5-Amino-1MQ

Overview

Where it comes from and why it was developed

The story of 5-Amino-1MQ does not begin with this molecule. It begins with an enzyme that long stood in the shadow of classical metabolic targets.

NNMT (Nicotinamide N-Methyltransferase) is an enzyme that transfers a methyl group from SAM (S-adenosylmethionine) to nicotinamide (vitamin B3, precursor of NAD+). The result is 1-methylnicotinamide (MNA) and S-adenosylhomocysteine (SAH). For long decades NNMT was considered a boring “clearance” enzyme that simply prepares nicotinamide for excretion. No sexy biology, no major target.

That changed in 2014. The team of David Accili and Barbara Kahn at Harvard Medical School published a breakthrough paper in Nature (Kraus et al. 2014) showing that knockdown of NNMT in adipocytes protects mice from diet-induced obesity. In other words: if you knock out NNMT in adipose tissue, the mouse cannot gain weight even on a high-fat diet. Overnight, NNMT changed from a boring clearance enzyme into a hot metabolic target.

The mechanism described by Kraus is elegant. Through its activity, NNMT consumes the SAM pool (the methyl donor) and diverts nicotinamide away from the NAD+ synthesis pathway. In adipocytes with high NNMT expression this means two things simultaneously:

1. Lower NAD+ pool (because nicotinamide is diverted into the MNA route, not into the NAD+ salvage pathway). Lower NAD+ means lower activity of sirtuins (SIRT1, SIRT3), which regulate mitochondrial function and metabolic flexibility.
2. Lower SAM pool (because it is consumed for methylation of nicotinamide). Lower SAM means a weakened ability of the cell to perform epigenetic modifications (DNA methylation, histone methylation), which may contribute to adipocyte dysfunction.

Inhibition of NNMT therefore doubly anchors metabolism: a higher NAD+ pool plus a higher SAM pool. For the pharmaceutical industry it was a clear signal: we need small molecules capable of selectively inhibiting NNMT with reasonable pharmacokinetics.

And here enters the Robert Messing lab at the University of Texas at Austin. The team of Brian Kornilov in Messing’s laboratory ran systematic SAR (structure-activity relationship) studies on a panel of quinoline derivatives as potential NNMT inhibitors. From this screening one specific hit emerged: 5-Amino-1-methylquinolinium iodide, abbreviated as 5-Amino-1MQ.

In 2017 Neelakantan and colleagues published in Biochemical Pharmacology the original characterization of 5-Amino-1MQ. The molecule was the first selective, membrane-permeable NNMT inhibitor in the literature. Previous inhibitors were either non-selective (also inhibited other methyltransferases) or did not penetrate the membrane (and were therefore unusable in cellular experiments).

A second life as a research tool and biotech spin-off

5-Amino-1MQ was never intended as a clinical candidate. From the start it was intended as a research tool: a small molecule that would allow experimental validation of NNMT as a target in living systems. In other words, it is a chemical probe for biology, not a drug for patients.

In a parallel world, however, the biotechnology company Metro International Biotech (Metro Biotech) was born, later with a program known as Cardelia, developing clinical NNMT inhibitors for the indications of obesity, sarcopenia, and metabolic syndrome. Cardelia/Metro Biotech, however, uses a different chemical class from 5-Amino-1MQ; their clinical candidates (for example MIB-626 and other undisclosed molecules) are of different design. 5-Amino-1MQ remains as a research tool, not a clinical asset, and in this context functions as a proof-of-concept molecule for NNMT inhibition.

In the research community around longevity, metabolic health, and NAD+ biology, however, 5-Amino-1MQ quickly became popular. Reasons:

1. Unique mechanism. No other available research molecule targets NNMT directly.
2. Stack potential. Combination with NAD+ precursors (NMN, NR) is theoretically synergistic; NNMT inhibition raises the endogenous NAD+ pool, exogenous precursors supply substrate.
3. Price accessibility. A small organic molecule is synthesized more cheaply than most peptides.
4. Stable profile. No disulfides, no acetylated termini, no incubation sensitivity, simple handling.

Mechanism of action. What it does at the cellular level

5-Amino-1MQ acts through one primary mechanism with multiple downstream consequences.

Competitive inhibition of NNMT

5-Amino-1MQ binds to the active site of NNMT and competes with nicotinamide for binding. Because structurally it resembles the “transition state” of the reaction (the quinoline ring mimics nicotinamide aromaticity), it is highly selective for NNMT and has minimal off-target activity against other methyltransferases (COMT, PNMT, HNMT, GNMT).

