5-Amino-1MQ: Dosage Chart, Benefits, and Why It Is Not Really a Peptide

5-Amino-1MQ is the compound on the research storefronts that nobody can quite classify. It sits between BPC-157 and GHK-Cu on the vendor pages, it ships in the same lyophilised vials, and a large share of the search traffic that reaches it types the word "peptide" after the name. It is not a peptide. It is 5-amino-1-methylquinolinium, a small molecule of about 160 daltons built on a two-ring quinoline scaffold, with no amino acids in it and no peptide bonds.

That is not a pedantic point, and this page opens with it because it changes everything downstream. A small molecule can be swallowed: it survives stomach acid, crosses membranes unaided, and needs no bacteriostatic water or insulin syringe unless you choose the injectable presentation. Every other compound the Bureau covers has to be injected, because a peptide taken by mouth is digested before it reaches anything. This one is the exception, and that is why the dosage numbers here look nothing like the microgram figures on the BPC-157 dosage page.

What 5-Amino-1MQ Actually Is

The chemistry states in a sentence. Quinoline is a benzene ring fused to a pyridine ring; methylate the nitrogen, add an amino group at the 5 position, and you have 5-amino-1-methylquinolinium. The molecule carries a permanent positive charge, so it is supplied as a salt, usually the iodide, and the salt weighs more than the cation does. That matters for one reason: a vendor quoting milligrams of salt is quoting less active compound than one quoting milligrams of free cation, and almost none of them say which.

Structurally it is a mimic. It resembles 1-methylnicotinamide, the product of the enzyme it blocks, closely enough to occupy that enzyme's active site. Building an inhibitor that looks like the reaction product is ordinary medicinal chemistry, and it is why this one is both potent at the target and small enough to swallow. For scale against the compounds on the weight loss peptides page: semaglutide weighs about 4,100 daltons, BPC-157 about 1,400, and this about 160.

The Mechanism: NNMT, Nicotinamide and the Methyl Budget

5-Amino-1MQ inhibits nicotinamide N-methyltransferase, universally abbreviated NNMT. The enzyme does one thing: it takes a methyl group from S-adenosylmethionine, the body's main methyl donor, and attaches it to nicotinamide. Two products come out, 1-methylnicotinamide and S-adenosylhomocysteine, and both are dead ends compared with what went in. That reaction drains two pools at once, and both matter for metabolism.

The first is nicotinamide, the salvage substrate for NAD+, the cofactor every step of cellular energy production depends on. Methylating it removes it from that pool permanently, because 1-methylnicotinamide cannot be recycled back. Block NNMT and more nicotinamide stays available to become NAD+ again, which is the overlap with the compounds on the NAD+ injection dosage page and the reason the two get stacked. The second pool is S-adenosylmethionine, usually written SAM, which every methylation reaction in the body draws on and of which NNMT is one of the largest single consumers in fat tissue. Blocking the enzyme leaves more SAM in the adipocyte, which changes the flux through polyamine synthesis and, in the mouse data, raises energy expenditure without touching appetite.

The reason any of this was investigated is that NNMT is not evenly expressed. It sits at high levels in white adipose tissue and liver, and its expression rises in obesity and in type 2 diabetes in rodents and in humans. An enzyme upregulated in the disease state, burning the cell's methyl currency and destroying the substrate for NAD+ recycling, is an obvious thing to try switching off.

Where the chain weakens is at the end of it. That NNMT is elevated in obese adipose tissue is an association, and the step from "more SAM and more nicotinamide inside a fat cell" to "the organism carries less fat" comes from rodent experiments, not a measured human outcome. It is a good hypothesis with real experimental support in animals. It is not a demonstrated human effect, and a vendor page describing it as one is ahead of the literature.

What the Preclinical Work Actually Showed

Three publications carry most of the weight, and the summaries in circulation blur them together. The foundational paper is Kraus and colleagues in Nature in 2014 (PMID 24717514), which did not use 5-amino-1MQ at all. They knocked NNMT down with an antisense oligonucleotide in mice on a high fat diet, and those mice were protected against diet induced obesity: less fat mass, smaller adipocytes and, critically, no reduction in how much food they ate. A compound that makes animals eat less is unremarkable. A knockdown that changes fat mass while intake stays flat points at energy expenditure and at the cell's internal metabolism, which is the claim being made for this class.

