Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of Roxadustat and Sobetirome (GC-1) — mechanism, side effects, legal status, and pricing.
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.
Sobetirome (GC-1) is a non-peptide small-molecule thyromimetic that selectively activates thyroid hormone receptor beta (TRβ) over TRα, designed to lower cholesterol and triglycerides without the cardiac effects of natural thyroid hormone. It completed Phase 1 trials in healthy volunteers for dyslipidemia (discontinued), but has no FDA or EMA approval and no validated human dose for any indication. Planned human trials in X-linked adrenoleukodystrophy were withdrawn before enrollment; all neurological data are preclinical only.
Roxadustat
Sobetirome (GC-1)
Category
Legal Status
Mechanism
Side Effects
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Roxadustat
No pricing data yet.
Check Roxadustat prices →Sobetirome (GC-1)
COA corpus from Disclosed Labs — independently tested batches only.
Roxadustat
3
COAs
99.8%
Avg purity
2
Labs
Sobetirome (GC-1)
1
COAs
97.3%
Avg purity
1
Labs
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.
Human data are limited to Phase 1 trials in healthy volunteers conducted by QuatRx Pharmaceuticals; company press releases (not peer-reviewed) reported LDL-C reductions up to 22% (single-ascending-dose, 1–450 mcg) and 41% (multiple-ascending-dose, 10–100 mcg/day × 14 days) with no significant heart-rate or TSH change. Development for dyslipidemia was discontinued and no Phase 2/3 data exist. Two planned human trials in X-linked adrenoleukodystrophy (NCT01787578, NCT03196765) were withdrawn before enrolling any participants; zero human neurological efficacy data exist. In Abcd1 knockout mice (X-ALD model), intraperitoneal dosing (0.1–1.0 mg/kg/day, 7–28 days) lowered serum and tissue very-long-chain fatty acid (VLCFA) levels; chronic oral dosing (0.4–2.0 mg/kg, 11–18 weeks) modestly reduced brain C26 VLCFA by 13–24% after 12 weeks, though the higher dose caused up to 20% body-weight loss requiring early termination. In experimental autoimmune encephalomyelitis mice, sobetirome reduced clinical disease severity, axonal degeneration, and oligodendrocyte loss versus vehicle controls.
Key references
Roxadustat and Sobetirome (GC-1) 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