AICAR (acadesine): research, side effects and dosage in studies

In short

AICAR, or acadesine, is a nucleoside that activates the cell's energy regulator AMPK. In mice it increased running endurance without training [1]C, but in humans it has been studied mainly as an infusion into a vein, mostly during heart surgery, and it has no marketing authorisation in the EU [6]A [27]regulator.

• Its reputation as an exercise mimetic comes from one mouse study: after four weeks of AICAR, sedentary mice ran 44% further [1]C. An effect on endurance has not been studied in humans.
• There are many human studies, but they are about heart surgery. In a pooled analysis of five randomised trials (4,043 patients) there were 27% fewer heart attacks [2]A, but the largest single trial (3,080 patients) was stopped because no benefit was seen [6]A.
• Taken by mouth, acadesine was poorly absorbed in humans, under 5%, and its half-life in the blood was about 1.4 hours [9]B.
• The best-known side effect is a rise in uric acid [2, 3]A. At very high doses into a vein, leukaemia patients also had kidney harm and a fall in blood pressure [11]B.
• WADA bans AICAR at all times (S4.4.1) [24]regulator. It is not listed on Fimea's medicines list [28]regulator, and it has no marketing authorisation in the EU [27]regulator.

What is AICAR?

AICAR is a molecule resembling a purine nucleoside, and its drug name is acadesine. In the literature the same substance is also called AICA riboside, and its chemical name is 5-amino-1-beta-D-ribofuranosyl-imidazole-4-carboxamide [3]A [21].

AICAR is not a peptide. It is a small molecule that resembles the body's own purine building blocks. The body also makes it: in athletes' urine samples it has been measured naturally at an average of 2,186 nanograms per millilitre [19]B.

The substance is known in two contexts. In the 1990s it was developed as a heart drug to protect the heart muscle during bypass surgery [2, 3]A. In 2008 a mouse study made it known as an "exercise mimetic", a substance that imitates the effects of exercise [1]C.

The same section of the WADA list also covers MOTS-c, which is also studied as an exercise mimetic [24]regulator. All substances on the site: Peptides A-Z.

Evidence at a glance

Each cell gives the kind of study and its source. The letter is the evidence level, not the result.

"-" = no such study is known.

What is AICAR studied for?

AICAR has been studied in humans in heart surgery, blood cancers and metabolic measurements, and in animals as an exercise mimetic. None of these is an approved use [27]regulator.

• Heart surgery: acadesine was given into a vein during bypass surgery and added to the heart's protective solution to prevent heart attacks. The two largest data sets together had over 7,000 patients [2, 6]A.
• Chronic lymphocytic leukaemia: in a phase 1/2 study, 24 patients received acadesine into a vein [11]B. In the EU the substance has orphan designations for this disease and for multiple myeloma [25, 26]regulator.
• Myelodysplastic syndromes: a French phase 1-2 trial was stopped after five patients because of kidney toxicity [29]E, not peer-reviewed.
• Type 2 diabetes: short infusion experiments measured how AICAR affects muscle glucose uptake and glucose output from the liver [12, 13, 14]B.
• Exercise mimetic: only in mice [1, 22]C.

In exercise-induced chest pain (angina), acadesine was tried in 12 patients at four doses, and it did not consistently change time to chest pain or exercise time [8]A.

How does AICAR work?

Laboratories widely use AICAR to activate the enzyme AMPK [15]. AMPK is the cell's energy regulator, and exercise activates it too [1]C [12]B. In human red blood cells AICAR is quickly converted to its monophosphate [9]B [10]B.

According to a systematic review, however, many effects of AICAR that have been put down to AMPK are in fact independent of AMPK [15].

As a heart drug, acadesine was thought to work in another way: it would increase adenosine locally in tissue short of oxygen [3]A.

In humans the results have been mixed. In healthy men an AICAR infusion increased muscle glucose uptake, but muscle AMPK was not activated. Exercise, by contrast, did activate AMPK [12]B. The same was seen in older people and in people with type 2 diabetes, and according to the researchers the effect ran through another signalling route (ERK1/2) [13]B. In the study of people with diabetes, phosphorylation of muscle AMPK did not increase, but phosphorylation of its target protein ACC did [14]B.

Has AICAR been studied in humans?

Yes, more than most substances on this site, but not as an exercise mimetic. The human studies are about heart surgery, leukaemia and short metabolic experiments. In all of them the substance was given into a vein under study conditions [2, 6]A [11, 12]B.