The second body of work is Neelakantan and colleagues, who built drug-like, membrane permeable small molecule NNMT inhibitors and tested them in the same model. The 2018 paper in Biochemical Pharmacology (PMID 29155147) reported that these inhibitors reversed high fat diet induced obesity in mice, a stronger claim than the knockdown paper's prevention result, and it is the work that put 5-amino-1MQ and its analogues on the map. Dosing was intraperitoneal, in the region of 20 mg per kilogram a day, over days rather than weeks.

The third, from the same group in 2019, reported that an NNMT inhibitor activated senescent muscle stem cells and improved the regenerative capacity of aged skeletal muscle in mice. This is the origin of the claim that 5-amino-1MQ preserves muscle while cutting. What it showed is an effect on satellite cell function in old animals. It did not measure lean mass in a dieting human, and nobody has.

The fair summary: the target is well characterised and the rodent evidence for inhibiting it is stronger than what sits behind several compounds written about far more confidently. The human evidence is zero. No published trial, no measured weight change in a person, and no pharmacokinetic study we could locate on PubMed as of September 2026, so nobody has published how much of an oral dose is absorbed, how long it lasts, or what it does to NAD+ in a human.

Oral Versus Injectable

This decision changes a protocol more than the number does, and it is genuinely open. The oral route is what the chemistry was designed for. Neelakantan's compounds were selected for membrane permeability precisely so they could be given systemically and reach the enzyme inside cells, and the consumer format that followed is a capsule or tablet at 50, 100 or 150 mg. Oral dosing is why 5-amino-1MQ has a life outside research storefronts, turning up in compounding pharmacy and clinic catalogues in a way BPC-157 never could.

The injectable route exists because research vendors sell what research vendors sell: a lyophilised powder, reconstituted with bacteriostatic water and drawn into an insulin syringe. The amounts quoted for it are lower, and the reasoning is sound in principle, because an oral dose has to survive the gut and the liver's first pass while an injected one does not. If oral bioavailability were 20 percent, 10 mg injected would deliver what 50 mg swallowed delivers.

The problem is the "if". Nobody has measured oral bioavailability in a person, so the conversion between routes is a guess dressed as arithmetic, and the published animal work used neither route. Note too that NNMT sits inside adipose and liver cells, both reached from the systemic circulation whichever route you pick. There is no local injection argument here the way there is for GHK-Cu. Injecting this one buys bioavailability, not targeting.

5-Amino-1MQ Dosage Chart

What follows describes what appears in practice, presented as research use information rather than instructions. None of it is validated in a human trial, and the amounts are conventions rather than the output of a dose response study.

The amount barely moves between goals while the duration does, which is the pattern the Bureau keeps meeting in compounds whose literature suggests something happens across a wide range of exposures and gives no guidance on where in that range to sit.

The oral figures are not arbitrary, though, even if they are not derived. Take the mouse dosing of roughly 20 mg per kilogram a day and convert it with the body surface area factor of 12.3 that regulators use for mouse to human scaling. That gives about 1.6 mg per kilogram, or roughly 110 mg for a 70 kilogram adult, and the 100 mg capsule sits almost exactly there. Whether somebody did that conversion or reverse engineered a round number the arithmetic later flattered is impossible to tell from a vendor page, and it assumes an oral bioavailability nobody has measured. It is the most defensible thing that can be said about the number, and it is still not a human dose.

Turning a Vial Into Syringe Units

Skip this if you have capsules. For the injectable presentation the arithmetic is the same as for any lyophilised vial: concentration is vial milligrams divided by millilitres of bacteriostatic water added, volume per dose is the amount divided by that concentration, and units on a U-100 insulin syringe are that volume in millilitres times 100. The reconstitution guide covers the mixing. One thing here works in your favour: amounts and vials are both quoted in milligrams, which removes the thousandfold microgram error that catches people out with BPC-157 and with kisspeptin. Vial sizes vary more than usual, though, because the same compound is sold as a research vial, as bulk powder by the gram and as finished capsules, so read the label rather than assuming.

Prefer the rows that put a dose between 10 and 50 units, where a one unit misread is a small error and the volume is still comfortable subcutaneously. The bac water guide covers the diluent, the injection guide covers needles and sites, and a reconstituted vial keeps roughly four weeks refrigerated per the storage guide. Capsules keep far longer, which is one more argument for the oral form.

