMPK and improves insulin sensitivity, synergizing with 5-Amino-1MQ's NAD+-driven metabolic boost.
L-Carnitine
L-carnitine shuttles fatty acids into mitochondria for oxidation. When 5-Amino-1MQ upregulates fat oxidation pathways, L-carnitine ensures the released fatty acids are efficiently burned rather than re-esterified.
Storage & Handling
Oral capsules: Store at room temperature (59–86°F / 15–30°C) in a cool, dry place away from direct sunlight and moisture. Shelf life is typically 12–24 months from manufacture. Injectable formulations: Store lyophilized powder refrigerated (36–46°F / 2–8°C). After reconstitution with bacteriostatic water, refrigerate and use within 4 weeks. Do not freeze reconstituted solution.
Pricing & Available Variants
Prices sourced from peptides.gg marketplace. Prices may vary.
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