Compounds
5-Amino-1MQ: What It Is, Dosage, Side Effects and Why It's Not a Peptide
5-Amino-1MQ is a small-molecule NNMT inhibitor sold alongside peptides. What the mouse studies showed, why there are no human trials, the doses actually tested (in mice), the unknown side effects, its real FDA status in October 2026, and the fat-loss options a clinician can prescribe instead.
Published October 12, 2026 · 15 min read
Key takeaways
- 5-Amino-1MQ is not a peptide. It is a small synthetic molecule, about 160 daltons with no amino acids, that blocks the enzyme nicotinamide N-methyltransferase (NNMT). It is sold alongside peptides because the same vendors and clinics stock it, inject it and describe it in the same language.
- The evidence is entirely in mice: injected at 20 mg/kg three times a day, obese mice lost about 5% of body weight and a third of their abdominal fat in 11 days without eating less; later studies showed better glucose tolerance, less fatty liver, and stronger aged muscle. Most of it comes from the group commercializing NNMT inhibitors.
- No human has ever taken 5-Amino-1MQ in a study. There is no published human trial and, as of October 2026, no registered one, so there is no human dose, no human side-effect profile and no idea whether the 25 to 50 mg capsules sold online do anything. In mice only 3.5% of an oral dose was absorbed.
- Its legal position is simple: it is not approved, fails every test for pharmacy compounding, and FDA warned a 503B facility in January 2026 for making it. Contrary to some reports, we could not find it on FDA's Category 2 list; it appears never to have been categorized at all.
- If the goal is fat loss, GLP-1 therapy has the human trials this compound never ran, and a clinician can prescribe it.
5-Amino-1MQ at a glance
- Also called
- 5-amino-1-methylquinolinium, 5A1MQ, 5-amino-1-methylquinolinium iodide, NNMT inhibitor, 5-amino-1MQ peptide (a misnomer)
- Class
- Small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT); a quinolinium salt about 160 daltons, not a peptide
- Route
- Sold as oral capsules and as vials for subcutaneous injection; in mice it was given by subcutaneous injection (oral bioavailability about 3.5%)
- FDA status
- Never FDA-approved and never tested in humans. Not a component of any approved drug, not on FDA's 503A bulks list and, per FDA's January 2026 warning letter to a 503B outsourcing facility, not on the 503B bulks list either. Never placed in Category 2 as far as we could verify.
- FDA Category 2 (compounding restricted)
- No
- Available by prescription (US)
- Not as a prescription product
- Best-studied use
- Diet-induced obesity, fatty liver, glucose tolerance and aged-muscle regeneration in mice; no human trials registered or published as of October 2026
- Typical monthly cost (telehealth, 2026)
- No legal prescription product exists; capsules and vials sold online are unapproved products with no verified content and are not priced here
What 5-Amino-1MQ is and why it is sold with peptides
Nicotinamide N-methyltransferase, NNMT, is an enzyme found mostly in the liver and in fat. Its day job is clearance: it attaches a methyl group to nicotinamide (vitamin B3), using S-adenosylmethionine (SAM) as the methyl donor, and the product, 1-methylnicotinamide, is excreted. In doing so it consumes two things cells care about, the nicotinamide that would otherwise be recycled into NAD+ and the SAM that would otherwise methylate DNA, histones and other molecules (Pissios 2017).
In 2014 a Harvard group reported in Nature that NNMT was the gene most strongly turned up in the fat of obese and diabetic mice, and that knocking it down in fat and liver with an antisense drug protected mice from diet-induced obesity by raising energy expenditure, through higher SAM and NAD+ and a faster polyamine cycle (Kraus 2014). That made NNMT a drug target. In 2017 a team at the University of Texas Medical Branch in Galveston published a series of small molecules built on a methylquinolinium scaffold that inhibit the enzyme, and identified 5-amino-1-methylquinolinium, 5-Amino-1MQ, as potent, selective and able to cross cell membranes (Neelakantan 2017). The lead scientist later founded a company, Ridgeline Therapeutics, to develop NNMT inhibitors, and most of the subsequent animal papers list its employees as authors.