Cycle Length and What Changes When

Eight to twelve weeks on, four weeks off, is the pattern in circulation. Unlike the growth hormone secretagogues there is no desensitisation argument forcing a break: NNMT is an enzyme being inhibited, not a receptor being downregulated. The reasons to break anyway are the general ones in the cycle length guide, plus the fact that NNMT is the body's route for disposing of excess methyl groups, and shutting that down for months on end shifts an accounting system nobody has measured in a person. Not a claim of harm, just a reason not to make indefinite use the default.

On expectations: nothing in the mechanism acts acutely. There is no appetite suppression to notice in week one, which is what separates it from the GLP-1 compounds on the fat loss peptides page and why so many logs read as unimpressive. If something is happening it is a shift in energy expenditure over weeks, against a diet doing the heavy lifting regardless.

Side Effects and the Open Questions

No controlled human safety data exists. That sentence does most of the work here. The anecdotal reports are mild and non-specific: nausea in the first few days, headache, facial flushing, and disrupted sleep when a dose is taken late. None of it is distinctive and none of it has a denominator. The mechanistic questions are more interesting and get less attention.

• 1-methylnicotinamide is not inert. Suppressing NNMT also reduces the metabolite the enzyme produces, and that metabolite has documented vascular and anti-inflammatory activity of its own. Removing it is a change, not the absence of one.
• The methyl group accounting. Raising SAM availability by blocking one of its largest consumers has knock-on effects on every other methylation reaction competing for the same pool. Nobody has measured what that looks like in a person over twelve weeks.
• The cancer literature cuts both ways. NNMT is overexpressed in several tumour types and its inhibition is being investigated as an anticancer strategy, which is reassuring in direction. It also means the enzyme is entangled in growth regulation in ways still being mapped.
• Purity is a small molecule question here, not a peptide one. A standard HPLC peptide purity assay is the wrong test for a quinolinium salt. What belongs on the certificate is identity confirmation, purity by an appropriate method, and heavy metals, because these synthesis routes use reagents a peptide synthesis does not. Read the testing guide with that difference in mind.

On regulatory status, once and plainly: 5-amino-1MQ is not an approved drug in any jurisdiction and not an established dietary supplement ingredient, so the capsules appearing in wellness catalogues sit in a space the FDA has not formally resolved. It also falls outside the peptide compounding debate the Bureau covered in the July 2026 advisory committee vote, because that process concerns peptides and this is not one. The legal status guide has the general framework.

Stacking

With NAD+ or its precursors. The coherent one. NNMT inhibition stops nicotinamide being thrown away; NAD+ dosing adds substrate to the same pool. One protects supply, the other increases it, which is easier to defend than most stacking arguments in this niche, and it remains untested as a combination in humans. The NAD+ dosage page has the amounts.

With a GLP-1 compound. The commonest real-world pairing, on the rationale that the mechanisms do not overlap: semaglutide, tirzepatide and retatrutide work through appetite and gastric emptying, this works inside the fat cell. Someone on a weekly GLP-1 who has stalled is the archetypal buyer. Keep the schedules separate so you know which one did what, and read the retatrutide guide or the semaglutide dosage guide for the injection side.

With repair compounds, in a blend. Pantheon sells a combination vial of BPC-157, TB-500 and 5-Amino-1MQ: two tissue repair peptides and a metabolic small molecule in one product. It suits someone wanting a single injection across two unrelated goals, and it costs you all control over the ratio. The Bureau's view of fixed-ratio blends, on the KLOW stack page, applies with extra force when the components have nothing to do with each other.

What it is not for: if the goal is libido or erectile function rather than fat mass, this is the wrong compound and NNMT has nothing to do with any of it. The compounds with human data there are on the erectile dysfunction page, the PT-141 page and the kisspeptin page. Readers buy them from the same storefronts and sometimes assume they interact. They share neither mechanism nor target.

Where to Buy 5-Amino-1MQ

Disclosure. Links in this section may earn the Bureau a commission; the scorecard method is on the vendor scorecard page. Formats and sizes change, so check the listing rather than trusting a figure on any guide page, this one included.

