5-Amino-1MQ : Key Benefits and Research Insights summary
Weight Loss and Fat Metabolism: Reduces body fat by inhibiting fat storage and increasing fat burning, as shown in in vitro studies on adipocytes.
Insulin Sensitivity and Glucose Control: Boosts NAD+ to improve mitochondrial efficiency and glucose uptake, potentially aiding type 2 diabetes management.
Muscle Health: Inhibits NNMT to preserve NAD+ precursors, supporting muscle strength and regeneration.
Anti-Aging Potential: NAD+ elevation activates sirtuins, which combat cellular aging and inflammation.
5-Amino-1-MQ mechanism of action
5-Amino-1MQ acts as a selective small molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme that methylates nicotinamide using S-adenosylmethionine (SAM) as a methyl donor.
By inhibiting NNMT, 5-Amino-1MQ reduces the production of 1-methylnicotinamide (MNA), a metabolite that would otherwise deplete cellular nicotinamide pools.
This inhibition prevents the degradation of nicotinamide, a key precursor for nicotinamide adenine dinucleotide (NAD+) synthesis via the salvage pathway.
The mechanism of the NAD+salvage pathway improves the function of skeletal muscle in aging. NAD+-Sirtuin1—FoxOs mitigates oxidative stress damage; NAD+-Sirtuin1- PGC-1α improves mitochondrial function; NAD+-Sirtuin1-AMPK promotes autophagy; NAD+-Sirtuin2 reduces chronic low-grade inflammation and enhances the quantity and functionality of MuSCs; NAD+ increases vesicles and remodels the endplate of NMJ.
As a result, intracellular NAD+ levels increase, enhancing the activity of NAD+-dependent enzymes such as sirtuins and poly(ADP-ribose) polymerases (PARPs).
Elevated NAD+ promotes mitochondrial biogenesis and function, improving cellular energy metabolism through enhanced oxidative phosphorylation.
In adipocytes, 5-Amino-1MQ suppresses lipogenesis by downregulating genes involved in fatty acid synthesis, such as those regulated by SREBP-1c.
The compound also improves glucose uptake and clearance by activating AMP-activated protein kinase (AMPK) pathways, which are sensitive to NAD+/NADH ratios.
At the molecular level, reduced NNMT activity shifts cellular methylation patterns, potentially altering epigenetic modifications via changes in SAM/S-adenosylhomocysteine (SAH) ratios.
This leads to decreased inflammation by modulating NF-κB signaling, as higher NAD+ supports sirtuin-mediated deacetylation of pro-inflammatory factors.
Overall, 5-Amino-1MQ's inhibition of NNMT restores metabolic homeostasis by boosting NAD+ availability, thereby counteracting age-related declines in cellular energy production.
Experimental studies frequently examine 5-Amino-1MQ as a research compound within NNMT-related metabolic pathways. Its interaction with NAD⁺ availability places it within a broader framework of cellular energy and aging research.
→ 5-Amino-1MQ research compound
→ NAD⁺ metabolism in research models