Heart surgery trials

• Pooled analysis 1997. A patient-level meta-analysis of five randomised, placebo-controlled trials included 4,043 bypass surgery patients. Acadesine reduced heart attacks around surgery by 27% and cardiac deaths within four days by 50%. Strokes were not significantly reduced [2]A.
• US trial 1995. 633 patients, two dose levels and placebo. Using the prespecified definition of heart attack, there was no difference between the groups (24%, 26% and 21%). A difference appeared only in an analysis done afterwards with a stricter definition [3]A.
• International trial 1995. 821 patients. There were not fewer heart attacks in the whole group, but in high-risk patients Q-wave heart attacks occurred in 10.0% instead of 19.7% with placebo [4]A.
• Long-term follow-up 2006. Of 2,698 patients, 100 had a heart attack around surgery. Within two years, 27.8% of them died in the placebo group and 6.5% in the acadesine group [5]A.
• RED-CABG 2012. The largest trial, with 3,080 intermediate- to high-risk patients at 300 sites. It was stopped because a prespecified interim analysis predicted that no benefit would be found. The primary outcome (death, stroke or severe heart failure) occurred in 5.0% of the placebo group and 5.1% of the acadesine group [6]A.

Overall: the early trials and their pooled analysis suggested a benefit [2]A, but the largest and newest trial did not confirm it [6]A.

Metabolic experiments

• Healthy men. 29 healthy men. At three hours, muscle glucose uptake was 2.1-fold with AICAR and 4.7-fold with cycling. Whole-body glucose use rose by 7% with AICAR [12]B.
• Age and diabetes. Glucose uptake rose 2.9-fold in young men, 1.8-fold in older men and 1.6-fold in men with type 2 diabetes. According to the researchers, age rather than diabetes weakened the effect [13]B.
• People with type 2 diabetes. In ten older men the infusion reduced glucose output from the liver, lowered blood sugar and reduced free fatty acids in the blood [14]B.

Leukaemia

In an open phase 1/2 study, 24 patients with relapsed chronic lymphocytic leukaemia received acadesine as a four-hour infusion. Leukaemia cells in the blood and the size of lymph nodes fell in some, but the results varied because of the small number of patients and the many dose levels [11]B.

Promising, but only in animals

AICAR's reputation as an exercise mimetic rests on animal studies. These findings have not been studied in humans.

• Endurance without training no human studies

  After four weeks of AICAR, sedentary mice ran on a treadmill about 23% longer and 44% further than control mice. Metabolic genes were switched on in the muscle [1]C. In trained mice AICAR increased endurance, and even more together with a PPAR-delta agonist [22]C.

  If it held in humans: the substance could increase endurance without training or strengthen the effect of training.

  Why it might not translate: the mice received the substance as an injection into the abdominal cavity [1]C, but in humans less than 5% of acadesine taken by mouth was absorbed [9]B. In humans an AICAR infusion did not activate muscle AMPK [12, 13]B, and exercise raised muscle glucose uptake more than twice as much as AICAR did [12]B. According to a review, whether exercise mimetics are feasible at all is disputed [23].

  Evidence now: there are several mouse studies from different groups [1, 22]C. No human endurance study has been published or registered (as of October 2026).

• Brain and memory no human studies

  In young mice, seven days of AICAR increased the number of new cells and the growth factor BDNF in the hippocampus, much like running. At fourteen days the effect reversed: the rise in new cells stopped, and genes linked to cell death and inflammation were switched on [16]C.

  If it held in humans: short treatment could support brain plasticity, but longer treatment could be harmful.

  Why it might not translate: the result comes from one mouse study, and the benefit was gone within two weeks [16]C.

  Evidence now: one study; there is no human study.

• Muscle diseases no human studies

  In a mouse model of spinal muscular atrophy (SMA), muscle wasting decreased, but survival and movement did not improve [17]C. In a mouse model of Huntington's disease the muscles shifted towards an endurance type, but the disease did not slow down [18]C.

  If it held in humans: the substance could change muscle structure in muscle diseases, but not necessarily the disease itself.

  Why it might not translate: in both models the change in muscle did not show in the course of the disease [17, 18]C.

  Evidence now: two independent mouse studies; there is no human study.

Who studies AICAR?

