AICAR 50 mg

AICAR 50 mg is a research peptide studied as an AMPK activator for metabolic research. It was clinically investigated for cardioprotection during CABG surgery and for chronic lymphocytic leukemia, but neither program resulted in FDA approval. It has no approved human use and is sold strictly for laboratory research purposes.

No established human dosage exists for AICAR in fitness or performance contexts. In clinical trials, it was administered intravenously at doses ranging from 0.1 mg/kg/min (CABG) to 210 mg/kg (CLL). In non-medical community contexts, subcutaneous doses of 10-50 mg daily or every other day are referenced. These community doses are roughly 500 times below animal study levels and are not supported by human clinical data.

AICAR has no relationship to the hypothalamic-pituitary-gonadal axis and is not part of any post-cycle therapy protocol. Its research focus has been on metabolic and cardiovascular endpoints, not hormonal recovery. PCT compounds such as Clomid and Nolvadex address entirely different biological systems.

AICAR is a cell-permeable nucleoside analog that is phosphorylated intracellularly to ZMP, which mimics AMP and activates AMPK. AMPK activation triggers metabolic pathways associated with exercise, including increased glucose uptake, fatty acid oxidation, and mitochondrial biogenesis. Some effects of AICAR are AMPK-independent, suggesting additional targets.

AICAR has a half-life of approximately 2-3 hours. In animal studies, metabolic effects were observed over days to weeks of treatment. In the mouse endurance study, effects were observed after a 4-week treatment period. No human data exists on the time course of AICAR effects for fitness or performance applications.

There is no single AMPK activator that is universally best. AICAR is a research tool commonly used to study AMPK biology. Other AMPK activators like metformin and A769662 work through different mechanisms. AICAR's lack of FDA approval and its WADA-prohibited status limit its legitimate use to laboratory research.

AICAR and GW501516 work through different mechanisms. AICAR activates AMPK by mimicking AMP, while GW501516 is a PPARδ agonist that modulates gene expression related to fatty acid oxidation. Both are WADA-prohibited substances and have been investigated for metabolic effects. AICAR's mechanism is more direct and acute, while GW501516's effects are mediated through transcriptional changes.

AICAR and MOTS-C have different mechanisms. MOTS-C is a mitochondrial-derived peptide that acts catalytically on the folate-methionine cycle, causing AICAR to accumulate endogenously. AICAR, when administered directly, activates AMPK more bluntly. MOTS-C is described as more "surgical" in comparison, targeting tissues where it naturally distributes.

No human dosing standards exist for AICAR in fitness contexts. The 50 mg vial strength is a research quantity. In animal studies, AICAR was administered at 0.5 mg/g/day, which for a 70 kg human would be approximately 35,000 mg daily—far beyond the 50 mg vial content. Community doses of 10-50 mg are extrapolated from animal studies but are roughly 500 times below the animal study levels on a body-weight basis.

AICAR 50 mg is labeled at 50 mg of AICAR per vial. It is supplied as a lyophilized powder in a 2 mL vial, requiring reconstitution before laboratory use.

Yes. Hyperuricemia is the most consistently reported adverse effect of AICAR in clinical trials. In the CABG meta-analysis, hyperuricemia occurred in 5.1% of acadesine-treated patients compared to 0.7% of placebo patients (OR 7.32, p < 0.001). AICAR metabolism increases uric acid burden. Individuals with a history of hyperuricemia or gout may be particularly at risk.

No. AICAR has never been approved by the FDA or any regulatory authority for human use. Its most advanced clinical development program (cardioprotection in CABG surgery) was completed in the 1990s and did not result in approval. As of April 2026, no active IND for AICAR in metabolic, endurance, or performance indications is publicly registered.