This product is a box of 10 vials.
What is 5-Amino-1MQ?
5-amino-1MQ (5-amino-1methylquinolinium), similar to methylquinolinium, acts as a short peptide that blocks the cytosolic enzyme nicotinamide N-methyltransferase (NNMT). This enzyme connects to obesity and type 2 diabetes while helping control energy balance in cells. Blocking NNMT causes major weight loss, less fat mass and smaller fat cells (adipocytes), plus lower cholesterol and glucose in the blood. Researchers actively study 5-amino-1MQ and related methylquinolinium compounds as possible treatments for obesity and diabetes. Blocking NNMT also seems to activate stem cells and boost muscle repair capacity.
Molecular Formula: C10H11N2
Molecular Weight: 159.21 g/mol
PubChem CID: 950107
CAS Number: 42464-96-0
Synonyms: 5-amino-1-methylquinolinium
Obesity
Nicotinamide N-methyltransferase serves as a cell enzyme present in many body areas, but it thrives most in liver and fat cells. Mouse research links high NNMT levels to lower amounts of the sugar transporter GLUT4. This transporter, found mainly in skeletal and heart muscle plus fat cells, ties closely to blood sugar control and diabetes risk. Rodent tests show mice with high GLUT4 production stay sensitive to insulin and resist type 2 diabetes better. In contrast, those with low GLUT4 face strong insulin resistance.
GLUT4 connects to basic metabolic rate and ideas of fast versus slow metabolism. People with naturally high GLUT4 levels tend to have quicker metabolism and burn more calories. Exercise boosts this transporter's production, which helps explain how physical activity fights weight gain, high blood sugar, and insulin issues. GLUT4 and NNMT link tightly, affecting baseline metabolism in mammals. Dr. Barbara Kahn from Harvard Medical School notes that the GLUT4-NNMT tie first sparked interest in targeting this enzyme for diabetes and obesity care. Animals with insulin resistance often show high NNMT in fat cells. Adjusting this gene counters insulin resistance and thus diabetes, while strongly impacting weight and obesity.
Human and animal metabolism runs with great efficiency, squeezing the most from few calories. Yet this same trait might drive obesity when calories abound. Making metabolism less efficient—causing the body to waste some calories—has long been a medical goal to tackle rising obesity. NNMT's role with GLUT4 could be the missing piece researchers seek. At its core, NNMT slows calorie use, leaving more for fat or glycogen storage. Lower NNMT cuts the shift of nicotinic acid (NA) to 1-methylnicotinamide (1-MNA). This change affects metabolism in two ways.
Overall, using an NNMT blocker like 5-amino-1MQ ramps up energy burn and cuts storage. Paired with raised GLUT4 expression from lower NNMT, this setup clears glucose from blood better and uses it directly during burn. Outcomes include less insulin need, lower resistance, reduced fat buildup, and higher energy metabolism. In just 10 days, treated mice dropped 7% in weight and 30% in fat mass. Their blood cholesterol matched lean mice, all without food intake shifts. Mice on 5-amino-1MQ lost 7% body mass in 10 days without eating changes, unlike controls.
Fresh evidence hints that 5-amino-1MQ's perks go beyond curbing NNMT and boosting inefficient metabolism plus GLUT4. Mouse studies suggest it reshapes fat cell function by raising GLUT4, prompting them to make different lipids with anti-diabetic and anti-inflammatory traits. These lipids, called PAHSAs (palmitic acid esters of hydroxy-stearic acids), ease insulin resistance alone and curb inflammation, improving odds against heart attacks and strokes. Though new, this side of 5-amino-1MQ suggests a wider range of benefits for this standout molecule.
Muscle Function
5-amino-1MQ affects skeletal muscle in several ways. Like in fat tissue, it boosts GLUT4 production there and raises metabolic inefficiency for more energy use. But recent mouse work shows inhibiting NNMT, including via 5-amino-1MQ, might speed muscle repair by sparking stem cells.
Studies on 24-month-old mice (elderly for their kind) found those treated with an NNMT blocker had far more stem cell activation in hurt muscle than untreated ones. Their repaired muscle fibers grew twice as thick in cross-section and gained stronger contraction power. Treated mice showed 70% more force in healed muscle than controls. Beyond quickening injury fixes, boosting muscle stem cells could help older folks stay independent longer. By aiding movement and cutting fall risks, NNMT blockers might greatly enhance life quality and self-reliance in aging adults.
Rising NNMT expression often marks muscle-wasting issues like Duchenne Muscular Dystrophy. Lowering NNMT could ease symptoms in some cases. This ties back to NNMT blocking stem cell growth and split. Compounds like 5-amino-1MQ, by dropping NNMT, might aid various muscle-loss conditions. NNMT block's full muscle effects aren't clear yet, but another angle involves NAD+ levels. Blocking NNMT raises NAD+, and tools like 5-amino-1MQ have boosted muscle work, heart health, and DMD in animal tests. Key drivers seem to be better mitochondrial function plus less inflammation and scarring, all from higher NAD+.
Cognition
NAD+ plays a vital part in brain energy balance. Low NAD+ links to many brain issues and harms neuron communication at synapses and nerve-muscle junctions. Mouse research shows falling NAD+ can weaken synaptic signals, hurt muscle, and harm overall thinking. While not tested directly here, 5-amino-1MQ likely affects brain NAD+ like elsewhere. This suggests it could treat thinking problems or act as a nootropic to sharpen average minds. Active interest explores 5-amino-1MQ's potential brain perks, though research must confirm.
Cancer
Strong evidence shows higher NNMT in all gastric cancers, plus pancreatic, kidney, and bladder types. Mice lacking NNMT gene resist these cancers, hinting NNMT causes them. Early work speculates blocking NNMT could treat or prevent some cancers, or at least curb their spread. It's unclear if 5-amino-1MQ, by lowering NNMT, affects these cancers.
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