Also known as: 5-amino-1-methylquinolinium · 5A1MQ · 5-amino-1-methylquinolinium chloride
| Parameter | Value | Source |
|---|---|---|
| Elimination Half-Life (Human) | Not established — no published human PK study | — |
| Elimination Half-Life (Animal) | Not reported in Kannt et al. 2018 | Kannt A et al. 2018[1] |
| Time to Peak (Tmax) | No published human data | — |
| Bioavailability | No published human data | — |
| Plasma Protein Binding | No published data | — |
| Route of Administration (Animal Studies) | Subcutaneous (murine models) | Kannt A et al. 2018[1] |
| Molecular Weight | ~174 Da | PubChem CID 11988697 |
| Full Clearance (5 × t½) | Cannot be calculated — human t½ unknown | — |
| FDA Approval Status | Not approved | — |
| Data Quality | Animal Study — no published human PK study identified as of May 2026 | |
No published human pharmacokinetic study for 5-amino-1MQ (5-amino-1-methylquinolinium) has been identified as of May 2026. The plasma half-life in humans is unknown. The primary published study — Kannt et al. (2018) in Scientific Reports — is a murine study that characterized the pharmacodynamic effects of 5-amino-1MQ on adipocyte size in diet-induced obese mice but did not report formal pharmacokinetic parameters including half-life.[1]
5-Amino-1MQ is a small aromatic amine with molecular weight of approximately 174 Da (as the free base). Based on structural features alone — small size, aromatic ring, basic nitrogen — one would expect reasonable oral bioavailability and hepatic metabolism, but this is an inference from chemistry, not from published human or animal ADME data. No clinically actionable half-life value can be stated.
A human pharmacokinetic characterization of 5-amino-1MQ would require an IND-enabled Phase 1 trial with serial blood sampling following single- and multiple-dose administration. LC-MS/MS assay development for plasma quantification of the quinolinium cation would be necessary. To date, no such study has been published in peer-reviewed literature or registered in ClinicalTrials.gov as of the review date for this page.[1]
For NNMT inhibitors, the plasma half-life is likely to be shorter than the biological effect duration, because the downstream consequences of NNMT inhibition — shifts in the SAM:SAH ratio, changes in histone methylation patterns, altered adipogenic gene expression — may persist after the compound has cleared from plasma. This is analogous to other enzyme inhibitors where the pharmacodynamic effect outlasts plasma exposure. However, this is a mechanistic inference; no quantitative data exists to compare plasma clearance against cellular effect duration for 5-amino-1MQ in any species.
This cannot be answered with published data. No human or animal pharmacokinetic study has characterized the clearance timeline for 5-amino-1MQ. A clearance timeline table (1–5 half-lives) is not presented here because there is no validated half-life value from which to calculate it. Presenting such a table would require fabricating data, which Halflife Labs' editorial policy prohibits.
If a human half-life were to be established in future clinical research, this section will be updated with a full clearance timeline based on that primary data.
Because no human PK data exists, no evidence-based dosing frequency recommendation can be made for 5-amino-1MQ. Any dosing protocol described by sellers, forums, or research communities is extrapolated from the murine study dose (which used ~100 mg/kg SC in mice — a dose that cannot be directly scaled to humans without allometric adjustment and safety validation).[1]
| Compound | Mechanism | Human PK Data? | Primary Evidence | Status |
|---|---|---|---|---|
| 5-Amino-1MQ | NNMT inhibitor | No | Murine adipocyte study | Not FDA-approved |
| SLU-PP-332 | ERR agonist (exercise mimetic) | No | Murine endurance study | Not FDA-approved |
| MK-677 (Ibutamoren) | GH secretagogue (oral) | Yes — human PK studies | Human PK studies; t½ ~6 h | Not FDA-approved |
| Tirzepatide | GIP/GLP-1R dual agonist | Yes — Human RCT | FDA NDA 215866; t½ ~5 days | FDA-approved |
| Route | Half-Life | Bioavailability | Notes |
|---|---|---|---|
| Subcutaneous (murine studies) | Not reported | Not reported | Route used in Kannt et al. 2018; no formal PK reported |
| Oral (human) | No published data | No published data | Small MW suggests potential oral absorption; not validated |
| Intravenous | No published data | 100% (definitional) | No published study in any species |
5-Amino-1MQ is not included in any standard workplace, military, or forensic drug panel. It is not a controlled substance in the United States.[1]
No published forensic detection study for 5-amino-1MQ in urine or blood has been identified. Detection in biological samples would require validated LC-MS/MS methods specific to the quinolinium structure, which have not been reported in the peer-reviewed literature as of May 2026.
5-Amino-1MQ inhibits NNMT — nicotinamide N-methyltransferase — a cytosolic enzyme that catalyzes the N-methylation of nicotinamide (NAM) using S-adenosylmethionine (SAM) as the methyl donor, producing 1-methylnicotinamide (MNA) and S-adenosylhomocysteine (SAH).[1]
NNMT serves as a metabolic sink for both NAD+ precursors and methyl groups. In white adipose tissue, NNMT expression is elevated in obesity. High NNMT activity: (1) consumes NAM, reducing flux through the NAD+ salvage pathway (NAM → NMN → NAD+) and potentially lowering cellular NAD+ levels in adipocytes; and (2) depletes the methyl donor SAM while accumulating SAH, which inhibits most methyltransferases including histone methyltransferases — effectively reducing histone H3K4me3 marks associated with genes promoting adipocyte differentiation and lipid storage.[1]
By inhibiting NNMT, 5-amino-1MQ theoretically reverses both effects: restoring NAD+ salvage flux and restoring SAM availability for other methylation reactions. In Kannt et al. (2018), DIO mice treated with 5-amino-1MQ showed reduced adipocyte cell size (not count) and attenuated body weight gain compared to vehicle-treated controls. The effect was modest and the study did not characterize dose-response, duration-response, or mechanisms beyond histological adipocyte size measurement.[1]
It is important to note that: (a) reduced adipocyte size in mice does not directly translate to human weight loss; (b) the translational relevance of NNMT inhibition in human obesity has not been validated in any published clinical trial; (c) NNMT is expressed in many tissues beyond adipose (liver, brain, kidney), and systemic inhibition could have off-target consequences that have not been characterized in safety studies.
Track injection timing, dose, and site rotation for research compounds including 5-amino-1MQ. On-device. No data shared externally. No account required.
Download Free — iOSThe Halflife app tracks 5-amino-1MQ alongside 44 other compounds — all with citation-backed pharmacokinetic data from FDA labels and published literature. Free on iOS.
Download on the App Store