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Head-to-head comparison of 3,5-Diiodo-L-thyronine (3,5-T2) and Roxadustat — 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.
Roxadustat (Evrenzo) is a small-molecule HIF-prolyl-hydroxylase inhibitor — not a peptide — that raises endogenous erythropoietin. It is an approved prescription drug for anemia of chronic kidney disease in China, Japan, and the EU, but the US FDA rejected it over safety signals. Because it boosts EPO/hemoglobin, it is diverted to the gray market for endurance doping and is WADA-prohibited at all times.
3,5-Diiodo-L-thyronine (3,5-T2)
Roxadustat
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 →Roxadustat
No pricing data yet.
Check Roxadustat prices →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
Roxadustat
3
COAs
99.8%
Avg purity
2
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
Roxadustat is supported by extensive human data as an approved anemia drug (China 2018, Japan 2019–2020, EU 2021 as Evrenzo) with numerous Phase 2/3 CKD trials. The US FDA advisory committee voted against approval in July 2021, citing thrombosis, seizures, infections, and mortality signals. No validated recreational or performance dose exists. Not FDA-approved; not a peptide.
3,5-Diiodo-L-thyronine (3,5-T2) and Roxadustat 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