• Amino Club: the vendor Bureau readers order from most this year, with the most detailed testing policy of the five we score and a certificate reachable from the vial itself. Code 100 takes 20% off a first order. Amino Club review.
• PSPeptides: the one to use outside the United States, and the vendor most likely to offer an oral format given the tablet line it already runs. Code PEPTIDEBUREAU takes 10% off and keeps the order counted for the Bureau.
• Apollo Peptide Sciences: a short catalogue, mostly GLP compounds under coded names. Test reports sit as a gallery image rather than in a library, so check the report's batch against what you received. Apollo review.
• Pantheon Peptides: the widest single-compound catalogue of the five, and the only one selling 5-Amino-1MQ inside a blend. Convenient, and you inherit somebody else's ratio. Pantheon review.

The buying guide and the fake vendor guide apply as usual, and the cost per mg index is the honest way to compare listings quoted in different vial sizes.

Key Takeaways

• 5-Amino-1MQ is 5-amino-1-methylquinolinium, a small molecule of about 160 daltons, not a peptide, which is why it can be taken by mouth
• It inhibits NNMT, the enzyme that consumes nicotinamide and S-adenosylmethionine in fat tissue and liver, and which is upregulated in obesity
• The strongest evidence is a 2014 Nature knockdown study that prevented diet induced obesity in mice with no change in food intake, plus inhibitor work that reversed it
• There is no published human trial, no measured human weight change and no human pharmacokinetic data as of September 2026
• The oral convention is 50 to 150 mg once daily, in eight to twelve week blocks with a four week break; injectable amounts in circulation are 5 to 10 mg a day
• The mouse dose of roughly 20 mg/kg converts by body surface area to about 110 mg for a 70 kg adult, which is where the 100 mg capsule sits
• Do not expect appetite suppression: the defining feature of the Nature result was that food intake did not change

Frequently Asked Questions

Is 5-amino-1MQ a peptide?

No. 5-Amino-1MQ is 5-amino-1-methylquinolinium, a small molecule built on a two-ring quinoline scaffold weighing roughly 160 daltons as the cation. It contains no amino acids and no peptide bonds, so it is not a peptide in the chemical sense. It is called one because it is sold on research peptide storefronts alongside BPC-157 and GHK-Cu, and because the search term stuck. The distinction is practical rather than pedantic: a small molecule can survive the stomach and cross membranes, which is why this is the rare compound on those storefronts taken by mouth rather than injected.

What is the dosage for 5-amino-1MQ?

The convention in circulation is 50 to 150 mg a day by mouth, most often 100 mg once in the morning, in blocks of eight to twelve weeks with a break of about four weeks afterwards. No published human dose finding study sits behind those numbers. What can be said is that the mouse work dosed by injection in the region of 20 mg per kilogram a day, and that converting that to a human equivalent by the standard body surface area factor lands in the same neighbourhood as the capsules being sold. Treat the range as a description of practice, not a recommendation.

Does 5-amino-1MQ actually cause fat loss?

In mice, blocking NNMT does. A 2014 Nature paper knocked the enzyme down with an antisense oligonucleotide in mice on a high fat diet and found they were protected against diet induced obesity, with smaller fat cells and no reduction in how much they ate. Follow-up work with small molecule NNMT inhibitors of this class reported reversal of diet induced obesity in the same model. In humans there is no published trial, no measured weight change and no pharmacokinetic data that we could locate on PubMed as of September 2026. The mechanism is real and the human evidence does not exist yet.

Is 5-amino-1MQ taken orally or injected?

Mostly orally. It was designed to be membrane permeable, and the consumer format is a capsule or tablet of 50, 100 or 150 mg. Injectable presentations exist, sold as a lyophilised vial reconstituted with bacteriostatic water like any research peptide, and the amounts quoted for that route are lower because nothing is lost to the gut or to first pass metabolism in the liver. The published animal work used intraperitoneal injection, which is neither of the routes people actually use. Nobody has measured oral bioavailability in a person, so the conversion between the two is guesswork.

What are the side effects of 5-amino-1MQ?

No controlled human safety data exists, so the honest answer is that nobody knows. The reports in circulation are mild and non-specific: nausea in the first few days, headache, flushing, and trouble sleeping when a dose is taken late in the day. The mechanistic questions are more interesting than the anecdotes. Blocking NNMT spares nicotinamide and raises S-adenosylmethionine in fat tissue, which is the point, but it also suppresses 1-methylnicotinamide, a metabolite with biological activity of its own, and it shifts the body's methyl group accounting in a way nobody has measured in a person over months.

Research use only. The compounds discussed are sold as research chemicals and are not approved for human use. Nothing here is medical advice. More compound guides are indexed on the guides page.