This material is supplied exclusively as a laboratory research chemical for in vitro scientific study. All descriptions and documentation are provided for informational and educational purposes only.
This compound is not approved for human or animal consumption, injection, ingestion, inhalation, topical use, or any other biological application. It must be handled only by qualified, trained personnel in a properly equipped laboratory.
This product is not a drug, supplement, food, cosmetic, or therapeutic agent, and it may not be rebranded, repackaged, or marketed as any such item. Misuse, mislabeling, or unauthorized application is strictly prohibited.
Nothing on this website constitutes medical advice, professional guidance, or a recommendation of use.
Note: AICAR does not use Smad signaling or ligand/receptor kinetics like myostatin-related peptides; instead, its biochemical relevance is AMPK activation, mitochondrial biogenesis, and metabolic gene expression. So the highly technical version will focus on AMPK pathway mechanics, second messengers, phosphorylation cascades, and downstream gene targets – the correct scientific domain.
AICAR (5-Aminoimidazole-4-carboxamide ribonucleotide) is an AMP analog and an established activator of the AMP-activated protein kinase (AMPK) pathway in metabolic research models. Inside cells, AICAR is converted to ZMP (AICA-ribotide), a synthetic analog of AMP. ZMP binds to the γ-subunit of AMPK, promoting allosteric activation and preventing dephosphorylation of the AMPK α-subunit at Thr172, the critical phosphorylation site for AMPK signaling.
Mechanism:
AICAR enters cells and is phosphorylated to ZMP
ZMP mimics rising AMP levels
ZMP binds the regulatory site of AMPK (γ-subunit)
AMPK becomes activated through:
Allosteric activation
Increased phosphorylation by LKB1 and CaMKKβ
Decreased dephosphorylation by phosphatases
Resulting signaling cascades studied:
Inhibition of mTORC1
Increased fatty-acid oxidation
Enhanced glucose uptake
Upregulation of mitochondrial biogenesis and oxidative capacity
Activated AMPK influences transcription factors and coactivators including:
✅ PGC-1α – mitochondrial biogenesis and oxidative phosphorylation
✅ SIRT1/SIRT3 coordination with AMPK for mitochondrial remodeling
✅ CPT1 and ACADs – fatty-acid β-oxidation genes
✅ GLUT4 – glucose transporter expression in metabolic models
✅ ACC (acetyl-CoA carboxylase) – phosphorylated and inhibited, reducing malonyl-CoA, enhancing fatty-acid entry into mitochondria
✅ TSC2 & Raptor phosphorylation – suppression of mTORC1 signaling
AICAR-mediated AMPK activation has been investigated in:
Glucose homeostasis models: increased glucose uptake via AS160 phosphorylation and GLUT4 translocation
Mitochondrial studies: induction of NRF1, NRF2, Tfam expression linked to mitochondrial replication
Lipid oxidation: upregulation of CPT1 and β-oxidation cycles
Autophagy research: ULK1 phosphorylation downstream of AMPK and mTOR inhibition
Energy stress simulations: ZMP accumulation mimics high AMP:ATP ratio without requiring caloric or hypoxic stress
AMPK activation triggers a broad phosphorylation cascade:
↑ p-AMPK (Thr172)
↓ p-ACC (Ser79) → disinhibits fatty-acid import into mitochondria
↑ p-TSC2 / p-Raptor → mTORC1 suppression
↑ p-ULK1 → autophagy initiation
↑ p-AS160 → GLUT4 translocation
These events make AICAR a powerful research tool in the controlled study of metabolic regulation and mitochondrial biology.
AICAR is supplied exclusively for laboratory, in-vitro scientific research.
It is not approved for human or animal use, medical treatment, or diagnostic procedures.
| Weight | N/A |
|---|---|
| Size | 50 Mg |
