Clenbuterol

Identity, and two regulatory lives

Clenbuterol resolves cleanly at the compound level and splits almost everywhere else. One PubChem record covers it: CID 2783, CAS 37148-27-9, molecular formula C12H18Cl2N2O, molecular weight 277.19, InChIKey STJMRWALKKWQGH-UHFFFAOYSA-N, UNII XTZ6AXU7KN, cross-referenced to ChEMBL49080, ChEBI 174690 and DrugBank DB01407, under the IUPAC name 1-(4-amino-3,5-dichlorophenyl)-2-(tert-butylamino)ethanol. The World Health Organization then assigns two ATC codes, R03AC14 and R03CC13, both filed under drugs for obstructive airway disease, which is the classification the molecule was built for. The material in circulation is a racemate, and the FDA Global Substance Registration System keeps separate substance records for each enantiomer. Those figures describe the free base; the hydrochloride salt is indexed separately at 313.6 g/mol, a 13 per cent difference in mass on anything weighed.

No United States approval for human use exists. The openFDA human drug-label endpoint and the Drugs@FDA endpoint were both queried on the name in August 2026 and both returned no matches. The only United States approval located is veterinary: NADA 140-973, an oral syrup for horses containing 72.5 micrograms of clenbuterol hydrochloride per millilitre, indicated for the management of airway obstruction. Its label carries three statements that describe the position precisely. Not for use in humans. Do not use in horses intended for human consumption. Federal law prohibits the extralabel use of this drug in food animals. Registration as a human respiratory medicine does exist in several European and Asian countries, which is what the two ATC codes record.

Sport regulates it as an anabolic agent rather than a bronchodilator, and has had to build an unusual rule around it. On 20 May 2021 the World Anti-Doping Agency's Executive Committee approved a Minimum Reporting Level of 5 ng/mL for clenbuterol, ractopamine, zilpaterol and zeranol, given effect through Technical Letter TL23 on 1 June 2021. Below that urinary concentration an accredited laboratory reports an Atypical Finding rather than an adverse analytical finding, and the results management authority is required to investigate whether contaminated meat explains it. The rule exists because of the findings set out further down this page.

The one randomised trial in healthy people

Hostrup and colleagues published the first randomised placebo-controlled trial of clenbuterol in healthy humans in The Journal of Physiology in 2025. Eleven men aged 18 to 40 completed two two-week cycles, one of oral clenbuterol at 80 micrograms per day and one of placebo, separated by a three-week washout. Lean mass rose 0.91 kg against placebo, with a 95 per cent confidence interval of 0.02 to 1.81 kg, and muscle protein content in vastus lateralis biopsies rose with it. Fat mass did not change. That single null result sits against the largest body of claim attached to this compound.

Cardiorespiratory measures moved the other way. Maximal oxygen uptake fell 7 per cent and exercise capacity fell 4 per cent, both at P below 0.001, while sprint power output, left ventricular mass, intravascular blood volume and haemoglobin mass were unchanged. In the biopsies, 3-hydroxyacyl CoA dehydrogenase activity was repressed and oxidative phosphorylation complex V abundance fell. Protein kinase A activation and ribosomal protein S6 phosphorylation were both marked at the start of a cycle and declined across it, which is a measurement of tolerance developing inside two weeks rather than an inference about it.

An acute study by Jessen and colleagues in 2020 measured the metabolic side of the same molecule. Six young men were assessed before and 140 minutes after a single 80-microgram oral dose. Resting energy expenditure rose 21 per cent and fat oxidation rose 39 per cent, while carbohydrate oxidation did not change; circulating glucose, lactate, insulin and fatty acids all rose. Maximal voluntary contraction torque fell 4 per cent. The two studies are not in conflict. One measured substrate use over an afternoon, the other measured stored fat over a fortnight, and only the first moved.

What the trials in patients measured

Late-onset Pompe disease produced the longest controlled human exposure on record. Koeberl and colleagues ran a 52-week double-blind randomised placebo-controlled phase 1/2 study in thirteen participants already receiving enzyme replacement therapy, eleven of whom completed it. Six-minute walk distance increased by a mean of 16 metres, which did not reach significance at P equals 0.08, though the same change expressed as per cent of predicted performance did at P equals 0.03. Maximum inspiratory pressure rose 8 per cent, two functional scores improved, and glycogen content in the vastus lateralis was halved at week 52. No change in the placebo group reached significance.

Overweight and obesity produced the second randomised placebo-controlled human dataset, and it measured something different again. Van Lier and colleagues randomised fourteen adults aged 40 to 70 with a body mass index between 25 and 35 to four weeks of oral clenbuterol at 40 micrograms per day or to placebo, in a double-blind crossover registered as NCT04921306. Insulin-stimulated glucose uptake during a hyperinsulinaemic-euglycaemic clamp, measured by 18F-FDG PET-MRI, was 15 per cent higher in vastus lateralis at P equals 0.072 and 13 per cent higher in the hamstring at P equals 0.039. Brown adipose tissue uptake did not change, at P equals 0.720. Quadriceps uptake was the primary outcome, and it did not reach significance.