So why does a quinolinium salt turn up in "peptide" catalogs and "peptide therapy" menus? Three reasons, none scientific. It was discovered as an injectable research compound, so it fits the vial-and-syringe format; its mechanism touches NAD+, which lets it be bundled with NAD+ injections and sold as a longevity-and-metabolism product; and the research-chemical vendors that sell BPC-157 and AOD-9604 are the only channel for it, so it inherits their shelf and their marketing. The label "5-amino-1MQ peptide" is simply wrong, and the distinction matters for one practical reason: a small molecule can in principle be taken by mouth, which peptides mostly cannot, and that is the basis for the capsules. Whether it works by mouth is a separate question, answered below.
What the evidence actually shows
| Claim | Grade | What the evidence shows | Sources |
|---|---|---|---|
| Reverses diet-induced obesity | D | Mice only. Diet-induced obese mice injected subcutaneously with 5-Amino-1MQ at 20 mg/kg three times a day for 11 days lost about 5% of body weight while saline controls gained 1.4%, with about 35% less epididymal fat, 30% smaller fat cells and 30% lower cholesterol, and no difference in food intake (9 mice per group). A 2024 study found 32 mg/kg once daily for 28 to 30 days limited weight gain to 0.9 g versus 5.4 g and fat gain to 1.3 g versus 4.7 g; 10 mg/kg did almost nothing. | Neelakantan 2018; Babula 2024 |
| Improves blood sugar and fatty liver | D | Mice only. The high dose improved oral glucose tolerance, suppressed the rise in insulin, reduced liver fat, liver weight and liver triglycerides, and normalized liver enzymes in obese mice. Combined with a switch to a lean diet, an NNMT inhibitor normalized body composition and liver fat to the levels of never-obese mice. | Babula 2024; Sampson 2021 |
| Builds or preserves muscle, fights sarcopenia | D | Mice only. In 24-month-old mice, 5 or 10 mg/kg injected twice daily activated muscle stem cells after injury, roughly doubled regenerating fiber size and increased peak torque by about 70%. In 22-to-24-month-old mice, two months of an NNMT inhibitor increased grip strength about 40% over sedentary controls, more than exercise alone, and the two were additive. From the developer's group. | Neelakantan 2019; Dimet-Wiley 2024 |
| Fat loss in humans | D | No evidence of any kind. No human study of 5-Amino-1MQ is indexed in PubMed, and a search of ClinicalTrials.gov on October 9, 2026 found no registered trial of the compound or of any NNMT inhibitor. | ClinicalTrials.gov 2026 |
| NNMT is a real target for obesity | C | Target validation, not drug validation. NNMT is overexpressed in the fat and liver of obese and diabetic mice, knockdown protects against obesity, and in humans adipose NNMT expression and circulating 1-methylnicotinamide rise with obesity and insulin resistance. A promising enzyme is not the same as a drug that is safe and effective in people. | Kraus 2014; Pissios 2017; Sun 2024 |
| Works as an oral capsule | D | Unlikely at the doses sold, on the only data available. In mice, oral bioavailability was 3.5% (limited gut absorption and first-pass metabolism); a subcutaneous dose produced about 30 times the blood exposure of a larger oral dose. Every published effect came from injections. No human absorption data exist. | Babula 2024 |
| Raises NAD+ | D | Mechanistic and rodent only. NNMT inhibition raised intracellular NAD+ and SAM in cultured fat cells and in mouse fat tissue. No human NAD+ measurement has been made, and raising NAD+ has not been shown to produce a clinical benefit in people. | Neelakantan 2018; Kraus 2014 |
| Safe | D | No human safety data. Mice showed no observable adverse effects at the doses used, but the high dose lowered lymphocytes by 31% and monocytes by 50%, and the compound inhibited MAO-A by 67% at 10 micromolar in an off-target screen. The longest exposure in any animal is about two months, in aged mice. | Babula 2024; Neelakantan 2018 |
| Anti-aging or longevity | D | The aged-muscle mouse data are the entire basis. No lifespan, healthspan or human aging outcome has been measured. | Dimet-Wiley 2024 |
Three things stand out.