When acadesine was studied as a heart drug, its pharmacokinetics were published by researchers of the US company Gensia Pharmaceuticals [9]B [10]B. Much of the heart surgery research was done by the McSPI research group coordinated in San Francisco [2, 3]A, and the first author of the RED-CABG trial was from Duke University's clinical research institute [6]A.

The EU orphan designations were granted to the Spanish company Advancell [25, 26]regulator, and the first author of the leukaemia study was from Brussels [11]B. As an exercise mimetic the substance was made known by a group at the Salk Institute in California [1]C, and doping tests have been developed by the German Sport University's laboratory in Cologne [19]B [20]D.

Who wrote this page: the editorial team

This page was written by the Molecular Recovery editorial team. The draft was made with the help of AI, and the claims were checked against the sources (AI policy). The page has not been medically reviewed. How we work: About us.

How long does AICAR stay in the body?

A short time. In healthy men, the half-life of acadesine given into a vein was on average 1.4 hours in the blood [9]B. In another study the unchanged substance could be measured in the blood for only two hours after the infusion [10]B.

• Absorption by mouth: under 5% when taken as a solution [9]B.
• Breakdown: acadesine is mainly broken down to uric acid. Six hours after the infusion, all of the labelled substance in the blood was uric acid [10]B.
• Excretion: only 5-8% of the dose was excreted unchanged in the urine [9]B [10]B.
• Red blood cells: in red blood cells the substance is converted to a monophosphate, which stays inside the cells [10]B. The slow final phase of the total labelled material lasted about a week, but it describes breakdown products, not AICAR itself [10]B.

What are the side effects of AICAR?

The best-known side effect is a rise in uric acid, because the body breaks acadesine down to uric acid [10]B. At heart surgery doses, other adverse events were as common as with placebo [2]A.

Measured in humans

• Uric acid. In the heart surgery trials uric acid rose transiently at the higher dose [2, 3]A, in the first trial by an average of 1.6 mg/dl without clinical consequences [7]A.
• Healthy volunteers. The substance was well tolerated at all doses studied. Mild, transient symptoms were reported both by those who received placebo and those who received the substance [9]B.
• Very high doses in leukaemia. The single doses in the leukaemia study were larger than the seven-hour heart surgery infusion dose. At these doses a rise in uric acid was common; it was not clinically significant and resolved with preventive allopurinol. There was also transient anaemia and a fall in platelets (not clinically significant), kidney impairment and infusion-related low blood pressure, which was clinically significant [11]B.
• Kidney toxicity. The trial in myelodysplastic syndromes was stopped because of kidney toxicity. The information comes from a registry, not a peer-reviewed publication [29]E, not peer-reviewed.

Seen in animals

In mice, two weeks of treatment switched on genes linked to cell death and inflammation in the brain, although the effect at seven days had been positive [16]C.

What has not been studied

Repeated use without medical supervision, injection under the skin and long-term use have not been studied. All human studies used infusions in hospital, and the longest treatment, in the leukaemia study, was five doses [11]B. Side effects more generally: side effects in studies.

Interactions and who has no data

Drug interactions have not been studied separately. In the leukaemia study, patients received allopurinol as prevention because of the rise in uric acid [11]B, but there is no research data on gout or other conditions linked to uric acid.

In people with type 2 diabetes the substance lowered blood sugar and reduced glucose output from the liver [14]B, but use together with diabetes medicines has not been studied. There is no research data on pregnancy, breastfeeding or children.

What speaks against it and what is not known

The largest human trial found no benefit, and the evidence for mimicking exercise comes only from mice.

Counter-evidence

• RED-CABG did not repeat the benefit. The 3,080-patient trial was stopped for futility; the primary outcome occurred in 5.0% of the placebo group and 5.1% of the acadesine group [6]A.
• The early findings came from subgroups. In two trials published in 1995, the prespecified outcome did not differ from placebo; a benefit was found only afterwards or in a subgroup [3, 4]A.
• Human muscle did not react like mouse muscle. In humans the infusion did not activate muscle AMPK [12, 13]B, although in mice that activation is the basis of the whole exercise mimetic idea [1]C.
• The effect does not run purely through AMPK. Many effects of AICAR are independent of AMPK [15].
• A change in muscle does not always help. In two disease models the mouse muscles changed, but the disease did not ease [17, 18]C.

