5-Amino-1MQ

Produktübersicht

5-Amino-1MQ blocks the enzyme NNMT, which is predominantly active in fat tissue and normally slows fat breakdown while reducing NAD+ levels. By inhibiting NNMT, 5-Amino-1MQ increases NAD+ — a cofactor central to cellular metabolism — thereby increasing metabolic rate and activating SIRT1, known as the "longevity gene" for its role in reducing risks of diabetes, obesity, cardiovascular disease, neurodegeneration, and cancer.

Mechanismus der Wirkung

NNMT inhibition by 5-Amino-1MQ elevates cellular NAD+ levels. Increased NAD+ enhances mitochondrial energy production, DNA repair capacity, and activates SIRT1 signaling. This shifts metabolism toward fat utilization while preserving muscle mass, improving insulin sensitivity, and supporting cellular health.

Wichtigste Vorteile

Fat Burning with Muscle Preservation — Shifts metabolic pathways to burn stored fat for energy while preferentially maintaining muscle tissue. Mouse studies show 47% reduction in fat mass with NNMT inhibition.

Metabolic Health & Weight Management — Stabilizes blood sugar, improves insulin sensitivity, and supports weight management in individuals at risk for or living with type 2 diabetes and metabolic comorbidities.

Anti-Aging & Langlebigkeit — SIRT1 activation is associated with healthier aging, reduced disease risk, and improved cellular resilience. A key addition to comprehensive anti-aging protocols.

Cognitive & Neurological Support — NAD+ elevation improves cellular energy availability for brain function, potentially protecting against neurodegenerative conditions.

Referenzen

1. Neelakantan H, et al. Selective and membrane-permeable small molecule inhibitors of NNMT reverse high fat diet-induced obesity in mice. *Biochem Pharmacol.* 2018;147.
2. Yu T, et al. Effects of nicotinamide N-methyltransferase on PANC-1 cells proliferation under metabolic stress. *Cell Physiol Biochem.* 2015;35(2):710–721.
3. Markert JM, et al. Differential gene expression profiling in human brain tumors. *Physiol Genomics.* 2001;5(1):21–33.