The mouse data are coherent and come from one source. The obesity, liver, glucose and muscle findings all point the same way, and they are what you would expect from the 2014 Nature paper. They also come almost entirely from the laboratory that invented the compound and the company founded to sell it, with the 2014 knockdown study as the independent anchor. That is normal in early drug development and it is a reason to wait for replication, not a reason to buy capsules.
The doses were large and injected. The headline study injected 20 mg/kg three times a day, about 34 mg/kg a day of the active molecule, under the skin (Neelakantan 2018). The 2024 study found that 10 mg/kg a day did almost nothing and 32 mg/kg a day worked (Babula 2024). Those are not small doses, and they were not swallowed.
No human has taken it in a study. This is the whole answer to "does it work" and "is it safe": nobody knows, and nobody is currently trying to find out in a registered trial (ClinicalTrials.gov 2026). The developer's published work remains preclinical.
What you are promised versus what is documented
Sales pages promise fat loss "without stimulants", a faster metabolism, higher NAD+, more muscle, better energy, anti-aging and "reversal of fat-cell growth", often with the phrase "clinically studied" attached. Sorted by the evidence:
- Documented in mice at injected doses: less weight gain and fat mass, smaller fat cells, lower cholesterol, better glucose tolerance, less liver fat, better muscle regeneration and strength in old mice.
- Mechanistic only: higher NAD+ and SAM in cells and mouse tissue.
- Not documented anywhere: any effect in a human; any effect of an oral capsule in any species at a dose resembling what is sold; safety beyond 30 days in any species.
"Clinically studied" is false. No clinical study exists.
5-Amino-1MQ vs AOD-9604, NAD+ and GLP-1 drugs
| 5-Amino-1MQ | AOD-9604 | NAD+ (injection or IV) | Semaglutide or tirzepatide | |
|---|---|---|---|---|
| What it is | Small-molecule NNMT inhibitor | 16-amino-acid fragment of growth hormone | Coenzyme, not a peptide | GLP-1 (and GIP) receptor agonists |
| Best human evidence for fat loss | None; mice only | Negative phase 2b trial, about 530 adults | None for fat loss | Large trials: 15% to 20% weight loss |
| Human safety data | None | Six company trials, 893 people, oral tablets | Small studies; infusion reactions | Extensive |
| FDA status | Never approved; no compounding basis; 503B warning letter January 2026 | Never approved; Category 2 from 2023, now listed as nominated but withdrawn | Not an approved drug; nominated for the 503A list and placed in Category 1 in FDA's 2023 update | Approved for obesity and type 2 diabetes |
| Can a US pharmacy legally make it? | No | No | Widely compounded; confirm the pharmacy's basis | Brand yes; compounded only for documented individual need |
Read the AOD-9604 profile for the other "fat-loss" product sold next to it, the NAD+ profile for the compound it is most often bundled with, and best peptides for weight loss for the ranking.