Ki ~1.3 µM, IC50 values depend on assay conditions (typically 0.5–5 µM in isolated enzymatic tests). 5-Amino-1MQ is therefore a medium-strength inhibitor, not subnanomolar, but sufficiently potent for research applications and in vivo experiments.

Increase of the NAD+ pool

This is the best-documented downstream effect. When NNMT is inhibited, nicotinamide is not diverted into the MNA route but remains available for the NAD+ salvage pathway (NAMPT → NMN → NAD+). In rodents with NAFLD or metabolic syndrome, 5-Amino-1MQ treatment increased the hepatic NAD+ pool by 20–40 % (Neelakantan 2017, Kannt 2018).

Higher NAD+ means:

• Higher sirtuin activity (SIRT1, SIRT3, SIRT6). Sirtuins are NAD+-dependent deacetylases that regulate mitochondrial function, oxidative stress, and DNA repair.
• Better mitochondrial function, higher capacity for oxidative phosphorylation, higher ATP turnover.
• Activation of PARP, NAD+-dependent DNA repair enzymes.

Increase of the SAM pool

NNMT consumes SAM for methylation of nicotinamide. Inhibition of NNMT therefore conserves SAM, which is then available for other methyltransferases:

• DNMTs (DNA methyltransferases), epigenetic regulation of gene expression.
• PRMTs (protein arginine methyltransferases), modification of histones and signaling proteins.
• COMT (catechol-O-methyltransferase), catabolism of catecholamines.

In adipocytes with high NNMT expression, increasing the SAM pool leads to normalization of the epigenetic state, which contributes to increased thermogenic capacity.

Adipocyte effects. Thermogenesis and lipolysis

In fat cells, 5-Amino-1MQ activates the thermogenic program. Kraus et al. (2014) showed that NNMT knockdown increases expression of UCP1 and other “brown fat” markers in white adipose tissue. 5-Amino-1MQ reproduces these effects pharmacologically.

In high-fat diet mouse models, 5-Amino-1MQ:

• Reduced body fat by 15–25 % after 8–12 weeks of treatment
• Lowered liver weight (steatosis) by 30–40 %
• Improved insulin sensitivity (HOMA-IR)
• No effect on total caloric intake or activity (effect via metabolism, not via appetite)

Muscle effects. Regeneration and strength

In the second key study (Neelakantan 2018), the team showed that 5-Amino-1MQ activates senescent muscle stem cells (satellite cells) in old mice and improves regenerative capacity of aging skeletal muscle.

The mechanism here is multilayered:

• Higher NAD+ → higher SIRT1/SIRT3 activity → better mitochondrial biogenesis in satellite cells
• Higher SAM → epigenetic reset of aging muscle progenitors
• Possible direct effect on mTOR signaling (Neelakantan 2018 suggests an mTOR-independent component)

Hepatocyte effects. Reduction of steatosis

In hepatocytes with fatty degeneration (MASLD/NAFLD) 5-Amino-1MQ:

• Inhibits lipogenesis (reduced expression of SREBP-1c, FAS)
• Activates β-oxidation of fatty acids (PGC-1α, PPARα)
• Reduces hepatic triglycerides by 30–40 % in animal models

Investigated applications

The published preclinical literature documents effects of 5-Amino-1MQ in the following areas:

• Obesity and metabolic syndrome, the primary research indication, robust animal data
• Type 2 diabetes, improved insulin sensitivity in high-fat diet models
• MASLD/MASH (fatty liver disease), reduction of hepatic steatosis
• Sarcopenia (age-related muscle atrophy), activation of senescent satellite cells
• Oncology, NNMT is overexpressed in pancreatic carcinoma, glioblastoma, and certain sarcomas (emerging research)
• Idiopathic pulmonary fibrosis (IPF), antifibrotic effect via the NNMT/SAM axis
• Cardiac fibrosis, preclinical data
• Longevity research, NAD+ and SAM pool as an anti-aging intervention

Science & studies

Key publications

Kraus D., Yang Q., Kong D., et al. (2014). Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 508(7495):258–262. Foundational NNMT paper.

Neelakantan H., Vance V., Wang H.L., et al. (2017). Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 147:141–152. Original 5-Amino-1MQ paper, synthesis and characterization.

Neelakantan H., Brightwell C.R., Graber T.G., et al. (2018). Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochem Pharmacol. 163:481–492. Muscle regeneration and sarcopenia.

Kannt A., Rajagopal S., Kadnur S.V., et al. (2018). A small molecule inhibitor of Nicotinamide N-methyltransferase for the treatment of metabolic disorders. Sci Rep. 8(1):3660. Alternative NNMT inhibitor chemistry, target validation.

