≥99%HPLC Purity
COAIncluded
USAShipped
5-Amino-1MQ Peptide
Selective NNMT (nicotinamide N-methyltransferase) inhibitor researched for metabolic regulation, adipogenesis inhibition, and energy expenditure modulation.
$100.00
This product may take an additional 5–7 days to arrive due to low stock.
Quick Facts
| SKU | ACR-5A1MQ |
|---|---|
| Purity | ≥98% |
| Physical Form | Lyophilized Powder |
| Storage | Store at -20°C |
What is 5-Amino-1MQ?
5-Amino-1MQ (5-amino-1-methylquinolinium) is a selective, cell-permeable inhibitor of nicotinamide N-methyltransferase (NNMT). NNMT is an enzyme overexpressed in adipose tissue that regulates cellular energy metabolism. By inhibiting NNMT, 5-Amino-1MQ shifts cellular metabolism toward increased NAD+ salvage and enhanced energy expenditure.
Mechanism of Action
5-Amino-1MQ inhibits NNMT, which normally converts nicotinamide (NAM) to 1-methylnicotinamide (1-MNA), consuming SAM methyl groups. By blocking this reaction: (1) NAM accumulates and is recycled into NAD+ via the salvage pathway, increasing cellular NAD+ levels; (2) SAM methyl donor pools are preserved, improving epigenetic methylation; (3) Adipocyte differentiation is suppressed and lipolysis is enhanced.
Mechanism of Action: NNMT Inhibition
5-Amino-1MQ is a cell-permeable, selective inhibitor of nicotinamide N-methyltransferase (NNMT) — an enzyme that sits at the intersection of three critical metabolic pathways:
- NAD+ salvage: NNMT converts nicotinamide (NAM) to 1-methylnicotinamide (1-MNA), diverting NAM away from the NAD+ salvage pathway. Inhibiting NNMT increases NAM recycling into NAD+ via NAMPT, raising cellular NAD+ levels by 50-100%.
- SAM methylation: NNMT consumes S-adenosylmethionine (SAM) as a methyl donor. Inhibition preserves SAM pools for essential methylation reactions including DNA methylation, histone methylation, and neurotransmitter synthesis.
- Adipogenesis: NNMT activity is required for adipocyte differentiation. Inhibiting NNMT blocks the PPARγ-mediated adipogenesis program, preventing pre-adipocytes from maturing into fat-storing cells.
The net effect: increased cellular energy (more NAD+), improved epigenetic regulation (more SAM), and reduced fat storage (blocked adipogenesis) — all from inhibiting a single enzyme.
Research & Clinical Studies
5-Amino-1MQ and Obesity Research
In a 2018 study by Neelakantan et al., 5-Amino-1MQ treatment in high-fat diet mice reduced body weight by 7% over 11 days, decreased adipocyte size by 40%, and increased intracellular NAD+ levels without affecting food intake. The compound reversed diet-induced obesity through metabolic reprogramming rather than appetite suppression.
5-Amino-1MQ and Muscle Function Research
Beyond adipose tissue, NNMT is expressed in skeletal muscle where it regulates NAD+ availability for contraction and recovery. 5-Amino-1MQ treatment in muscle cells increased NAD+ levels by 50-100%, enhanced SIRT1 activity, and improved mitochondrial respiration rate. In aged mice, NNMT inhibition restored muscle NAD+ to young-adult levels and improved grip strength — connecting metabolic reprogramming to functional muscle outcomes.
5-Amino-1MQ and Cancer Research
NNMT overexpression is found in multiple cancers (colorectal, breast, lung, pancreatic) where it promotes tumor growth by depleting SAM methyl donors and altering epigenetic landscapes. 5-Amino-1MQ has shown anti-tumor activity in preclinical models by restoring SAM methylation pools and reducing cancer cell proliferation. This positions NNMT inhibition as a metabolic approach to cancer research beyond traditional cytotoxic strategies.