Dosage: what was studied versus what sellers circulate
| Setting | Dose and route | Subjects | Result |
|---|---|---|---|
| Neelakantan 2018 | 20 mg/kg subcutaneously, three times a day (about 34 mg/kg a day of active compound) for 11 days | 9 diet-induced obese mice per group | About 5% weight loss vs 1.4% gain; about 35% less abdominal fat |
| Babula 2024 | 10 or 32 mg/kg subcutaneously once a day for 28 to 30 days | 8 obese mice per group | 32 mg/kg limited weight and fat gain and improved glucose tolerance; 10 mg/kg did little |
| Neelakantan 2019 | 5 or 10 mg/kg per injection twice daily under the skin, for 2 or 4 weeks starting a week before muscle injury | 24-month-old mice | Faster regeneration, about 70% higher peak torque |
| Babula 2024, pharmacokinetics | Single 30 mg/kg oral dose vs 25 mg/kg subcutaneous | Mice | Oral bioavailability 3.5%; subcutaneous exposure about 30 times higher |
| Seller listings for capsules (2026) | 25 to 50 mg by mouth once or twice a day, "cycled" | None | Never tested in any species |
| Seller listings for injections (2026) | Vials for subcutaneous injection, doses stated in mg, 5 to 7 days a week | None | Never tested in humans; mouse doses would scale to a different order of magnitude |
What the mouse doses would mean in a person
Doses do not transfer between species by body weight; the standard FDA conversion uses body surface area, under which a mouse dose is divided by about 12 to estimate a human-equivalent dose. The effective 32 mg/kg a day in mice corresponds to roughly 2.6 mg/kg in a person, about 180 mg a day for a 70 kg adult, by subcutaneous injection, with the 10 mg/kg mouse dose (about 60 mg a day human-equivalent) having done little. A 50 mg capsule, of which mice absorbed 3.5%, is not in the same arithmetic. This is not a dose and should not be read as one; it is the reason the capsules are unlikely to replicate the mouse studies, and the reason the injectable vials are a human experiment without a protocol.
There is no reconstitution example to give, because no legal vial exists; the reconstitution calculator is for prescribed peptides with a labeled concentration.
Side effects and who should not use it
In humans: unknown. No one has recorded a side-effect profile for 5-Amino-1MQ in people, because no one has given it to people under observation. Anecdotal reports online mention nausea, headache, sleep disturbance and injection-site irritation; such reports cannot be tied to the compound, the dose, the purity of the product or the person.
In mice: little at the doses used, with two signals. The published studies reported no observable adverse effects. In the 30-day study, the high dose lowered circulating lymphocytes by about 31% and monocytes by about 50% compared with controls, which the authors interpreted as a metabolic effect rather than toxicity, and an off-target screen found the compound inhibited monoamine oxidase A by 67% at 10 micromolar (Babula 2024). No formal toxicology study has been published.
Theoretical concerns, from NNMT biology.
- Methylation balance. NNMT is a major consumer of SAM in the liver; inhibiting it raises SAM, which is the point in fat tissue but has unexamined consequences for DNA and histone methylation elsewhere over months or years (Pissios 2017).
- Nicotinamide clearance. NNMT is how the liver disposes of excess nicotinamide. Blocking it while taking NAD+ precursors, as the marketing suggests, pushes nicotinamide upward, and high nicotinamide inhibits the sirtuins and PARP enzymes that NAD+ products are supposed to support.
- MAO-A inhibition. If the mouse screen result applied at human exposures, 5-Amino-1MQ could interact with SSRIs, SNRIs, tricyclics and other serotonergic drugs. Nobody has checked.
- Cancer biology, which cuts both ways. NNMT is overexpressed in many cancers and supports tumor growth, invasion and treatment resistance, which is why NNMT inhibition is being explored as a cancer therapy; it has also been found to shape the tumor microenvironment in ways that are not uniformly bad for the host (Wang 2022). An untested drug acting on an enzyme this entangled with cancer biology is not something to take with a cancer history.
- Immune cells. The drop in lymphocytes and monocytes in mice has no human correlate and no explanation.
Who should not use it. Since nobody can be advised to use it, the list is categorical: anyone pregnant, breastfeeding or trying to conceive; anyone with a cancer history; anyone on antidepressants or other MAO-sensitive drugs; anyone with liver disease, since NNMT is a liver enzyme and the drug is cleared there. Athletes should assume WADA treats it as a non-approved substance, prohibited at all times under section S0 of the Prohibited List.
