Editorial note: this article summarises published research on SLU-PP-332, AICAR and 5-Amino-1MQ. Baclabs does not sell SLU-PP-332, AICAR, 5-Amino-1MQ or any peptide; we supply bacteriostatic water and reconstitution consumables. Nothing here is medical advice.
SLU-332 (properly SLU-PP-332), AICAR and 5-Amino-1MQ are sold alongside metabolic peptides and share a marketing label, “exercise in a pill”, but none of them is a peptide and none has been shown to do in humans what it does in mice. Each targets a different node of energy metabolism: SLU-PP-332 switches on a nuclear receptor programme that resembles endurance training, AICAR mimics the low-energy signal that activates AMP-activated protein kinase (AMPK), and 5-Amino-1MQ blocks an enzyme that drains the cell’s NAD+ and methyl donor pools.
This article explains the three mechanisms, reports the doses and results from the rodent papers behind the headlines, and sets out the regulatory and anti-doping position.
What an “exercise mimetic” is supposed to be
Endurance exercise reprogrammes skeletal muscle: more mitochondria, a shift towards oxidative fibres, greater fatty-acid oxidation and better glucose handling. The signalling runs through energy sensors (AMPK) and nuclear receptors (PPARδ, the oestrogen-related receptors ERRα/β/γ). An exercise mimetic is a drug that triggers part of this programme without the contraction. The concept was made concrete by Narkar and colleagues in 2008, who showed that four weeks of AICAR alone improved running endurance in sedentary mice by about 44 per cent [1].
SLU-332 (SLU-PP-332): a pan-ERR agonist
SLU-PP-332 was developed in Thomas Burris’s laboratory at Saint Louis University (the “SLU”) as a synthetic agonist of all three oestrogen-related receptors, with the strongest activity at ERRα, orphan nuclear receptors that control genes for mitochondrial biogenesis and fatty-acid oxidation.
In the 2023 ACS Chemical Biology paper, a single 50 mg/kg intraperitoneal dose given an hour before treadmill testing, on top of 7–15 days of 50 mg/kg twice daily, let mice run about 70 per cent longer and roughly 45 per cent further than vehicle-treated animals. Chronic treatment increased oxidative type IIa fibres and myosin IIA protein. The effect vanished in mice with ERRα deleted specifically in skeletal muscle, which is the strongest piece of evidence that the mechanism is what the authors claim [2].
The 2024 Journal of Pharmacology and Experimental Therapeutics paper extended this to obesity. Diet-induced obese mice kept on a high-fat diet and given 50 mg/kg twice daily weighed about 12 per cent less than controls after 28 days, gained far less fat, and showed improved glucose tolerance; ob/ob mice on the same regimen for 12 days also lost weight [3].
“SLU 332 exercise in a pill”: the gap between mouse and human
The phrase is fair as a description of the mouse data and misleading as a description of what anyone can buy. There is no human pharmacokinetic, safety or efficacy study of SLU-PP-332. The mouse dose of 100 mg/kg/day by intraperitoneal injection has no human equivalent; oral bioavailability, half-life and off-target effects in people are unknown. Burris’s group has since described a successor, SLU-PP-915, a signal that SLU-PP-332 was a research tool rather than a drug candidate. Products sold under this name are unlicensed research chemicals of uncertain identity and purity.
AICAR: the original AMPK activator
AICAR (5-aminoimidazole-4-carboxamide ribonucleoside) is taken up by cells and phosphorylated to ZMP, an analogue of AMP. ZMP binds AMPK’s regulatory subunit as if the cell were short of energy, switching on glucose uptake and fatty-acid oxidation and switching off lipid and protein synthesis. This is the same pathway that MOTS-c activates, covered in the MOTS-c and SS-31 article.
In the 2008 Cell study, untrained mice given AICAR at 500 mg/kg/day intraperitoneally for four weeks increased running endurance by around 44 per cent, with induction of oxidative and mitochondrial genes in muscle. Combining a PPARδ agonist (GW1516) with training produced larger gains [1].
The human record: acadesine
AICAR is unusual among “research chemicals” in having a substantial human history under its clinical name, acadesine, an intravenous agent developed to protect the heart during coronary artery bypass grafting. The large randomised RED-CABG trial was stopped early for futility: acadesine did not reduce the composite of death, stroke or left-ventricular dysfunction [4]. It has human exposure data but no approved indication, and no human trial has tested it for endurance or fat loss.
WADA status
The World Anti-Doping Agency lists activators of AMPK, naming AICAR and MOTS-c specifically, under section S4.4.1 of the Prohibited List, and PPARδ agonists such as GW1516 under the same section. Both classes are banned at all times [5]. The US Anti-Doping Agency’s guidance adds that AICAR “has not been extensively studied in people” and that excessive AMPK activation carries theoretical risks including effects on cell division [6].
5-Amino-1MQ: an NNMT inhibitor
5-Amino-1MQ (5-amino-1-methylquinolinium) works on a different axis. Nicotinamide N-methyltransferase (NNMT) transfers a methyl group from S-adenosylmethionine (SAM) to nicotinamide, producing 1-methylnicotinamide. In doing so it consumes both the NAD+ precursor and the cell’s main methyl donor. NNMT is over-expressed in the fat and liver of obese animals, and inhibiting it raises intracellular NAD+ and SAM and suppresses lipogenesis in adipocytes.
