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AICAR Overview, Dosing & Safety | Peptide Database

AICAR (Acadesine) 5-Aminoimidazole-4-carboxamide Ribonucleotide | AMPK Activator Community Research Join others researching AICAR — share findings, ask questions, and learn from real experiences AICAR is a cell-permeable nucleoside analog that activates AMP-ac

Written by Peptide Therapy Guide Editorial Team
For education only

This guide cannot diagnose a condition or recommend a personal treatment plan. Discuss medical questions with a qualified professional.

AICAR (Acadesine)

5-Aminoimidazole-4-carboxamide Ribonucleotide | AMPK Activator

Community Research

Join others researching AICAR — share findings, ask questions, and learn from real experiences

AICAR is a cell-permeable nucleoside analog that activates AMP-activated protein kinase (AMPK), a key regulator of cellular energy homeostasis. Originally studied for cardiac ischemia protection, it gained attention as an 'exercise mimetic' due to its metabolic effects.

Once inside cells, AICAR is phosphorylated to ZMP, which mimics AMP and activates AMPK. This triggers metabolic pathways typically activated during exercise: increased glucose uptake, fatty acid oxidation, and mitochondrial biogenesis.

Molecular Data

Research Indications

Directly activates the master metabolic regulator through ZMP accumulation.

Increases fat burning through AMPK-mediated pathways.

Enhances glucose uptake independent of insulin in some tissues.

Animal studies showed increased running endurance; human data limited.

AMPK activation promotes new mitochondria formation over time.

Original clinical interest; may protect heart tissue during reduced blood flow.

Dosing Protocols

Subcutaneous injection once daily. Progressive dosing protocols are common to assess tolerance.

Standard Protocol

1-3mg

Daily

SubQ

Gradual Introduction

1mg → 2mg → 3mg

Daily, titrating over 4 weeks

Advanced Protocol

3-5mg

Daily for 8-12 weeks

Reconstitution Instructions

AICAR lyophilized powder (typically 50mg vial)

Bacteriostatic water (3.0mL recommended)

Insulin syringes (29-31 gauge)

Alcohol swabs

1 Allow vial to reach room temperature

2 Clean rubber stopper with alcohol swab

3 Add 3.0mL bacteriostatic water for ~16.7mg/mL concentration

4 Inject slowly along vial wall to avoid foaming

5 Gently swirl to dissolve; never shake

6 Label with date and store refrigerated at 2-8°C

7 Use within 4 weeks of reconstitution

Interactions

What to Expect

Side Effects & Safety

Common Side Effects

Injection site reactions

Mild fatigue during adaptation

Potential hypoglycemia

Stop Signs - Discontinue if:

Severe hypoglycemia symptoms

Lactic acidosis symptoms (muscle pain, weakness, difficulty breathing)

Unusual cardiac symptoms

Severe fatigue or weakness

Contraindications

Diabetes (risk of hypoglycemia)

Cardiac conditions

Pregnancy or breastfeeding

Competitive athletes (WADA prohibited)

Quality Checklist

Good Signs

White to off-white lyophilized powder

Clear solution after reconstitution

Certificate of Analysis with purity testing

Warning Signs

Slight yellowing may occur but should dissolve clearly

Bad Signs

Discolored or clumped powder

Cloudy solution after reconstitution

Particulate matter visible

Frequently Asked Questions

Does AICAR actually work as an 'exercise mimetic' in humans?

Animal studies show AICAR increased running endurance by 44% without training. However, this was mice, not humans. Humans have never been adequately tested for AICAR's endurance effects, so calling it an exercise mimetic is speculative. The compound does activate AMPK and increase fat oxidation, but real-world performance gains in people are unproven.

Is AICAR banned in sports and why?

Yes, AICAR is WADA prohibited. While it's not anabolic per se, it provides competitive advantage through enhanced metabolic efficiency and endurance. Athletes competing under WADA rules must avoid it entirely due to testing likelihood and strict liability regulations.

What's the risk of hypoglycemia on AICAR if I'm not diabetic?

AICAR increases glucose uptake independent of insulin in some tissues, creating theoretical hypoglycemia risk especially in non-diabetics with normal insulin sensitivity. Diabetics face more serious risk, which is why AICAR is contraindicated in diabetes. Monitor blood glucose closely, particularly during initial doses.

How does AICAR differ from GW501516 for metabolic enhancement?

AICAR activates AMPK, the master metabolic regulator, increasing fatty acid oxidation and glucose uptake. GW501516 is a PPARδ agonist with different downstream effects. They're often stacked because they target complementary pathways—AMPK plus PPARδ activation produces synergistic metabolic effects.