Legal status in the United States
5-Amino-1MQ is not a peptide, so most of the 2023 to 2026 peptide regulation does not reach it directly. What does reach it is the general law of compounding and the law against selling unapproved drugs. Here is exactly what we verified for October 2026.
- Not approved. FDA has never approved 5-Amino-1MQ for any use, and it is not a component of any approved drug.
- No basis for 503A compounding. A state-licensed pharmacy may compound a bulk substance only if it has a USP monograph, is a component of an approved drug, or appears on FDA's 503A bulks list (FDA 503A bulks list). We found no USP monograph, there is no approved drug, and it is not on the bulks list.
- Not in Category 2, as far as we can find. Several sites state that FDA placed 5-Amino-1MQ in Category 2 in 2023. We checked FDA's September 29, 2023 category update, which lists the nineteen Category 2 additions of that action and the full Category 2 list of twenty-three substances; 5-Amino-1MQ is not on either list, and neither are the capsules (FDA 503A categories 2023). Two specialist summaries of that action also do not name it. FDA stopped assigning interim categories to new nominations on January 7, 2025, so a later nomination would not have received one (Health Law Alliance 2026). The accurate statement is that 5-Amino-1MQ was never nominated and categorized, which leaves it with no compounding basis at all; "not in Category 2" is not a permission.
- FDA has acted on it once, under 503B. On January 20, 2026, FDA issued a warning letter to GenoGenix LLC, an outsourcing facility in Boca Raton, Florida, after a July 2025 inspection. Among the violations, FDA stated that the facility was compounding with bulk substances, including 5-Amino-1MQ and NAD+, that do not appear on the 503B bulks list and are not used to compound drugs on the shortage list, so the products did not qualify for the 503B exemptions (FDA warning letter 2026). That is the clearest statement of FDA's position: a licensed facility making it was told to stop.
- The capsule market. Some compounding pharmacies and telehealth clinics have sold 25 to 50 mg capsules described as "compounded 5-Amino-1MQ", and research-chemical vendors sell capsules and vials under research-use labels. Neither has a legal basis, and FDA's 2026 warning letters to peptide vendors established that a research label does not survive a dosing guide. Possessing it is not a crime; selling it for human use is the violation. The peptide legal tracker explains the three tests and the enforcement pattern.
Cost and what a clinician can actually prescribe
There is no legal price. Capsules and vials are listed online at prices we neither quote nor link to; what they buy is an unverified chemical, not a medication, and the number is not comparable to anything a pharmacy dispenses.
If the reason for the search is fat loss, the options a licensed clinician can prescribe in October 2026, ranked by evidence, are GLP-1 therapy (semaglutide, tirzepatide), with 15% to 20% weight loss in large trials, at about $299 to $449 a month for a brand pen or $150 to $350 compounded under the conditions in our legal tracker; tesamorelin, for visceral fat specifically, available only as the brand Egrifta at about $2,400 to $2,800 a month because it cannot be compounded; and, far behind, sermorelin. The compounded semaglutide versus tirzepatide guide and the cost guide have the figures and their sources.
If the reason is NAD+ or "metabolic health", the honest answer is that NNMT inhibition is an interesting hypothesis with a 2014 Nature paper behind it and no human test, and that a clinician cannot prescribe it.
Bottom line
5-Amino-1MQ is a legitimate research compound with a real mechanism, good mouse data and a company trying to turn it into a drug. None of that is available to you. What is available is a capsule or vial, sold outside the law, at a dose and route the mouse studies do not support, with no human safety data of any kind, acting on an enzyme tied to methylation, NAD+ and cancer biology in ways that have never been studied for longer than about two months in any animal.
The right response to a promising target is to wait for the trial. If fat loss cannot wait, the drugs that passed their trials are a prescription away.
Frequently asked questions
+What is 5-Amino-1MQ, and is it a peptide?