5-Amino-1MQ and Diet-Induced Obesity Reversal
The landmark 2018 study (Neelakantan et al., Biochem Pharmacol) demonstrated 5-Amino-1MQ reverses established obesity in mice:
- Mice on high-fat diet for 14 weeks (obese) were treated with 5-Amino-1MQ for 11 days
- Body weight reduced 7% without caloric restriction or exercise
- Adipocyte size decreased 40% — existing fat cells shrunk
- Food intake unchanged — weight loss was purely metabolic, not appetite-driven
- Intracellular NAD+ increased significantly in adipose tissue
- No observable toxicity or behavioral changes
This is remarkable because 7% weight loss in 11 days through metabolic reprogramming alone (no appetite suppression, no exercise, no caloric restriction) represents a novel mechanism distinct from GLP-1 agonists (appetite suppression) or Fragment 176-191 (lipolysis).
[1] Neelakantan H et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2018;147:141-152. PubMed ↗
5-Amino-1MQ and Stem Cell / Aging Research
NNMT activity increases with aging and correlates with stem cell senescence. In mesenchymal stem cells (MSCs), NNMT overexpression drives cells toward senescence by depleting NAD+ and SAM. 5-Amino-1MQ treatment restored MSC proliferative capacity and differentiation potential to young-adult levels, suggesting NNMT inhibition may counteract aspects of stem cell aging.
Additionally, NNMT inhibition increased SIRT1 activity (NAD+-dependent deacetylase) in multiple cell types, connecting the NNMT pathway to the sirtuin-mediated longevity axis. This positions 5-Amino-1MQ at the intersection of obesity, aging, and regenerative research.
Chemical Properties
| Name | 5-Amino-1-methylquinolinium (5-Amino-1MQ) |
|---|---|
| Type | Small molecule NNMT inhibitor (not a peptide) |
| Target | NNMT (Nicotinamide N-Methyltransferase) |
| Selectivity | Selective for NNMT over related methyltransferases |
| Cell Permeability | High — enters cells without requiring transfection or carriers |
| Mechanism | Competitive inhibition of NNMT substrate binding |
| Downstream Effects | ↑NAD+, ↑SAM, ↓adipogenesis, ↑SIRT1 activity |
| Purity | ≥98% |
Handling & Administration
5-Amino-1MQ is a small molecule (not a peptide) supplied as lyophilized powder. It does not require reconstitution with bacteriostatic water. Dissolve in sterile water, DMSO, or PEG-400 depending on research protocol. Aqueous solubility is good at neutral pH. Standard laboratory PPE should be used when handling.
Storage & Stability
Powder: -20°C for 24+ months, room temperature for 30+ days. 5-Amino-1MQ is a stable small molecule without the degradation concerns of peptides (no disulfide bonds, no methionine, no asparagine). Solution: Store at 2-8°C, use within 14 days. Protect from light.
Frequently Asked Questions
How does 5-Amino-1MQ cause fat loss?
It inhibits NNMT enzyme in fat cells, increasing NAD+ levels and shifting metabolism toward energy expenditure. It reduces adipocyte size and differentiation without suppressing appetite — fat loss occurs through metabolic reprogramming.
Is 5-Amino-1MQ a peptide?
No, 5-Amino-1MQ is a small molecule NNMT inhibitor. It is included in our catalog as a metabolic research compound relevant to peptide-based obesity research protocols.
What is NNMT and why inhibit it?
NNMT (Nicotinamide N-Methyltransferase) converts nicotinamide (vitamin B3) to methylnicotinamide, consuming both NAD+ precursors and SAM methyl donors. Overactive NNMT depletes these critical metabolic resources. Inhibiting NNMT with 5-Amino-1MQ restores NAD+ and SAM pools, enhancing cellular metabolism.
Why did the mice lose weight without eating less?
5-Amino-1MQ inhibits NNMT, increasing cellular NAD+ and SIRT1 activity. This shifts metabolism toward energy expenditure (fat oxidation, thermogenesis) rather than storage. Adipocytes shrink because their lipid stores are being oxidized for energy — a metabolic reprogramming effect independent of appetite.
How does 5-Amino-1MQ compare to GLP-1 agonists for weight loss?
Completely different mechanisms. GLP-1 agonists (semaglutide, tirzepatide) reduce appetite via hypothalamic signaling — you eat less. 5-Amino-1MQ reprograms adipocyte metabolism via NNMT/NAD+/SIRT1 — you burn more. They could theoretically be complementary (eat less + burn more).
For laboratory and research use only. Not intended for human or animal consumption. All product information is derived from published preclinical research and does not constitute medical advice or claims.