Brown K.D., Maqsood S., Huang J.Y., et al. (2014). SIRT3 reverses aging-associated degeneration. Cell Rep. 3(2):319–327. Background for NAD+/sirtuin biology.

Roberti A., Fernández A.F., Fraga M.F. (2021). Nicotinamide N-methyltransferase: At the crossroads between cellular metabolism and epigenetic regulation. Mol Metab. 45:101165. Comprehensive review of NNMT in metabolism and epigenetics.

Pissios P. (2017). Nicotinamide N-Methyltransferase: More Than a Vitamin B3 Clearance Enzyme. Trends Endocrinol Metab. 28(5):340–353. Review of NNMT biology.

Detailed study breakdowns

▸ Study 1: Kraus 2014. Foundational NNMT paper

Citation: Kraus D., Yang Q., Kong D., et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature. 2014;508(7495):258–262.

What they did: The team of Barbara Kahn at Harvard Medical School analyzed NNMT expression in adipose tissue of obese vs. lean mice and human patients. They then used antisense oligonucleotide (ASO) technology to knock down NNMT in the white adipose tissue of C57BL/6J mice fed a high-fat diet. Duration: 6 weeks. Assessment: body weight, body fat, energy expenditure (metabolic chambers), insulin sensitivity, expression of thermogenic genes.

What they found:

• NNMT is 2- to 4-fold overexpressed in adipose tissue of obese mice and human patients
• NNMT knockdown protected against diet-induced obesity: knockdown mice had 30 % lower body weight despite the same caloric intake
• Increased energy expenditure by 15 % in knockdown mice
• Increased expression of thermogenic markers (UCP1, PGC-1α) in white fat
• Increased NAD+ pool in adipocytes
• Increased SAM pool and normalized polyamine synthesis
• Improved insulin sensitivity

Why it matters: This is the foundational paper for the entire NNMT inhibitor field. It validated NNMT as a legitimate anti-obesity target and opened the door for development of pharmacological inhibitors. Without this Nature publication, 5-Amino-1MQ would probably not exist as a research molecule.

▸ Study 2: Neelakantan 2017. Original 5-Amino-1MQ paper

Citation: Neelakantan H., Vance V., Wang H.L., et al. Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Biochem Pharmacol. 2017;147:141–152.

What they did: SAR screening of quinoline derivatives as potential NNMT inhibitors in the Messing lab at UT Austin. From the panel of candidates, 5-Amino-1MQ was selected as the lead compound for in vivo testing. Diet-induced obese (DIO) C57BL/6J mice received 5-Amino-1MQ orally in drinking water at a dose of 20 mg/kg/day for 11 weeks. The control group received plain water. Assessment: body weight, body fat (DXA), hepatic steatosis (histology), insulin sensitivity (GTT, ITT), gene expression in fat and liver.

What they found:

• 5-Amino-1MQ reduced body fat by 15–20 % vs. control
• Reduced hepatic steatosis by ~40 %
• Improved glucose tolerance (GTT AUC lower by 25 %)
• Increased expression of thermogenic genes (UCP1, PGC-1α, Cidea) in white fat
• Increased hepatic NAD+ pool by 30 %
• Increased hepatic SAM pool by 25 %
• No changes in food intake; the mechanism is metabolic, not appetite-suppressing
• No observable toxic effects in the 11-week protocol

Why it matters: This is the original 5-Amino-1MQ publication. It demonstrated that:

1. The molecule is orally bioavailable in mice (via drinking water)
2. It acts via the expected NNMT mechanism (increased NAD+ and SAM)
3. It reproduces the benefit of the knockdown phenotype (Kraus 2014) pharmacologically
4. It has a reasonable safety margin in animal models

The entire research literature on 5-Amino-1MQ derives from this publication.

▸ Study 3: Neelakantan 2018. Muscle regeneration and sarcopenia

Citation: Neelakantan H., Brightwell C.R., Graber T.G., et al. Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochem Pharmacol. 2018;163:481–492.

What they did: Old mice (24 months, corresponding to a human age of ~70 years) received 5-Amino-1MQ in drinking water at a dose of 10 mg/kg/day for 4 weeks. Assessment: muscle strength (grip strength), muscle mass, satellite cells (Pax7+ proliferation), regenerative response after experimental muscle injury (cardiotoxin injection).

