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01 — Identity
Name & Classification
5-Amino-1-Methylquinolinium (5-Amino-1MQ) is technically a small molecule rather than a peptide, but is widely categorized alongside research peptides in the longevity and metabolic optimization space. Its chemical designation is 5-amino-1-methylquinolinium.
It is a selective inhibitor of NNMT (Nicotinamide N-methyltransferase) — an enzyme highly expressed in fat tissue that consumes SAM (S-adenosylmethionine) and reduces NAD⁺ precursor availability. By blocking NNMT, 5-Amino-1MQ effectively boosts intracellular NAD⁺, activates SIRT1, and shifts fat cells toward energy expenditure rather than storage.
02 — Origin
When It Was Developed
2010s
NNMT identified as a key regulator of fat cell metabolism. Initial research at Weill Cornell Medicine and other institutions established NNMT overexpression as a driver of obesity and insulin resistance.
2015
5-Amino-1MQ first described as a potent, cell-permeable NNMT inhibitor. Early cell culture studies showed it dramatically reduced fat accumulation and increased energy expenditure in adipocytes.
2018–2021
Animal studies published showing 5-Amino-1MQ reduced body weight, fat mass, and metabolic disease markers in diet-induced obese mice without caloric restriction. Showed NAD⁺ elevation as primary mechanism.
2021–Present
Growing use in the longevity and metabolic optimization space. Oral bioavailability established. No human clinical trials published to date; classified as a research chemical.
03 — Research History
Research Background
The core insight behind 5-Amino-1MQ is that NNMT acts as a metabolic brake in fat tissue — it consumes methyl donors and NAD⁺ precursors, suppressing the very pathways that drive fat burning. In obese individuals, NNMT is chronically overexpressed in adipose tissue, creating a feedback loop that perpetuates fat storage.
By inhibiting NNMT, 5-Amino-1MQ restores the SAM/SAH ratio, elevates intracellular NAD⁺, and activates SIRT1 — the longevity-associated deacetylase that promotes mitochondrial biogenesis and fat oxidation. Studies in obese mice showed decreases in body fat of 7–10% without any change in food intake, and significant improvements in insulin sensitivity.
Unlike NMN or NR (which boost NAD⁺ by adding precursors), 5-Amino-1MQ boosts NAD⁺ by stopping its consumption — a fundamentally different and potentially more targeted approach, especially in adipose tissue.
04 — Key Benefits
Proposed Benefits
Inhibits NNMT — reduces fat storage drive in adipocytes
Elevates intracellular NAD⁺ by blocking NAD⁺ precursor consumption
Activates SIRT1 — promotes fat oxidation and mitochondrial biogenesis
Reduces body fat and adipocyte size in animal models
Improves insulin sensitivity and glucose metabolism
Subcutaneous injectable — 50mg vial, precise mcg dosing
Increases energy expenditure without reducing food intake
Complementary to NMN/NR — different mechanism, additive NAD⁺ effect
05 — Reconstitution
50mg Vial — Subcutaneous Injectable
50mg + 3.0mL BAC
subcutaneous injection — 166.7 mcg per unit (0.01 mL)
36–46°F / 2–8°C
storage (recon)
🧊
RECONSTITUTED SHELF LIFE
30 days after mixing
Standard 30-day window. Refrigerate 36–46°F / 2–8°C, protected from light. Do NOT freeze.
Storage: 2–8°C (fridge) · Protected from light · Do NOT freeze
Preload syringes/cartridges to minimize vial disturbance
Reconstitute 50mg vial with 3.0mL bacteriostatic water = 166.7 mcg/unit. Inject subcutaneously — abdomen or outer thigh. Refrigerate after reconstitution, use within 30 days. Do not freeze reconstituted vial.
06 — Dosage
Dosage Reference (SC Injectable — 50mg/3.0mL = 166.7 mcg/unit)
| Level | Dose | Units (syringe) | Context |
| LOW | 150 mcg | ~1 unit | Conservative start — sensitive individuals or first cycle |
| STANDARD | 250 mcg | ~1.5 units | Most common research dose — active metabolic optimization |
| HIGH | 500 mcg | ~3 units | Aggressive protocol — monitor methylation markers closely |
Start at 150mcg daily and titrate up based on response. Monitor homocysteine and methylation markers — NNMT inhibition affects the SAM/methionine cycle. Individual sensitivity varies significantly.