Spinal and bulbar muscular atrophy was studied by Querin and colleagues in twenty patients given oral clenbuterol at 0.04 mg per day for twelve months, of whom sixteen completed. Six-minute walk distance and forced vital capacity both increased between baseline and month twelve at P below 0.001, while Medical Research Council strength scores and the revised ALS Functional Rating Scale did not move. Serum creatine kinase rose. The paper carries a Classification of Evidence assigned by the journal under the American Academy of Neurology scheme: Class IV, the weakest tier. Neurology gives no reason for the class in the indexed abstract; this record's own reading is that the open-label design with no control arm accounts for it.

Amyotrophic lateral sclerosis produced the clearest signal on tolerability, and it was negative. Li and colleagues enrolled 25 participants in an open-label trial with no placebo and no randomisation. Twenty-four experienced adverse events, most often tremors, cramps, insomnia and spasticity, and fourteen withdrew early, thirteen of them because of adverse events. The authors reported slower functional decline during treatment than before it, and then stated plainly that the comparison is limited by sample size, dropout and the absence of blinding. ClinicalTrials.gov holds twelve registered studies naming clenbuterol as an intervention; four have posted results, the largest completed enrolment is 41 people, and two studies that have not reported carry enrolment targets of 90 and 72.

The heart-failure programme, and how it ended

Cardiology reached this compound through myocardial atrophy. George and colleagues gave oral clenbuterol to seven patients supported by a left ventricular assist device, up-titrated to 720 micrograms daily and continued for three months. Ejection fraction did not change. Left ventricular end-diastolic dimension increased from 4.73 to 5.24 centimetres at P below 0.01, and no change in myocyte size or collagen deposition was seen at explantation. Skeletal muscle moved instead: body weight rose from 75.5 to 79.2 kg, lean mass from 21.1 to 23.6 kg, and quadriceps maximal voluntary contraction from 37.0 to 45.8 kg. Creatine phosphokinase was elevated in four of the seven.

A multicentre attempt to reproduce the British recovery protocol in the United States was registered as NCT00585546, enrolled eighteen participants, and was terminated. The registry's whyStopped field reads, in full: No longer could obtain clenbuterol. The reason recorded is supply, not efficacy; the trial ended because the drug could no longer be obtained, and no efficacy result was reported. Nothing has replaced it, and no cardiac outcome trial of clenbuterol in any population appears in the registry.

What the record does not contain is a controlled measurement of cardiac structure under prolonged exposure in healthy people. The two-week crossover found left ventricular mass unchanged, which is a result about fourteen days and nothing longer. Every human cardiac finding beyond that comes from case reports of overdose, or from patients whose hearts were already failing.

Animals, and where the rat dose-response separated

The rodent literature is where the anabolic reputation was built, and the same experiment recorded where the response changed direction. Burniston and colleagues infused rats with clenbuterol across a thousand-fold range for fourteen days. At 10 micrograms per kilogram per day and above, protein content rose in the heart by 12 to 15 per cent, the soleus by 12 per cent, the plantaris by 18 to 29 per cent and the tibialis anterior by 11 to 22 per cent, with matching myofibre hypertrophy. At 100 micrograms and 1 milligram per kilogram, myocyte death appeared in soleus, diaphragm and plantaris, and the area fraction of collagen in the myocardium increased.

Bone was measured separately and moved in one direction only. Bonnet and colleagues gave clenbuterol at 2 mg per kilogram per day subcutaneously to twelve-week-old female Wistar rats for six weeks. The study ran three arms across 39 animals — clenbuterol, salbutamol at 4 mg per kilogram per day, and saline — so roughly thirteen rats per arm. Trabecular number fell 40.40 per cent and trabecular bone volume fell 42.85 per cent, both at P below 0.001, with lower bone mineral density and lower ultimate force on biomechanical testing. Muscle mass rose and fat mass fell in the same animals, and a fall in leptin accompanied the bone loss, which tracked fat mass rather than muscle mass. Salbutamol in the same experiment altered neither bone microarchitecture nor body composition.

Horses supply the only sustained exercise data in a large mammal. Kearns and McKeever divided 23 unfit Standardbred mares across four groups for eight weeks: clenbuterol at 2.4 micrograms per kilogram twice daily with exercise, clenbuterol alone, exercise alone, and control. Maximal oxygen uptake fell 6.2 per cent in the group given both clenbuterol and exercise, and time to exhaustion fell about 20 per cent in both clenbuterol groups. The clenbuterol-only group recorded no significant change in maximal oxygen uptake. Exercise alone raised maximal oxygen uptake 6.5 per cent and time to exhaustion 32.3 per cent. The training effect and the drug effect ran in opposite directions.