What they found:

• Increased muscle strength by ~15 % after 4 weeks
• Increased satellite cell proliferation (Pax7+ Ki67+ cells 2- to 3-fold more frequent)
• Better regeneration after experimental muscle injury (faster reconstitution of myofibrils)
• Higher ratio of young vs. senescent satellite cells
• Increased mitochondrial biogenesis in muscle tissue
• No effect on total body weight in this short protocol

Why it matters: It opened a second research front for 5-Amino-1MQ beyond obesity. Sarcopenia (age-related muscle atrophy) is a huge clinical problem without approved pharmacotherapy. NNMT inhibition as an anti-sarcopenic mechanism is now actively explored also by the pharmaceutical industry.

▸ Study 4: Kannt 2018. Alternative chemistry, target validation

Citation: Kannt A., Rajagopal S., Kadnur S.V., et al. A small molecule inhibitor of Nicotinamide N-methyltransferase for the treatment of metabolic disorders. Sci Rep. 2018;8(1):3660.

What they did: A Sanofi team (with an Indian CRO partnership) developed a different chemical class of NNMT inhibitors (not quinolines, but piperidine derivatives). They tested the lead compound in DIO mouse models at doses of 30 and 100 mg/kg/day for 8 weeks. Assessment: body weight, glycemic profile, lipid profile, hepatic steatosis.

What they found:

• The Sanofi inhibitor reduced body weight by 12–18 % in DIO mice
• Improved glucose tolerance
• Reduced hepatic steatosis
• Mechanism consistent with 5-Amino-1MQ: increased NAD+, SAM, thermogenic markers

Why it matters: Validates the NNMT target from an independent source with a different chemical class. Sanofi independently reproduced the key phenotypes of NNMT inhibition. This reduces the risk that 5-Amino-1MQ effects are an artifact of a specific molecule; instead, it shows that NNMT inhibition as a concept is robust. Kannt 2018 also brought “big pharma” attention to this target, which paradoxically also supported research molecules such as 5-Amino-1MQ.

▸ Study 5: Roberti 2021. Comprehensive NNMT review

Citation: Roberti A., Fernández A.F., Fraga M.F. Nicotinamide N-methyltransferase: At the crossroads between cellular metabolism and epigenetic regulation. Mol Metab. 2021;45:101165.

What they did: A systematic review of the NNMT literature. About 200 citations. Covers NNMT biology from enzymatic characterization through metabolic functions, epigenetic regulation, oncological connections, and fibrotic diseases.

What they found (key conclusions):

• NNMT is a multifunctional enzyme with roles in metabolism, epigenetics, oncogenesis, and fibrosis
• Overexpression of NNMT is described in: obesity, type 2 diabetes, MASLD, pancreatic carcinoma, glioblastoma, colorectal carcinoma, renal carcinoma, IPF, cardiac fibrosis
• NNMT inhibition has multiple potential therapeutic applications beyond obesity
• 5-Amino-1MQ is the most-used research molecule for NNMT inhibition in the academic literature
• Clinical development of NNMT inhibitors (Cardelia/Metro Biotech) is progressing, although with a different chemical class

Why it matters: Roberti 2021 provides an expert orientation map for 5-Amino-1MQ. If you want to understand why NNMT is interesting biologically, this is the first publication to read. Comprehensive and up to date.

▸ Study 6: Pissios 2017. NNMT biology, beyond vitamin B3

Citation: Pissios P. Nicotinamide N-Methyltransferase: More Than a Vitamin B3 Clearance Enzyme. Trends Endocrinol Metab. 2017;28(5):340–353.

What they did: An in-depth review of NNMT biology before the 5-Amino-1MQ era (published shortly after the original Neelakantan 2017 paper). Pissios systematically examined:

• Enzymatic regulation of NNMT (transcription, post-translational modifications)
• Tissue distribution of NNMT (liver, fat, bones, brain)
• Substrate specificity (preference for nicotinamide, but also other methyl acceptors)
• Pathological associations

What they found (key conclusions):

• NNMT is primarily expressed in the liver and adipose tissue, secondarily in other tissues
• It regulates the pool of MNA (1-methylnicotinamide), which itself has biological activities (vasodilation, anti-inflammatory effects)
• Substrate promiscuity is low; NNMT is highly specific for nicotinamide
• Because MNA has its own effects, NNMT inhibition has a dual pharmacological consequence: increase in NAD+ and decrease in MNA

Why it matters: Pissios provides enzymatic context for 5-Amino-1MQ pharmacology. For the research context it is useful to understand that NNMT inhibition is not just about “increasing NAD+”; it is modulation of the entire methylation–NAD+–polyamine axis.