5-Amino-1MQ (5-amino-1-methylquinolinium) is a small synthetic molecule, about 160 daltons, that blocks the enzyme nicotinamide N-methyltransferase (NNMT). It is not a peptide; it has no amino acids. It was designed at the University of Texas Medical Branch in 2017 as a tool to test whether inhibiting NNMT could treat obesity, and in mice it reduced fat mass and improved glucose handling. It is sold next to peptides because the same research vendors and clinics stock it, inject it and market it with the same metabolic language.
+Does 5-Amino-1MQ work for fat loss?
In mice, yes, at high injected doses: diet-induced obese mice lost about 5% of body weight in 11 days and about 35% of their abdominal fat pad while controls gained, without eating less, and a 28-day once-daily study limited weight and fat gain and improved glucose tolerance. In people, nobody knows. As of October 2026 there is no published human study and no registered clinical trial, so every claim about fat loss in humans is an extrapolation from rodents.
+What is the dosage of 5-Amino-1MQ?
There is no human dose, because it has never been given to people in a study. The mouse studies used 20 mg per kilogram injected three times a day for 11 days, or 10 to 32 mg per kilogram injected once a day for 28 to 30 days, with the lower dose doing little. Scaled by body surface area the effective mouse dose corresponds to roughly 2.6 mg per kilogram in a human, by injection, which is an illustration of the gap, not a dose. Capsules sold online are usually 25 to 50 mg; in mice only about 3.5% of an oral dose was absorbed.
+5-Amino-1MQ oral vs injection: which is better?
Neither has human data. In mice, oral bioavailability was 3.5% because of poor gut absorption and first-pass metabolism, while subcutaneous injection delivered roughly 30 times the exposure, so the published effects come from injections. That does not make injecting an unregulated vial a good idea; it means the oral capsules most people buy may deliver very little of what the mouse studies delivered, and the injections have never been tested for safety in people.
+What are the side effects of 5-Amino-1MQ?
Unknown in humans. In mice, the published studies reported no observable adverse effects at the doses used, but the high dose in the 28-day study lowered circulating lymphocytes by about 31% and monocytes by about 50%, and the compound inhibited the enzyme MAO-A by 67% in a laboratory screen, which would matter for anyone on antidepressants if the same happened in people. NNMT also helps the liver clear excess nicotinamide and regulates methylation chemistry, so the long-term effects of blocking it are a theoretical concern that no human study has examined.
+Is 5-Amino-1MQ FDA approved or legal in 2026?
It is not approved for anything. A licensed pharmacy may compound a substance only if it has a USP monograph, is part of an approved drug or is on FDA's 503A bulks list; 5-Amino-1MQ meets none of those tests, and in January 2026 FDA warned a 503B outsourcing facility that it was compounding with 5-Amino-1MQ, which is not on the 503B list. Possessing it is not a crime. Selling it for human use without approval is. Contrary to some reports, we could not find it on FDA's Category 2 list; it was never nominated and categorized at all.
+Can you take 5-Amino-1MQ with NAD+ or a GLP-1 drug?
There is no human data on either combination. Mechanistically, NNMT consumes nicotinamide, so blocking it is expected to raise nicotinamide and NAD+ levels, which is why it is marketed with NAD+ products; adding NAD+ precursors on top pushes the same pathway further with no evidence of benefit. With a GLP-1 drug, a clinician cannot prescribe 5-Amino-1MQ and should not be asked to supervise a research chemical alongside a prescription. If a provider offers the pair, the GLP-1 is the part with evidence.
+Does 5-Amino-1MQ build muscle?
In old mice, NNMT inhibitors improved muscle stem cell activity and regeneration after injury and increased grip strength by about 40% over two months, with gains that added to exercise. These are promising animal findings about aging muscle, from the company developing NNMT inhibitors. There is no human study, and the doses in the muscle-injury study (5 or 10 mg per kilogram of body weight per injection, twice daily under the skin, for 2 or 4 weeks starting a week before the injury) do not resemble a 50 mg capsule.
+Is 5-Amino-1MQ safe long term, and does it affect cancer?
