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 Amlexanox — mechanism, dosing, 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."
Amlexanox is a non-peptide small-molecule 2-amino-chromeno[2,3-b]pyridine-3-carboxylic acid derivative (CAS 68302-57-8, MW 298.29 g/mol). Originally approved in 1996 as a topical oral paste for aphthous ulcers (FDA, now discontinued) and in Japan for allergic conditions, it was later characterized as a selective ATP-competitive inhibitor of the non-canonical IκB kinases TBK1 and IKKε. It is NOT approved for any metabolic, obesity, or performance indication; it is sold by research-chemical vendors labeled research-use-only and promoted off-label by biohacking outlets for fat loss. No validated human dose exists for metabolic applications.
AICAR
Amlexanox
Category
Legal Status
Mechanism
Dose Range
Route
COA-verified vendors · trust score ≥70 required · single-vial price — bulk/bundle deals may be lower
AICAR
Amlexanox
COA corpus from Disclosed Labs — independently tested batches only.
AICAR
3
COAs
99.3%
Avg purity
3
Labs
Amlexanox
1
COAs
99.6%
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
In diet-induced obese and ob/ob mice, amlexanox treatment increased energy expenditure via thermogenesis, produced weight loss, improved insulin sensitivity, and decreased hepatic steatosis; these metabolic benefits require intact FGF21 signaling. In LDL-receptor-knockout mice on Western diet, amlexanox reduced triglycerides, cholesterol, circulating monocytes/eosinophils, macrophage plaque accumulation, and atherosclerotic lesion size. One randomized, double-blind, placebo-controlled proof-of-concept trial in 42 obese patients with type 2 diabetes and NAFLD showed statistically significant HbA1c and fructosamine reductions versus placebo, with a responder subgroup showing improved insulin sensitivity and reduced hepatic fat; rash occurred in several participants (two required biopsy). No obesity or diabetes indication has been approved by any regulator.
AICAR and Amlexanox 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.
Frequency
Dosing Notes
Side Effects
Contraindications
Lab Testing
Disclosed Labs