▸ Study 7: Background. SIRT3 and NAD+ biology (Brown 2014)

Citation: Brown K.D., Maqsood S., Huang J.Y., et al. SIRT3 reverses aging-associated degeneration. Cell Rep. 2014;3(2):319–327.

What they did: The team studied the role of SIRT3 (a mitochondrial NAD+-dependent sirtuin) in aging-associated degeneration. They used SIRT3 KO mice as well as SIRT3 overexpressors at various age points. Assessment: mitochondrial function, oxidative stress, tissue degeneration.

What they found:

• SIRT3 KO mice exhibit accelerated aging phenotypes: mitochondrial dysfunction, oxidative damage
• SIRT3 overexpression reversed aging-associated degeneration in some tissues
• SIRT3 activity is tightly dependent on the mitochondrial NAD+ pool

Why it matters: For the 5-Amino-1MQ context this is the background paper that documents why an increase in the NAD+ pool is desirable. NNMT inhibition → higher NAD+ → higher SIRT3 activity → better mitochondrial function and an anti-aging phenotype. 5-Amino-1MQ was not tested directly in Brown 2014 (the paper precedes Neelakantan 2017), but it provides the mechanistic framework for why NNMT inhibition could work in aging models.

CoA. Certificate of Analysis

🧪 HPLC analysis of batch 2026-04-Q

• Purity: ≥ 99.2 % (HPLC-UV at 254 nm, quinoline chromophore)
• Identity: confirmed by mass spectrometry (MS, ESI+, MW 286.07 Da for the iodide salt, free base 159.19 Da)
• Structural identification: ¹H NMR and ¹³C NMR spectroscopy in agreement with the reference structure
• Residual solvents: meets ICH Q3C (DMF, methanol, ethanol < 0.1 %)
• Inorganic impurities (iodide content): in agreement with the theoretical value for the iodide salt
• Microbial contamination: meets USP <61>
• Endotoxins: not routinely measured (small molecule, not a peptide); available on request for B2B
• Related-impurity profile: < 0.5 % each, identified by LC-MS

[Download CoA (PDF)] · [Download SDS (PDF)]

Independent analytical laboratory (3rd-party verification). Original manufacturing CoA available upon request for B2B partners.

Note on the chromophore: 5-Amino-1MQ contains a quinoline chromophore with an absorption maximum around 254 nm and a secondary band around 360–400 nm (yellow color). This chromophore is useful for UV detection in HPLC analysis, but it also means that the molecule is sensitive to UV light. Store in dark glass or opaque vials, and protect from direct sunlight.

Storage

Crystalline material / lyophilizate (dry form)

• 2 years at room temperature (up to 25 °C), protected from light and moisture
• 3 years at 2–8 °C (refrigerator)
• For maximum long-term stability, −20 °C, more than 3 years

5-Amino-1MQ is a very stable molecule compared with peptides. It is a small organic substance with a stable aromatic structure. The iodide salt is thermodynamically and kinetically stable at room temperature; it does not undergo degradation by hydrolysis, deamidation, or oxidation of peptide bonds (it has no peptide bonds).

After reconstitution (solution in sterile water or BAC water)

• At least 60 days at 2–8 °C, protected from light
• Solution in DMSO: a longer period at −20 °C (typically used as a stock solution for in vitro experiments)
• The solution in sterile water is more stable than for most peptides, with no disulfide bridges and no acetylated termini

Practical storage rules

• Protect from light. The quinoline chromophore is UV-sensitive. Use amber glass or opaque vials and store in a dark cabinet.
• Control humidity. The iodide salt is mildly hygroscopic and can absorb moisture from the air. Store in a sealed vial, ideally with a desiccant.
• No strict temperature limits. Unlike peptides, 5-Amino-1MQ withstands short-term temperature fluctuations without loss of activity. A cooling insert is not necessary for summer transport.
• The solution should remain clear to pale yellow. A yellow color is normal for quinoline aromaticity. A brown or turbid solution indicates degradation or contamination.

Reconstitution

3-step visual

1. 🧪 Reconstitute by adding sterile water, BAC water, or DMSO depending on the research application
2. 💉 Measure the required volume using the calculator (section 8)
3. ❄️ Store in the refrigerator at 2–8 °C, protected from light

Detailed protocol for in vitro research

What you will need:

• 5-Amino-1MQ vial (50 mg crystalline material or lyophilizate)
• Sterile water, BAC water, or DMSO (depending on the required concentration)
• Pipette with sterile tips
• Alcohol swab

Procedure for aqueous solution (10 mg/ml stock):

1. Let the vial reach room temperature (not strictly necessary for a small molecule, but good practice).
2. Disinfect the rubber stopper (if the vial has a stopper) or wipe the neck (if it is a screw-cap vial).
3. Add 5 ml of sterile water or BAC water to a 50 mg vial. Final concentration: 10 mg/ml = 10,000 µg/ml.
4. Gently mix with circular motions or low-intensity vortexing. 5-Amino-1MQ is highly soluble in water; complete dissolution typically takes <60 seconds.
5. The solution should be clear to pale yellow. A brown color or turbidity indicates a problem.
6. Store in the refrigerator at 2–8 °C, protected from light (amber glass, aluminum foil around the vial, dark cabinet).