References

Review of AMPK role in exercise-induced metabolic adaptations and AICAR as pharmacological activator.

Mice treated with AICAR showed 44% increase in running endurance without training.

Disclaimer

This information is for educational and research purposes only. Consult a healthcare professional before use.

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Research context

Read sources and limitations before applying a claim.

Research Indications

FDA-approved for treatment of essential hypertension as monotherapy or in combination with other antihypertensives. Provides consistent 24-hour blood pressure reduction. Particularly effective for AAS-induced hypertension where elevated blood pressure is driven by RAAS activation and increased erythropoiesis. FDA-approved for reduction of cardiovascular morbidity in patients at high risk. The ONTARGET trial demonstrated non-inferiority to ramipril for the composite of cardiovascular death, MI, stroke, and hospitalization for heart failure in over 25,000 high-risk patients. Angiotensin II receptor blockade counteracts the pro-hypertrophic and pro-fibrotic effects of supraphysiological androgen levels on the myocardium. Preclinical and observational data support the use of ARBs to attenuate left ventricular hypertrophy in steroid users. Widely recommended in harm reduction protocols. Reduces intraglomerular pressure and proteinuria by blocking angiotensin II-mediated efferent arteriolar constriction. Slows progression of chronic kidney disease, particularly in patients with diabetic nephropathy or hypertensive nephrosclerosis. Relevant for AAS users where elevated blood pressure and NSAID co-use may compromise renal function. Telmisartan's partial PPAR-gamma agonism improves insulin sensitivity without the weight gain associated with full PPAR-gamma agonists like pioglitazone. May reduce the risk of new-onset diabetes in hypertensive patients. The metabolic benefit is particularly relevant for users of compounds that impair glucose tolerance (e.g., growth hormone, trenbolone).

Source: peptide-db.com ↗

Community Research

Join others researching Tamoxifen — share findings, ask questions, and learn from real experiences Tamoxifen is a first-generation selective estrogen receptor modulator (SERM) that has been in clinical use since the 1970s. It is FDA-approved for the treatment and prevention of estrogen receptor-positive breast cancer and remains one of the most widely prescribed cancer therapies worldwide. In the context of performance enhancement, tamoxifen is used extensively for post-cycle therapy (PCT) to restore the hypothalamic-pituitary-testicular axis after suppression from anabolic steroids, and for on-cycle gynecomastia prevention by blocking estrogen receptors in breast tissue. Tamoxifen acts as an estrogen antagonist in breast and hypothalamic tissue while functioning as a partial estrogen agonist in bone, the uterus, and the cardiovascular system. Its active metabolite endoxifen, produced via CYP2D6 metabolism, is responsible for much of its pharmacological activity. Tamoxifen competitively binds to estrogen receptors (primarily ERalpha) and exerts tissue-selective effects depending on the local coactivator and corepressor environment. In breast tissue and the hypothalamus, tamoxifen acts as an estrogen antagonist, blocking estradiol-mediated signaling. At the hypothalamus and anterior pituitary, this antagonism removes estrogen-driven negative feedback on GnRH secretion, leading to increased pulsatile GnRH release and subsequent elevation of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). The rise in LH stimulates Leydig cell testosterone production, which is the basis for its use in post-cycle therapy. In bone tissue, tamoxifen acts as a partial estrogen agonist, providing a protective effect on bone mineral density. Tamoxifen is a prodrug that requires hepatic metabolism via CYP3A4 and CYP2D6 to generate its active metabolites, particularly endoxifen, which has approximately 100-fold greater affinity for the estrogen receptor than the parent compound.

Source: peptide-db.com ↗
Practical and safety references

These excerpts are educational, not personalised medical instructions.

Dosage reference

Is survodutide's 6-day half-life long enough for once-weekly dosing?

Yes, the ~6-day half-life allows effective once-weekly dosing because peak levels remain therapeutic throughout the week. This contrasts with semaglutide (7-day half-life) - survodutide's slightly shorter half-life still covers the weekly interval adequately.

Source: peptide-db.com ↗
Side effects

Common Side Effects

Severe hepatic stress (elevated ALT, AST, GGT, bilirubin) Pronounced aggression and irritability HDL cholesterol suppression and LDL elevation Elevated blood pressure Headaches (frequently reported, may be related to blood pressure changes) Suppression of endogenous testosterone production Oily skin and acne Decreased appetite (potentially related to liver stress)

Source: peptide-db.com ↗
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