Neelakantan and colleagues at the University of Texas Medical Branch reported in 2018 that 5-Amino-1MQ, given to diet-induced obese mice at 20 mg/kg subcutaneously three times daily (about 34 mg/kg/day) for 11 days, produced a 2.0 g weight loss (about 5 per cent) against a 0.6 g gain in controls, a 35 per cent reduction in epididymal white fat, more than 30 per cent smaller adipocytes and about 30 per cent lower plasma cholesterol, with no change in food intake [7]. A 2024 paper from the same group examined body composition, fatty-liver pathology and insulin resistance in obese mice and characterised the compound’s plasma pharmacokinetics [8]. There is no human trial, no human safety data, and no regulatory status anywhere.
Doses reported in the literature
The figures below are the doses used in the cited studies. They are not recommendations and cannot be scaled to humans by body weight.
| Compound | Target | Model | Dose in source | Reported effect |
|---|---|---|---|---|
| SLU-PP-332 | ERRα/β/γ agonist | Mice, 7–15 days [2] | 50 mg/kg IP twice daily | ~70% longer running time |
| SLU-PP-332 | ERRα/β/γ agonist | Obese mice, 28 days [3] | 50 mg/kg IP twice daily | ~12% lower body weight |
| AICAR | AMPK activator | Sedentary mice, 4 weeks [1] | 500 mg/kg/day IP | ~44% more endurance |
| Acadesine (AICAR) | Adenosine regulation | CABG patients [4] | IV infusion, perioperative | No benefit; stopped for futility |
| 5-Amino-1MQ | NNMT inhibitor | Obese mice, 11 days [7] | 20 mg/kg SC three times daily | ~5% weight loss, 35% less fat |
Reconstitution and diluent notes
These compounds do not follow the peptide pattern. SLU-PP-332 and 5-Amino-1MQ are small molecules; vendors mostly sell them as capsules or as powder for oral use, and 5-Amino-1MQ is not generally injected. AICAR is sometimes sold as lyophilised powder in vials of 50 mg or more for injection, and the standard formula applies: concentration (mg/mL) = vial content ÷ diluent volume, so 50 mg in 2 mL gives 25 mg/mL, or 250 mcg per unit on a U-100 syringe. Any vial that will be punctured repeatedly needs a preserved diluent; the difference between bacteriostatic and sterile water is set out in bacteriostatic water vs sterile water, and the 28-day rule in bacteriostatic water storage and shelf life. Baclabs supplies UK-stocked bacteriostatic water in 30 mL vials; the reconstitution guide covers the method.
In the metabolic peptides guide, these three occupy the “rodent only” tier alongside MOTS-c. By comparison, AOD-9604 at least reached phase 2b before failing.
Frequently asked questions
Is SLU-332 the same as SLU-PP-332?
Yes. SLU-332 is a vendor shorthand for SLU-PP-332, the pan-ERR agonist from Thomas Burris’s laboratory. There is no separate compound called SLU-332. The full name is worth using when checking certificates of analysis, because the shortened form does not identify a defined chemical structure.
Does SLU-332 work as “exercise in a pill” in humans?
Nobody knows. All published data are in mice at 50 mg/kg twice daily by intraperitoneal injection, showing longer running times and about 12 per cent lower body weight in obese animals. There is no human trial, no human safety data and no approved product. Claims of human effects are extrapolation.
Is AICAR banned in sport?
Yes. AICAR is named on the WADA Prohibited List under S4.4.1 as an AMPK activator and is prohibited at all times. MOTS-c is listed in the same clause, and PPARδ agonists such as GW1516 sit alongside it.
What does 5-Amino-1MQ do?
It inhibits NNMT, an enzyme that consumes NAD+ precursors and methyl donors. In obese mice, 11 days of injections produced about 5 per cent weight loss and a 35 per cent fall in white fat without reducing food intake. There is no human evidence of any kind, and its oral products are unregulated.
References
- AMPK and PPARδ agonists are exercise mimetics. Narkar et al., Cell, 2008
- Synthetic ERRα/β/γ agonist induces an ERRα-dependent acute aerobic exercise response and enhances exercise capacity. Billon et al., ACS Chemical Biology, 2023
- A synthetic ERR agonist alleviates metabolic syndrome. Billon et al., Journal of Pharmacology and Experimental Therapeutics, 2024
- Effect of adenosine-regulating agent acadesine on morbidity and mortality associated with coronary artery bypass grafting: the RED-CABG randomized controlled trial. Newman et al., JAMA, 2012
- The Prohibited List, section S4.4 (metabolic modulators). World Anti-Doping Agency, 2026
- What athletes should know about AICAR and other prohibited AMPK activators. US Anti-Doping Agency, 2023
- Selective and membrane-permeable small molecule inhibitors of nicotinamide N-methyltransferase reverse high fat diet-induced obesity in mice. Neelakantan et al., Biochemical Pharmacology, 2018
- Nicotinamide N-methyltransferase inhibition mitigates obesity-related metabolic dysfunction. Babula et al., Diabetes, Obesity and Metabolism, 2024
Disclaimer: This content is for educational purposes only and does not constitute medical advice. Bacteriostatic water is supplied for reconstitution of substances intended for research and for use as directed by a healthcare professional. Peptides and medicines discussed here may be unlicensed in the UK or prescription-only; consult a qualified clinician before using any medicine. Baclabs does not sell peptides.