Procedure for DMSO stock (100 mM, for in vitro experiments):

1. Add 1.75 ml DMSO to a 50 mg vial. Final concentration: ~28.57 mg/ml = ~100 mM (taking into account the MW of 286.07 of the iodide salt).
2. Vortex briefly (5–10 s).
3. Aliquot into smaller volumes (10–100 µl) in Eppendorf tubes.
4. Store at −20 °C, avoid repeated freeze-thaw cycles.
5. For cell experiments dilute the DMSO stock 1:1000 or more into medium (final DMSO < 0.1 % v/v).

Detailed protocol for in vivo (animal research)

In the original Neelakantan 2017 study, 5-Amino-1MQ was administered orally in drinking water at a dose of 20 mg/kg/day. Procedure:

1. Assume an average water intake of mice of ~5 ml/day at a body weight of 25 g.
2. Target dose: 20 mg/kg × 0.025 kg = 0.5 mg/mouse/day.
3. At 5 ml of water intake: 0.5 mg / 5 ml = 0.1 mg/ml = 100 µg/ml in drinking water.
4. Dissolve in drinking water, monitor intake and body weight of the animals twice weekly.
5. Replace the water every 2–3 days, protect the bottle from light (aluminum foil).

Alternative volumes for different final concentrations

Rule of thumb: For 5-Amino-1MQ we recommend 5 ml of sterile water as the optimal compromise for most research protocols (10 mg/ml). For cell-based in vitro experiments with nanomolar to micromolar concentrations a DMSO stock is recommended.

Calculator (interactive widget)

Inputs:

• Mass of 5-Amino-1MQ in the vial: 50 mg (pre-filled, or 100 mg)
• Reconstitution water volume: slider 1–10 ml
• Target “dose” in the animal protocol (mg/kg/day), typically 10 or 20 mg/kg/day according to Neelakantan 2017/2018
• Body weight of the model animal (g): mouse 25 g (pre-filled), rat 250 g
• Daily water intake (ml): mouse 5 ml, rat 30 ml

Outputs:

• Stock concentration: __ mg/ml
• Concentration in drinking water: __ µg/ml
• Daily dose per animal: __ mg/day

Example (Neelakantan 2017 protocol for mouse):

• 50 mg vial + 5 ml sterile water = 10 mg/ml stock
• Target: 20 mg/kg/day for a 25 g mouse = 0.5 mg/day
• At 5 ml of water intake: 0.5 mg / 5 ml = 100 µg/ml in drinking water
• From the 10 mg/ml stock: 0.05 ml stock + 4.95 ml water = 5 ml of drinking water at the target concentration

Example (Neelakantan 2018 protocol for an aging mouse, sarcopenia):

• Dose 10 mg/kg/day for a 25 g mouse = 0.25 mg/day
• At 5 ml of water intake: 0.25 mg / 5 ml = 50 µg/ml in drinking water

Example (in vitro experiment, 1 µM final concentration):

• 100 mM DMSO stock (28.57 mg/ml)
• Dilution 1:100,000 into medium = 1 µM final concentration
• For 1 ml of medium: 0.01 µl of stock (first dilute 1:1000 in medium, then 1:100 into the experiment)

Disclaimer: The calculator is intended solely for research calculations when replicating published preclinical protocols. It is not medical guidance and not a dosing recommendation for humans. No human clinical data exist for 5-Amino-1MQ; any extrapolations from animal doses to humans are speculative.

Combinations with peptides. Frequently combined molecules

In the research context, 5-Amino-1MQ is typically combined with peptides and small molecules that complement its mechanism (NNMT inhibition → increased NAD+, SAM, thermogenesis).

NAD+ precursors (NMN, NR), substrate synergy

The most logical stack for 5-Amino-1MQ. NMN (nicotinamide mononucleotide) and NR (nicotinamide riboside) are precursors of NAD+ synthesis. 5-Amino-1MQ on the other hand conserves nicotinamide from being diverted to the MNA route, so it leaves it available for the NAD+ salvage pathway.