What the evidence does not support

• "AICAR is exercise in a pill": taken by mouth, under 5% was absorbed in humans [9]B, and endurance has not been studied in humans.
• "AICAR burns fat in humans": in people with type 2 diabetes the infusion reduced fatty acids in the blood in an experiment lasting hours [14]B; weight loss has not been studied.
• "AICAR is safe because the body makes it": at high doses kidney harm and a fall in blood pressure have been reported [11]B.
• "AICAR is an approved medicine": it has no marketing authorisation in the EU [27]regulator.

What is not known

• Whether AICAR increases human endurance. It has not been studied.
• What repeated use without medical supervision does. All human studies were short hospital infusions [6]A [11]B.
• Why the large heart surgery trials reached different results. The researchers have not given a single clear reason.

AICAR dosage in studies

AICAR has no approved dosage. In humans it was given under study conditions per kilogram of body weight, mostly into a vein; Dixon 1991 also studied it by mouth. Below are the doses used in studies. They are not recommendations.

What the figures do not tell you. The human doses are infusions given in hospital per kilogram of body weight and per unit of time, not treatment instructions. The mouse dose cannot be converted to a human dose by body weight, and the injection route of the mouse study has not been studied in humans [1]C. In humans, under 5% of the substance taken by mouth was absorbed [9]B. Human doses with sources: AICAR doses in studies. Unit converter: AICAR calculator. On reading study doses: dosage in studies.

AICAR vs exercise: what is the difference?

The only direct comparison in humans concerned muscle glucose uptake, and there exercise was clearly more effective.

In healthy men, a three-hour AICAR infusion raised muscle glucose uptake 2.1-fold and cycling 4.7-fold. Exercise activated muscle AMPK; AICAR did not [12]B.

In mice, running and AICAR produced similar changes in muscle and brain over seven days. In muscle the effect lasted, but in the brain only the benefit of running continued at two weeks [16]C. The researchers concluded that only running consistently benefited the brain.

The group of exercise mimetics also includes MOTS-c, which has its own page. No study has compared the two.

The same group of exercise mimics also includes SLU-PP-332. A comparison of the three: Exercise mimetics: AICAR, SLU-PP-332 and MOTS-c.

AICAR combinations

Combinations with AICAR have only been studied in mice. The best known is AICAR together with a PPAR-delta agonist.

In trained mice, four weeks of AICAR combined with the PPAR-delta agonist GW0742 lengthened running time more than AICAR alone [22]C. In the original 2008 work, a PPAR-delta agonist and training together increased endurance [1]C.

Combinations have not been studied in humans. PPAR-delta agonists are in the same section of the WADA list as AICAR [24]regulator. On blends in general: blends.

Is AICAR legal in Finland?

AICAR, or acadesine, has no marketing authorisation in the EU, so it cannot be marketed as a medicine [27]regulator. It is not listed on Fimea's medicines list [28]regulator.

• Marketing authorisation. The EMA data set of centrally authorised medicines (14 Oct 2026) contains no product with acadesine [27]regulator.
• An orphan designation is not a marketing authorisation. The EU granted acadesine orphan designations for chronic lymphocytic leukaemia in 2005 and for multiple myeloma in 2011 [25, 26]regulator. A designation is a development-stage status, not permission to sell or use the substance.
• Medicines list. The fact that a substance is not on the medicines list does not settle a product's status. Under the Medicines Act, Fimea decides when needed whether a substance or product is a medicine [30]regulator.
• The label "for research use only" means the product is not intended for humans.

Overview of the law: Peptides and the law in Finland. Bringing substances back from travel: Travelling with peptides.

This is not legal advice. Disclaimer.

Is AICAR doping?

Yes. On the WADA 2026 Prohibited List, AICAR is named in section S4.4.1, activators of AMPK. Class S4 substances are prohibited at all times, in and out of competition [24]regulator.

According to a review, WADA added AMPK activators to the list after the mouse study was published just before the 2008 Beijing Olympics [21] [1]C.

Testing is difficult because the body makes AICAR itself. The Cologne laboratory measured natural levels in urine samples from 499 athletes as reference values, and levels varied by sex, sport and type of sample collection [19]B.

How to judge the quality of an AICAR product

There is no certainty about what an AICAR product contains without analysis, and a deviation has been measured for this substance.

In 2010 the Cologne doping laboratory bought AICAR from online sellers. The substance was genuine, but there was clearly less of it than the label stated. The parcels were labelled as amino acids and green tea extract, and the products were labelled "for research only" [20]D.

On a certificate of analysis (COA) look at the method: liquid chromatography, HPLC, gives purity and mass spectrometry (MS) identifies the molecule. A shortfall in content shows only if the certificate states the amount, not just purity. A guide: How to read a COA.