Contamination, and what a positive test means

Residues in edible tissue have been reaching people since at least 1992. Salleras and colleagues investigated 113 cases of poisoning in Catalonia that year: more than half of those affected recorded nervousness, tachycardia, muscle tremors, myalgia and headache, incubation ran from fifteen minutes to six hours, and symptoms lasted from ninety minutes to six days. Clenbuterol was detected in 47 urine samples at 11 to 486 parts per billion and in none of the serum samples. Illness was associated with eating veal liver at P below 0.0001, irrespective of how the liver had been cooked. Nobody died.

The scale of the problem for testing became visible in 2011. Thevis and colleagues reported that of 208 doping control samples collected during the FIFA U-17 World Cup in Mexico, 109 contained clenbuterol at 1 to 1556 picograms per millilitre, and 14 of 47 meat samples collected from team hotels contained it at 0.06 to 11 micrograms per kilogram. Only 5 of 24 teams returned samples with none, and at least one of those was reported to be on a strict no-meat diet. No player was sanctioned. The Minimum Reporting Level described earlier is the administrative answer to that dataset.

Exposure at population scale was quantified most recently in Taiwan. Liao and colleagues analysed spot urine from 1554 participants in the nationally representative 2019 Human BioMonitoring Program using isotope dilution online solid-phase extraction with tandem mass spectrometry. Clenbuterol was the most frequently detected beta-adrenergic agonist at 31.4 per cent, against 4.2 per cent for the legally permitted ractopamine, and against a zero detection rate in contemporaneous official market surveillance of meat. Detection was associated with red meat consumption at an adjusted odds ratio of 1.39, with a confidence interval of 1.08 to 1.79.

Recorded harms

Kumari and colleagues assembled the case literature systematically, searching four databases from 1990 to October 2021 and including 23 studies covering 24 athletes. Daily amounts reported across those cases ranged from 20 micrograms to 30 milligrams, mostly taken orally, a span of three orders of magnitude. Recorded events were supraventricular tachycardia, atrial fibrillation, hypotension, chest pain, myocardial injury, myocarditis, myocardial ischaemia, myocardial infarction, cardiomyopathy, hepatomegaly, hyperglycaemia and death. Cardiac complications were the most frequent category. Case series select for severity by construction, so this is a record of what has been reported, with no denominator behind it.

Within the controlled trials the pattern is milder. Tremors, cramps, insomnia and spasticity were the commonest events in the ALS cohort, where thirteen of 25 participants withdrew because of them. Creatine kinase rose in the spinal and bulbar muscular atrophy trial (PMID 23645595), creatine phosphokinase was elevated in four of seven device-supported patients (PMID 16962470), and the Pompe trial recorded mild elevations of creatine kinase among its transient minor adverse events (PMID 30025991). The two healthy-volunteer studies did not report a muscle enzyme measurement at all, so the record covers patients rather than every scale of exposure.

One finding about illicit supply belongs in a safety record. In a 2016 case series of ten patients hospitalised after heroin use in Virginia, clenbuterol was detected in all of them; the reported findings included a serum potassium nadir of 2.5 mEq/L, a lactate of 9.4 mmol/L, a glucose of 179 mg/dL and a peak creatine phosphokinase of 953 units/L, and all ten survived with supportive care (PMID 27431866). The exposure was an adulterant in the heroin rather than an intended dose, and what prompted testing was chest pain and adrenergic symptoms after heroin use.

What is not known

No phase 3 trial of clenbuterol exists in any indication. The twelve studies registered on ClinicalTrials.gov are small: the largest completed enrolment is 41 participants, two studies that have not reported carry enrolment targets of 90 and 72, four have posted results, one was withdrawn before enrolling and one was terminated with the reason recorded as no longer being able to obtain the drug. The longest controlled human exposure on record is 52 weeks in thirteen people with a rare metabolic myopathy. Everything asserted about physique or performance use rests on a single randomised crossover in eleven men over two weeks, which found no change in fat mass and a fall in maximal oxygen uptake. Body composition has never been measured in women taking it, and the two healthy-volunteer studies enrolled men only; the rat bone study used female animals only, so neither sex has a complete dataset. Cardiac structure under prolonged exposure in healthy people is uncharacterised. Left ventricular mass was unchanged at fourteen days, but the only sustained cardiac measurements in a large mammal come from eight weeks in horses, and the human cardiac literature beyond that is case reports of overdose and of adulterated illicit drugs. Bone has not been measured in any human study despite the rat work recording a 40 per cent loss of trabecular number at six weeks in an arm of about thirteen animals. The published human pharmacokinetics rest on a 1985 study that does not state its sample size, no absolute oral bioavailability figure could be traced to any primary source, and the enantiomers are dispositionally distinct without a human disposition study to describe how. Reproductive, developmental, carcinogenicity and chronic-exposure toxicology were not located in any species. Clenbuterol holds no human approval in the United States, material obtained outside a licensed supply chain has been documented as an adulterant in other drugs, and nothing published establishes a threshold below which harm in a person does not occur.

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