Nobody knows. NNMT is overexpressed in many cancers and appears to help tumors grow and resist treatment, which is why NNMT inhibitors are being studied as cancer drugs; that cuts in the compound's favor in theory, but the same enzyme is central to how cells balance methylation and NAD+ and the effects of suppressing it for months or years have never been examined; the longest animal exposure is about two months, in aged mice. Anyone with a cancer history should not experiment with it.
Sources
- StudyKraus D et al. Nicotinamide N-methyltransferase knockdown protects against diet-induced obesity. Nature 2014;508:258-62. (2014)
- StudyNeelakantan H et al. Structure-activity relationship for small molecule inhibitors of nicotinamide N-methyltransferase. J Med Chem 2017;60:5015-28. (2017)
- StudyNeelakantan 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;147:141-52. (2018)
- StudyNeelakantan H et al. Small molecule nicotinamide N-methyltransferase inhibitor activates senescent muscle stem cells and improves regenerative capacity of aged skeletal muscle. Biochem Pharmacol 2019;163:481-92. (2019)
- StudySampson CM et al. Combined nicotinamide N-methyltransferase inhibition and reduced-calorie diet normalizes body composition and enhances metabolic benefits in obese mice. Sci Rep 2021;11:5637. (2021)
- StudyDimet-Wiley AL et al. Nicotinamide N-methyltransferase inhibition mimics and boosts exercise-mediated improvements in muscle function in aged mice. Sci Rep 2024;14:15554. (2024)
- StudyBabula JJ, Bui D, Stevenson HL, Watowich SJ, Neelakantan H. Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. Diabetes Obes Metab 2024;26:5272-82. (2024)
- ReviewPissios P. Nicotinamide N-methyltransferase: more than a vitamin B3 clearance enzyme. Trends Endocrinol Metab 2017;28:340-53. (2017)
- ReviewWang W et al. Complex roles of nicotinamide N-methyltransferase in cancer progression. Cell Death Dis 2022;13:267. (2022)
- ReviewSun WD et al. Nicotinamide N-methyltransferase (NNMT): a novel therapeutic target for metabolic syndrome. Front Pharmacol 2024;15:1410479. (2024)
- SourceClinicalTrials.gov. Search for 5-amino-1-methylquinolinium and 5-amino-1MQ, run October 9, 2026: no registered studies. (2026)
- RegulatoryFDA. Bulk drug substances nominated for use in compounding under section 503A: notice of updates to the 503A categories and full Category 1, 2 and 3 lists, updated September 29, 2023. Copy hosted by the Alliance for Pharmacy Compounding. (FDA 503A categories 2023) (2023)
- RegulatoryFDA. Warning letter to GenoGenix LLC (outsourcing facility, Boca Raton, Florida), January 20, 2026: compounding with bulk drug substances, including 5-Amino-1MQ and NAD+, that do not appear on the 503B bulks list. (FDA warning letter 2026) (2026)
- NewsYastrovskaya D. FDA's bulk drug substance Categories 1, 2 and 3 for compounders (interim categorization of new nominations ended January 7, 2025). Health Law Alliance, October 7, 2026. (Health Law Alliance 2026) (2026)
- RegulatoryFDA. Bulk drug substances used in compounding under section 503A of the FD&C Act (the 503A bulks list and interim categories).
- RegulatoryFDA. Bulk drug substances nominated for use in compounding under section 503A: Category 1, 2 and 3 lists and updates (updated May 14, 2026). (2026)
Written by
The Peptide Doctrine Editorial Team
Our editors write from primary sources — peer-reviewed studies, FDA documents and pharmacy records — and grade every claim by the strength of its evidence. See our editorial policy for how articles are researched, reviewed and updated.
Disclosure. The Peptide Doctrine is an independent editorial project. It currently has no sponsor and runs no advertising: we accept no payment for reviews, rankings or placements, we run no affiliate links, and we do not sell or link to "research-use" peptide vendors. Content is educational and is not medical advice.
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