07 — Monitoring
Biomarkers, Lab Tests & Ranges
5-Amino-1MQ primarily affects NAD⁺ metabolism, fat mass, insulin sensitivity, and methylation status. Monitor the following before, at 6 weeks, and at end of cycle.
▸ NAD⁺ & Metabolic
| Biomarker | Lab Test | Clinical Range | Optimal Range |
| NAD⁺ (whole blood) | Intracellular NAD⁺ (Jinfiniti) | CLINICALNo standard reference | OPTIMAL>40 µM whole blood |
| Fasting Insulin | Serum Insulin (fasting) | CLINICAL2–25 µIU/mL | OPTIMAL2–6 µIU/mL |
| Fasting Glucose | Fasting Blood Glucose | CLINICAL70–99 mg/dL | OPTIMAL75–90 mg/dL |
| HbA1c | Hemoglobin A1c | CLINICAL<5.7% | OPTIMAL4.6–5.3% |
▸ Body Composition & Lipids
| Biomarker | Lab Test | Clinical Range | Optimal Range |
| Triglycerides | Lipid Panel | CLINICAL<150 mg/dL | OPTIMAL<80 mg/dL |
| HDL Cholesterol | Lipid Panel | CLINICAL>40 (M) / >50 (F) mg/dL | OPTIMAL55–80 mg/dL |
| Body Fat % (DEXA) | DEXA Scan | CLINICALM: <25% / F: <32% | OPTIMALM: 10–18% / F: 18–24% |
| Adiponectin | Serum Adiponectin | CLINICAL3–30 µg/mL | OPTIMAL>15 µg/mL |
▸ Methylation & Safety
| Biomarker | Lab Test | Clinical Range | Optimal Range |
Homocysteine Methylation status proxy | Serum Homocysteine | CLINICAL<15 µmol/L | OPTIMAL5–8 µmol/L |
SAM / SAH ratio Methylation capacity | Plasma SAM/SAH (specialty labs) | CLINICALSAM/SAH >4.5 | OPTIMALSAM/SAH >6.0 |
| AST / ALT | CMP | CLINICALAST 10–40 / ALT 7–56 U/L | OPTIMALAST <26 / ALT <26 U/L |
| CBC | Complete Blood Count | CLINICALStandard ranges | OPTIMALMid-range; WBC 4.5–6.0 |
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⚠ 5-Amino-1MQ has no published human clinical trials. Optimal ranges are functional medicine targets. Monitor methylation markers (homocysteine) closely — NNMT inhibition affects the methionine cycle. Consult a qualified practitioner.
08 — Cycle Protocol
Cycle Length, Frequency & Timing
▸ How Long to Cycle
ANIMAL RESEARCH
8–12 Weeks
Mouse studies showing fat loss ran 8–12 weeks of continuous daily dosing with significant body composition changes observed from week 4 onward.
PRACTITIONER CONSENSUS
8–16 Weeks
Practitioners commonly use 8–16 week cycles given the oral route and favorable safety profile. Off-period of 4–8 weeks between cycles is advised to assess methylation markers.
Because 5-Amino-1MQ affects the SAM/methionine cycle, methylation status should be monitored (homocysteine, SAM/SAH) especially in individuals with MTHFR variants or high homocysteine at baseline. Consider pairing with methylated B vitamins (methylfolate, methylcobalamin).
▸ Frequency & Timing
| Variable | Recommendation | Why |
| Frequency | Daily (1–2×/day) | Animal studies used daily dosing. Some practitioners split dose AM/PM for more consistent NNMT inhibition across the day. |
| Fasted vs Fed | Fed state acceptable | Fasting not required — inject AM with or without food. No insulin interaction concerns at these doses. |
| Morning (AM) | ✓ Preferred | AM injection aligns with peak metabolic activity and fat oxidation windows. |
| Injection Site | SC abdomen or thigh | Subcutaneous injection — rotate sites daily to prevent fibrosis. Abdomen or outer thigh preferred. |
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