Liothyronine (T3, Cytomel)
Synthetic T3 (3,5,3'-triiodothyronine), Pfizer 1956 FDA-approved hypothyroidism Rx (Cytomel). Cutting-cycle off-label thermogenic +10-30% REE via direct mitochondrial β-oxidation + Na/K-ATPase upregulation; WADA in-competition banned for non-Rx athletes.
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WHAT IS LIOTHYRONINE (T3, CYTOMEL)?
Detailed overview
Liothyronine (Cytomel) is the synthetic form of endogenous T3 (3,5,3'-triiodothyronine), the pharmacologically active form of thyroid hormone. With FDA approval since 1956 by Pfizer, it is primarily indicated for hypothyroidism where T4 monotherapy fails to produce full remission of cognitive symptoms (Bunevicius 1999 NEJM PMID 9989958 is the classic T3 add-on trial). 70 years of clinical literature plus documented bodybuilding off-label use since the 1980s (Hochberg 1989). T3 acts as a nuclear TR-α and TR-β receptor agonist, triggering direct gene-transcription activation that raises tissue metabolic rate by 10-30% through the nuclear-receptor cascade. The direct mechanism includes mitochondrial β-oxidation upregulation plus Na/K-ATPase density elevation in skeletal muscle, raising resting energy expenditure (REE). In AAS cutting context the T3 cycle (25-75 μg/day, 12.5 μg titration step) is used to balance muscle retention with fat-burning; however, hypothyroid shutdown risk is high (endogenous TSH suppression is dose-dependent, with >100 μg/day for 12+ weeks chronic carrying potential secondary hypothyroidism risk). The WADA list places T3 under S4.5 thyroid hormone modulator, in-competition banned for non-Rx athletes (NADA Switzerland 2023, USADA 2024 update). T4 vs T3: T4 has slower on/off plus a 7-day half-life enabling slow titration; T3 has a 24-hour half-life and fast action but sudden endogenous TSH suppression.
Mechanism of action
Nuclear TR-α + TR-β receptor agonist, gene-transcription activation, +10-30% REE
Dosing
Clinical 25-50 μg/day; off-label cutting-cycle 25-75 μg/day, titration 12.5 μg/step
Half-life
~24 hours (steady-state within 7 days)
Onset
Metabolic-rate increase 24-48 hours, fat-loss effect 1-2 weeks
Legal status
FDA + EMA Rx (hypothyroidism), registered in HU + PL. WADA: S4.5 in-competition banned for non-Rx athletes.
Data console
Lab data
Safety
Side effects, stop signs, contraindications
Side effects · 7
- Tachycardia, palpitations and atrial fibrillation: T3 directly raises heart rate and myocardial oxygen demand; overdosing can trigger arrhythmias (notably atrial fibrillation).
- Endogenous HPT-axis (TSH) suppression and iatrogenic secondary hypothyroidism: exogenous T3 dose-dependently suppresses your own TSH output, causing rebound hypothyroidism and slow recovery after longer or high-dose use.
- Thyrotoxicosis syndrome on overdose: hyperthermia, sweating, heat intolerance, marked unintended weight and muscle loss, since T3 at high doses is protein-catabolic.
- Tremor, anxiety, irritability and insomnia: the increased adrenergic tone and metabolic rate cause dose-dependent neuropsychiatric symptoms.
- Reduced bone density (osteoporosis risk): chronic high-dose use (>50 μg/day, >1 year) accelerates bone turnover and lowers bone mineral density.
- Increased SHBG and lower free testosterone: T3 raises sex-hormone-binding globulin, reducing the free testosterone fraction even alongside an AAS stack.
- Disturbed glucose metabolism and hypoglycemia risk: T3 increases glucose turnover, so combined with insulin or oral antidiabetics hypoglycemia can occur, especially during dose titration.
Contraindications · 7
- Pre-existing cardiac arrhythmia (atrial fibrillation, ventricular tachycardia): absolute contraindication, as T3 raises heart rate and can provoke life-threatening arrhythmia.
- Untreated adrenal insufficiency: thyroid hormone raises the metabolic demand for cortisol and can precipitate an adrenal crisis without cortisol replacement.
- Coronary artery disease, severe angina or recent myocardial infarction: relative/absolute contraindication due to increased myocardial oxygen demand and ischemia risk.
- Hashimoto autoimmune thyroiditis: contraindicated for off-label cutting use, as anti-TPO and anti-Tg titers can rise and the risk of autoimmune flare is high.
- Pheochromocytoma: absolute contraindication, as the heightened adrenergic tone can provoke a hypertensive crisis.
- Pregnancy and breastfeeding for off-label weight-loss purposes: prohibited, as a thyrotoxic state harms the fetus; only legitimate for diagnosed hypothyroidism under endocrinologist supervision.
- Type 1 diabetes mellitus: relative contraindication, as combining T3 with insulin disrupts glucose control and can cause hypoglycemia.
Related Performance Compounds
Same therapeutic category
Studies
Related research and clinical findings
Thyroxine vs thyroxine plus triiodothyronine in treatment of hypothyroidism after thyroidectomy for Graves' disease.
Bunevicius R, Jakuboniene N, Jurkevicius R, Bunevicius A, Lasas L, Prange AJ Jr
Discontinuation of levothyroxine therapy in patients with subclinical hypothyroidism: a pilot randomized clinical trial.
Maraka S, Owen RR, Singh Ospina NM
Thyroid Hormones and Cardiovascular Function and Diseases.
Razvi S, Jabbar A, Pingitore A, Danzi S, Biondi B, Klein I, Peeters R, Zaman A, Iervasi G
Acute Effects of Liothyronine Administration on Cardiovascular System and Energy Metabolism in Healthy Volunteers.
Chen S, Wohlford GF, Vecchie' A
Factitious thyrotoxicosis and thyroid hormone misuse or abuse.
Persani L, dell'Acqua M, Ioakim S, Bonomi M
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The information here is for educational and scientific purposes only. Performance-enhancing compounds (AAS, prohormones, stimulants, doping agents) are illegal without prescription in Hungary and most of the EU, and carry serious health and legal risks. WADA bans them in competitive sport. This is NOT a usage guide, and we do not encourage any illegal use. If you do use them, medical supervision and regular bloodwork are ESSENTIAL. Severe endocrine, cardiovascular, hepatic and psychiatric side effects are possible.