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.
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.
| Dose | Format | Context |
|---|---|---|
| 50 mg | 1 capsule | LOW / INTRO |
| 100 mg | 2 capsules | COMMON |
| 150–200 mg | 3–4 capsules | STANDARD |
| 250–300 mg | 5–6 capsules | HIGH |
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.
| 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% |
| 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 |
| 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 |
| 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 | ✓ With food preferred | As an oral small molecule, taking with food improves tolerability and may improve absorption. Unlike injectable peptides, fasting is not required or particularly beneficial. |
| Morning (AM) | ✓ Preferred (first dose) | AM dosing with breakfast aligns with peak metabolic activity and fat oxidation windows. If split dosing, take second dose with lunch rather than in the evening. |
| Evening (PM) | ~ Avoid as primary dose | No strong evidence against PM dosing but AM aligns better with the metabolic processes the molecule targets. Avoid late evening to prevent potential sleep disruption from metabolic activation. |