Understand the source comparison
Mechanism of Action: Cellular Metabolism vs CNS Appetite Control
5-Amino-1MQ works by competitive inhibition of NNMT, an enzyme that methylates nicotinamide (a form of vitamin B3) into N-methylnicotinamide. When NNMT is overactive. Common in obesity and metabolic syndrome. Cellular NAD+ pools are depleted because nicotinami
No winner is assigned.
This page preserves a source comparison for education. It does not add a rating, recommendation or clinical judgment.
- 5-Amino-1MQ works by competitive inhibition of NNMT, an enzyme that methylates nicotinamide (a form of vitamin B3) into N-methylnicotinamide. When NNMT is overactive. Common in obesity and metabolic syndrome. Cellular NAD+ pools are depleted because nicotinamide gets shunted into methylation rather than NAD+ salvage pathways. Reduced NAD+ impairs mitochondrial respiration, sirtuins (SIRT1, SIRT3), and AMPK signaling, all of which are required for efficient fat oxidation. By blocking NNMT, 5-Amino-1MQ restores NAD+ availability, reactivates SIRT1-mediated mitochondrial biogenesis, and shifts substrate preference from glucose storage to lipid catabolism. The effect is metabolic reprogramming at the cellular level. Not appetite suppression.
- Tesofensine blocks the reuptake of serotonin, norepinephrine, and dopamine in the synaptic cleft by inhibiting their respective transporter proteins (SERT, NET, DAT). This prolongs neurotransmitter signaling in regions of the hypothalamus and limbic system that regulate satiety, reward-driven eating, and basal metabolic rate. The appetite suppression is direct and CNS-mediated. Patients report reduced hunger within 48–72 hours of dosing. Phase 2 trials demonstrated 10.6% mean body weight reduction at 24 weeks on 0.5mg daily tesofensine versus 2% placebo, with most effect attributed to reduced caloric intake rather than increased thermogenesis. Unlike 5-Amino-1MQ, tesofensine doesn't alter intracellular metabolism. It changes eating behaviour.