The future: what comes next?

No ongoing human study was found. The acadesine trials in the ClinicalTrials.gov registry have ended or been stopped, the latest because of kidney toxicity [29]E, not peer-reviewed, and the largest heart surgery trial was stopped for futility [6]A.

The EU orphan designations are still in force, but the EMA pages have not been updated since 2013 [25, 26]regulator. According to a review, the feasibility of the whole exercise mimetic idea is disputed [23].

FAQ

Read the research yourself: sources

Every source opens the original publication or the regulator's page. The level shows what the source itself reports.

1. Narkar VA, Downes M, Yu RT, et al. AMPK and PPARdelta agonists are exercise mimetics. Cell. 2008;134(3):405-415. PMID 18674809 C
2. Mangano DT. Effects of acadesine on myocardial infarction, stroke, and death following surgery. A meta-analysis of the 5 international randomized trials. The Multicenter Study of Perioperative Ischemia (McSPI) Research Group. JAMA. 1997;277(4):325-332. PMID 9002496 A
3. Multicenter Study of Perioperative Ischemia (McSPI) Research Group. Effects of acadesine on the incidence of myocardial infarction and adverse cardiac outcomes after coronary artery bypass graft surgery. Anesthesiology. 1995;83(4):658-673. PMID 7574044 A
4. Menasché P, Jamieson WR, Flameng W, Davies MK. Acadesine: a new drug that may improve myocardial protection in coronary artery bypass grafting. Results of the first international multicenter study. J Thorac Cardiovasc Surg. 1995;110(4 Pt 1):1096-1106. PMID 7475138 A
5. Mangano DT, Miao Y, Tudor IC, Dietzel C. Post-reperfusion myocardial infarction: long-term survival improvement using adenosine regulation with acadesine. J Am Coll Cardiol. 2006;48(1):206-214. PMID 16814669 A
6. Newman MF, Ferguson TB, White JA, et al. Effect of adenosine-regulating agent acadesine on morbidity and mortality associated with coronary artery bypass grafting: the RED-CABG randomized controlled trial. JAMA. 2012;308(2):157-164. PMID 22782417 A
7. Leung JM, Stanley T 3rd, Mathew J, et al. An initial multicenter, randomized controlled trial on the safety and efficacy of acadesine in patients undergoing coronary artery bypass graft surgery. Anesth Analg. 1994;78(3):420-434. PMID 7818622 A
8. Holdright DR, Sparrow JL, Wright CL, Steiner J, Fox KM. Effect of acadesine, a new metabolic agent, on exercise-induced myocardial ischemia in chronic stable angina. Cardiovasc Drugs Ther. 1994;8(2):193-197. PMID 7918131 A
9. Dixon R, Gourzis J, McDermott D, et al. AICA-riboside: safety, tolerance, and pharmacokinetics of a novel adenosine-regulating agent. J Clin Pharmacol. 1991;31(4):342-347. PMID 2037706 B
10. Dixon R, Fujitaki J, Sandoval T, Kisicki J. Acadesine (AICA-riboside): disposition and metabolism of an adenosine-regulating agent. J Clin Pharmacol. 1993;33(10):955-958. PMID 8227467 B
11. Van Den Neste E, Cazin B, Janssens A, et al. Acadesine for patients with relapsed/refractory chronic lymphocytic leukemia (CLL): a multicenter phase I/II study. Cancer Chemother Pharmacol. 2013;71(3):581-591. PMID 23228986 B
12. Cuthbertson DJ, Babraj JA, Mustard KJ, et al. 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside acutely stimulates skeletal muscle 2-deoxyglucose uptake in healthy men. Diabetes. 2007;56(8):2078-2084. PMID 17513706 B
13. Babraj JA, Mustard K, Sutherland C, et al. Blunting of AICAR-induced human skeletal muscle glucose uptake in type 2 diabetes is dependent on age rather than diabetic status. Am J Physiol Endocrinol Metab. 2009;296(5):E1042-E1048. PMID 19190259 B
14. Boon H, Bosselaar M, Praet SF, et al. Intravenous AICAR administration reduces hepatic glucose output and inhibits whole body lipolysis in type 2 diabetic patients. Diabetologia. 2008;51(10):1893-1900. PMID 18709353 B
15. Višnjić D, Lalić H, Dembitz V, Tomić B, Smoljo T. AICAr, a widely used AMPK activator with important AMPK-independent effects: a systematic review. Cells. 2021;10(5):1095. PMID 34064363 (review)
