DOI: 10.11648/j.ajcbe.20261001.12 ISSN: 2639-9989

A Quantum-Biochemical Model of AA-5-HT-Induced Cytotoxicity in HL-60 Cells via FAAH Inhibition and Cannabinoid Receptor–Mediated Signal Interference

Atakuru Paulin
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Acute promyelocytic leukemia (APL) remains one of the most aggressive hematological malignancies, necessitating the discovery of novel therapeutic agents with improved efficacy and reduced toxicity. N-arachidonoyl-5-hydroxytryptamine (AA-5-HT), a hybrid indole–fatty acid amide compound isolated from Dialium corbisieri , has demonstrated potent cytotoxic activity in HL-60 leukemia cells, characterized by G 1 phase cell cycle arrest at low micromolar concentrations (2.3µM). Despite these promising findings, its mechanism of action remains incompletely understood. Here, we propose a quantum-biochemical hypothesis integrating molecular pharmacology with principles derived from quantum theory to explain AA-5-HT-induced cytotoxicity. We hypothesize that AA-5-HT inhibits fatty acid amide hydrolase (FAAH), leading to accumulation of anandamide (AEA), which in turn activates Gi/o-coupled cannabinoid receptors (CB 1 /CB 2 ). This activation suppresses the PI3K/AKT signaling pathway, resulting in decreased AKT phosphorylation, upregulation of cyclin-dependent kinase inhibitors (p21, p27), reduced retinoblastoma protein phosphorylation, and consequent G 1 arrest. From a quantum-biochemical perspective, AA-5-HT acts as a perturbator that shifts intracellular signaling probabilities, promoting destructive interference of pro-survival pathways and stabilizing a non-proliferative cellular state. This framework provides a novel conceptual model for understanding anticancer mechanisms and suggests new experimental directions for validating AA-5-HT as a therapeutic candidate.

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