Understand the source comparison
5-Amino-1MQ vs Tesofensine: Mechanism and Outcome Comparison
Primary Mechanism NNMT enzyme inhibition → increased NAD+ → mitochondrial fat oxidation Triple monoamine reuptake inhibition (serotonin, norepinephrine, dopamine) → appetite suppression 5-Amino-1MQ targets cellular metabolism; tesofensine modulates hunger sign
No winner is assigned.
This page preserves a source comparison for education. It does not add a rating, recommendation or clinical judgment.
- Primary Mechanism
- NNMT enzyme inhibition → increased NAD+ → mitochondrial fat oxidation
- Triple monoamine reuptake inhibition (serotonin, norepinephrine, dopamine) → appetite suppression
- 5-Amino-1MQ targets cellular metabolism; tesofensine modulates hunger signaling in the CNS
- Site of Action
- Peripheral (adipose tissue, liver, muscle). Does not cross BBB
- Central nervous system (hypothalamus, limbic regions)
- Entirely different biological compartments
- Weight Loss Mechanism
- Increased basal energy expenditure and fat oxidation without appetite reduction
- Reduced caloric intake due to appetite suppression and reward pathway modulation
- 5-Amino-1MQ: metabolic; tesofensine: behavioural
- Clinical Trial Data
- Preclinical and early human feasibility studies. No Phase 3 trials
- Phase 2 RCT: 10.6–12.8% mean weight reduction at 24 weeks (0.5–1.0mg daily)
- Tesofensine has stronger human efficacy data; 5-Amino-1MQ remains investigational
- Side Effect Profile
- Minimal reported AEs in animal models; human long-term data absent
- Insomnia, dry mouth, elevated HR (+7–9 bpm), mild hypertension
- 5-Amino-1MQ appears well-tolerated; tesofensine has documented cardiovascular signals
- Research Context
- NAD+ metabolism studies, mitochondrial dysfunction, metabolic syndrome models
- Appetite regulation, obesity pharmacology, CNS reward pathway research
- Use 5-Amino-1MQ for metabolism studies; tesofensine for appetite/CNS work