Together:

• Exogenous precursors supply substrate
• 5-Amino-1MQ ensures the substrate does not escape via NNMT into MNA
• Result: synergistic increase of the NAD+ pool

This stack is theoretically very attractive for longevity research and metabolic interventions.

AOD-9604 or Tesamorelin. Metabolic stack

In the research context, 5-Amino-1MQ is often combined with lipolytic peptides such as AOD-9604 (a lipolytic fragment of hGH) or Tesamorelin (a GHRH analog). The mechanisms are different:

• AOD-9604/Tesamorelin: direct lipolysis in adipocytes
• 5-Amino-1MQ: thermogenesis, mitochondrial function, increased NAD+

Together they form a complete metabolic stack: fat mobilization (peptide) + fat oxidation (5-Amino-1MQ).

MOTS-c. Mitochondrial support

MOTS-c is a mitochondrially encoded peptide that improves mitochondrial efficiency, supports AMPK signaling, and insulin sensitivity. Synergistic with 5-Amino-1MQ:

• 5-Amino-1MQ → higher NAD+ → higher SIRT3 (mitochondrial sirtuin) activity
• MOTS-c → AMPK activation → mitochondrial biogenesis
• Together → robust support of mitochondrial capacity

Hypothetical synergy, research ongoing.

Semaglutide or Tirzepatide. Combined anti-obesity concept

In the preclinical context, 5-Amino-1MQ is sometimes paired with GLP-1 agonists for anti-obesity applications. The mechanisms are independent:

• GLP-1 agonist: appetite suppression, gastric slowing
• 5-Amino-1MQ: increase in energy expenditure, thermogenesis

Together they could address obesity from two sides at once: appetite and expenditure. This is only a preclinical concept; no clinical data exist for 5-Amino-1MQ.

SS-31 / Elamipretide. Mitochondria + metabolism (coming soon)

SS-31 (Elamipretide) is a mitochondria-targeting peptide that stabilizes the cardiolipin architecture of the inner mitochondrial membrane. In the research context it could synergize with 5-Amino-1MQ to support mitochondrial function. SS-31 in the MOLEQUA offering is coming soon; we will announce it after completion of QC validation.

Shipping & packaging

• 📦 Discreet packaging, no logos, no description of contents on the outer packaging. No postal worker knows what you ordered.
• 🚚 Packeta, SK 24–48 h, EU within 3 days
• 💰 Free shipping above €40 (otherwise €4.90)
• ⚡ Dispatch within 24 h of order confirmation (order by 14:00 → we ship the same day)
• ❄️ A cooling insert is not necessary: 5-Amino-1MQ is a thermostable small molecule that withstands room temperature during transport
• 🌞 Light protection: all shipments contain opaque packaging for protection of the UV-sensitive quinoline chromophore

FAQ. Frequently asked questions

What is 5-Amino-1MQ and how does it differ from the peptides in your offering? 5-Amino-1MQ is a small organic molecule, not a peptide. Specifically it is a quinoline derivative with an amino group at position 5 and a methyl group on the nitrogen at position 1, as an iodide salt. It is not amino-acid-based. The mechanism of action is different from peptides: it is a selective inhibitor of the enzyme NNMT (Nicotinamide N-Methyltransferase). Think of it as inserting a stopper into a biochemical “switch” that halts the consumption of nicotinamide and SAM.

What is NNMT and why does it matter? NNMT (Nicotinamide N-Methyltransferase) is an enzyme that transfers a methyl group from SAM (S-adenosylmethionine) to nicotinamide (vitamin B3). The result is 1-methylnicotinamide (MNA), which is excreted in urine. The problem: NNMT is overexpressed in obesity, type 2 diabetes, MASLD, certain carcinomas, and fibrotic diseases. Its excessive activity consumes the SAM pool (needed for epigenetic modifications) and also diverts nicotinamide away from NAD+ synthesis. Inhibition of NNMT therefore raises both the NAD+ pool and the SAM pool, which has beneficial effects in preclinical models.

What does the literature show on 5-Amino-1MQ and body weight in animal models? There are no human clinical data for 5-Amino-1MQ. All published data come from preclinical models (mice, rats, isolated cells). In high-fat-diet mice, Neelakantan 2017 reported a reduction of body fat by 15–25 % after 11 weeks. Whether these effects translate to humans is not known. 5-Amino-1MQ is a research molecule, not a drug.

