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Head-to-head comparison of 3,5-Diiodo-L-thyronine (3,5-T2) and AICAR — mechanism, side effects, legal status, and pricing.
3,5-Diiodo-L-thyronine (3,5-T2) is a non-peptide endogenous iodothyronine produced by deiodination of T3 and T4. It is not an approved drug and has no registered human clinical trials as a study intervention. The only direct human-administration data come from a single 2-person case report. WADA/anti-doping status for 3,5-T2 specifically is unconfirmed; a 2019 secondary source suggested thyroid hormones as a class were not prohibited, but no current primary WADA citation was found.
AICAR (acadesine / AICA riboside) is a purine nucleoside analog and AMP-mimetic — not a peptide — that activates AMPK. Studied in registered human trials under the name acadesine (for cardioprotection and leukemia, not performance), it is not FDA-approved for any indication and is WADA-prohibited at all times. It is sold on the gray market as an "exercise mimetic."
3,5-Diiodo-L-thyronine (3,5-T2)
AICAR
Category
Legal Status
Mechanism
Side Effects
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3,5-Diiodo-L-thyronine (3,5-T2)
No pricing data yet.
Check 3,5-Diiodo-L-thyronine (3,5-T2) prices →AICAR
COA corpus from Disclosed Labs — independently tested batches only.
3,5-Diiodo-L-thyronine (3,5-T2)
2
COAs
97.4%
Avg purity
2
Labs
AICAR
3
COAs
99.3%
Avg purity
3
Labs
No approved human drug or registered interventional clinical trial exists. The only direct human-administration data are from a single 2-person case report: oral 3,5-T2 (~5 μg/kg body weight) for 28 days reportedly raised resting metabolic rate by ~15% and lowered body weight by ~4 kg, with no significant changes in principal clinical parameters and no observed side effects. Endogenous 3,5-T2 has been measured in healthy human serum (~0.22–0.33 nM) and as a metabolite in liothyronine (T3) pharmacokinetic trials. Preclinical rodent studies show 3,5-T2 rapidly increases resting metabolic rate (faster than T3), reduces adiposity in high-fat-diet models by increasing fat oxidation, stimulates liver and skeletal muscle mitochondrial bioenergetics, and activates AMPK in skeletal muscle. One rat regimen (25 μg/100g BW, 4 weeks) showed no HPT-axis suppression or cardiac hypertrophy at that specific dose/duration; however, one mouse model (unsaturated-fat diet) showed no improvement in NAFLD or insulin sensitivity.
Key references
As acadesine, AICAR was tested in registered human trials by IV infusion: the large RED-CABG cardioprotection trial (JAMA 2012) was stopped for futility, and a Phase I/II study in relapsed/refractory CLL established 210 mg/kg IV as the optimal dose. No human trial evaluated AICAR for exercise, fat loss, or longevity, and no validated non-IV dosing exists. Not FDA-approved; not a peptide.
3,5-Diiodo-L-thyronine (3,5-T2) and AICAR are both in the Metabolic category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
Contraindications
Lab Testing