Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Informational only. Not medical advice.INFORMATIONAL PLATFORM ONLY — NOT MEDICAL ADVICE, DIAGNOSIS, OR TREATMENT
Head-to-head comparison of AICAR and Sobetirome (GC-1) — mechanism, side effects, legal status, and pricing.
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."
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 Planned human trials in X-linked adrenoleukodystrophy were withdrawn before enrollment; all neurological data are preclinical only.
AICAR
Sobetirome (GC-1)
Category
Legal Status
Mechanism
Side Effects
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
AICAR
Sobetirome (GC-1)
COA corpus from Disclosed Labs — independently tested batches only.
AICAR
3
COAs
99.3%
Avg purity
3
Labs
Sobetirome (GC-1)
1
COAs
97.3%
Avg purity
1
Labs
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.
Key references
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data are limited to Phase 1 trials in healthy volunteers conducted by QuatRx Pharmaceuticals; company press releases (not peer-reviewed) reported LDL-C reductions up to 22% (single-ascending-dose, 1–450 mcg) and 41% (multiple-ascending-dose, 10–100 mcg/day × 14 days) with no significant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 Two planned human trials in X-linked adrenoleukodystrophy (NCT01787578, NCT03196765) were withdrawn before enrolling any participants; zero human neurological efficacy data exist.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.
AICAR 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
Disclosed Labs