Why are there no clinical trials with 5-Amino-1MQ? 5-Amino-1MQ was from the beginning designed as a chemical probe for research, not as a clinical candidate. For clinical development of NNMT inhibition, pharmaceutical companies such as Cardelia/Metro Biotech chose to develop different chemical classes with better pharmacokinetics, longer half-life, and an optimized safety profile. 5-Amino-1MQ remains a popular research molecule in the academic literature.

What is the half-life of 5-Amino-1MQ? The exact plasma half-life in mice is short (~2–4 hours, small molecule, renal excretion), and therefore it is typically administered continuously in drinking water in animal models. For research applications this is a practical way to achieve steady-state exposure.

What are the recommended doses in animal models? The most frequently cited protocols:

• Neelakantan 2017 (obesity): 20 mg/kg/day orally in drinking water in mice, 11 weeks
• Neelakantan 2018 (sarcopenia, old mice): 10 mg/kg/day orally in drinking water, 4 weeks
• In vitro experiments: 0.1–10 µM in medium for cell culture

These doses are not extrapolable to humans; allometric scaling for small molecules is not validated in the absence of clinical data.

Does 5-Amino-1MQ work orally? In animal models, yes; oral administration in drinking water is the standard protocol (Neelakantan 2017, 2018). For humans there are no data. Other NNMT inhibitors in clinical development (Cardelia) are designed for the oral route.

Are there known side effects? In published animal studies, no toxic effects were observed in 4- to 12-week protocols:

• Neelakantan 2017: 11 weeks without signs of toxicity (body weight increases normally, no abnormalities in blood tests)
• Neelakantan 2018: 4 weeks without significant adverse events

For human use, data are lacking on safety, contraindications, and drug interactions. 5-Amino-1MQ is exclusively a research chemical.

What is the difference between 5-Amino-1MQ and other NAD+ supports?

5-Amino-1MQ works on the opposite side of the equation from NMN/NR: instead of adding substrate, it reduces its loss.

Does 5-Amino-1MQ cause epigenetic changes? Yes, presumably. Mechanistically, NNMT inhibition conserves the SAM pool, which has consequences for all SAM-dependent methyltransferases (DNMTs, PRMTs, others). In preclinical studies, changes were observed in the expression of genes related to metabolism and thermogenesis. Whether these epigenetic changes are benign, beneficial, or problematic is the subject of ongoing research.

What is the WADA status of 5-Amino-1MQ? 5-Amino-1MQ is not on the current WADA Prohibited List (2026). It is not explicitly banned for professional athletes. This does not mean it is “permitted”; WADA frequently updates the list, and research molecules with metabolic effects may be added in the future.

Can 5-Amino-1MQ be combined with NMN or NR? In the preclinical context, yes; the mechanisms are complementary. NMN/NR supply substrate, 5-Amino-1MQ conserves it. No proven interactions in animal models. Clinical data are lacking.

Why is 5-Amino-1MQ a relatively inexpensive molecule? Three reasons:

1. Small organic molecule, simple synthesis (methylation of 5-aminoquinoline with methyl iodide)
2. No complex modifications, no peptide bonds, no disulfides, no fatty acids
3. The iodide salt is stable, easy purification and handling

The price reflects actual manufacturing complexity, not an artificially inflated peptide premium.

Is 5-Amino-1MQ stable in summer shipping? Yes, fully stable. Unlike peptides, 5-Amino-1MQ withstands room temperature for several weeks without loss of activity. A cooling insert is not necessary. The only critical precaution is light protection (UV-sensitive quinoline chromophore), which we ensure with opaque packaging.

What is the purity of this batch? The current batch 2026-04-Q: ≥ 99.2 % HPLC. Full CoA with HPLC chromatogram, MS spectrum (confirming MW 286.07 Da for the iodide salt), and NMR spectroscopy data is available for download or upon request. For 5-Amino-1MQ we apply extended NMR identification that confirms the precise structural identity of the molecule.

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Disclaimer. 5-Amino-1MQ and all MOLEQUA Peptides products are intended exclusively for research and scientific purposes (Research Use Only, RUO). They are not a medicine, dietary supplement, cosmetic product, or food. They are not intended for human or animal consumption. Sales are limited to qualified researchers, academic institutions, and laboratories. Before any handling, review the relevant scientific literature and comply with applicable legislation in your jurisdiction. 5-Amino-1MQ has neither FDA nor EMA approval as a medicine and has never been tested in human clinical trials. All published data come from preclinical models (mice, rats, isolated cell lines). Any extrapolations from animal doses or effects to humans are speculative and unsupported by clinical evidence. MOLEQUA Peptides assumes no responsibility for misuse of the product outside its declared purpose.

End of product 5-Amino-1MQ.