16. Guerrieri D, van Praag H. Exercise-mimetic AICAR transiently benefits brain function. Oncotarget. 2015;6(21):18293-18313. PMID 26286955 C
17. Cerveró C, Montull N, Tarabal O, et al. Chronic treatment with the AMPK agonist AICAR prevents skeletal muscle pathology but fails to improve clinical outcome in a mouse model of severe spinal muscular atrophy. Neurotherapeutics. 2016;13(1):198-216. PMID 26582176 C
18. Paré MF, Jasmin BJ. Chronic 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside treatment induces phenotypic changes in skeletal muscle, but does not improve disease outcomes in the R6/2 mouse model of Huntington's disease. Front Neurol. 2017;8:516. PMID 29021780 C
19. Thomas A, Beuck S, Eickhoff JC, et al. Quantification of urinary AICAR concentrations as a matter of doping controls. Anal Bioanal Chem. 2010;396(8):2899-2908. PMID 20225061 B
20. Thevis M, Geyer H, Thomas A, Schänzer W. Trafficking of drug candidates relevant for sports drug testing: detection of non-approved therapeutics categorized as anabolic and gene doping agents in products distributed via the Internet. Drug Test Anal. 2011;3(5):331-336. PMID 21538997 D
21. Niederberger E, King TS, Russe OQ, Geisslinger G. Activation of AMPK and its impact on exercise capacity. Sports Med. 2015;45(11):1497-1509. PMID 26186961 (review)
22. Manio MC, Inoue K, Fujitani M, Matsumura S, Fushiki T. Combined pharmacological activation of AMPK and PPARδ potentiates the effects of exercise in trained mice. Physiol Rep. 2016;4(5):e12625. PMID 26997622 C
23. Weihrauch M, Handschin C. Pharmacological targeting of exercise adaptations in skeletal muscle: benefits and pitfalls. Biochem Pharmacol. 2018;147:211-220. PMID 29061342 (review)
24. World Anti-Doping Agency. 2026 Prohibited List, section S4.4.1: activators of the AMP-activated protein kinase (AMPK), e.g. AICAR. WADA regulator
25. European Medicines Agency. EU/3/05/280: orphan designation for treatment of B-cell chronic lymphocytic leukaemia (acadesine), granted 27 May 2005; status positive (page last updated 31 Jul 2013). EMA regulator
26. European Medicines Agency. EU/3/11/881: orphan designation for treatment of multiple myeloma (acadesine), granted 5 Aug 2011; status positive (page last updated 31 Jul 2013). EMA regulator
27. European Medicines Agency. Medicine data (centrally authorised medicines, data set generated 14 Oct 2026): no product with acadesine as active substance. EMA regulator
28. Finland. Lääkeluettelo (Fimea medicines list), 230/2025, annexes 1 and 1 A: acadesine (AICAR) is not listed (searched 15 Oct 2026). Finlex regulator
29. ClinicalTrials.gov. NCT01813838: GFM-Acadesine: A Phase I-II Trial of Acadesine (Groupe Francophone des Myelodysplasies; phase 1-2; started Jun 2013; 5 participants; status terminated, reason given: "Renal toxicity"). Read 15 Oct 2026. ClinicalTrials.gov E, not peer-reviewed
30. Finland. Medicines Act (Lääkelaki) 395/1987, section 6: Fimea decides, when needed, whether a substance or product is to be regarded as a medicine. Finlex regulator

Sources searched and read on 15 Oct 2026: PubMed abstracts, ClinicalTrials.gov, the EMA orphan designations and medicine data, and Fimea's medicines list. The WADA 2026 Prohibited List was read on 15 Sep 2026. The mouse dose is from the full text of the publication, other dose details from the abstracts.

Evidence levels: A = randomised human trial or meta-analysis · B = observational human study or case series · C = animal study · D = cell or laboratory study · E = not peer-reviewed · regulator = a regulator's assessment or decision, not research evidence. The marker official means official product information (summary of product characteristics or label); it is not research evidence. For a review, the level shows what kind of research the statement rests on. No level: statements that something has not been studied, reviews' interpretations, named hypotheses and the general rules in our certificate-of-analysis guide.

Content is general information about research, not medical advice. If you have symptoms, contact a healthcare professional.