Overview

• Queen Mary University of London researchers report in Communications Biology that the bi‑steric TOR inhibitor prolongs chronological lifespan in fission yeast.
• The compound acts primarily on TORC1, slowing aspects of growth while extending survival in the yeast model.
• Genome-wide and cell biology screens identify agmatinases as a metabolic feedback mechanism that restrains TOR activity to promote longevity.
• Agmatinase loss sped up cell growth but caused premature aging, while agmatine or putrescine supplementation extended lifespan under specific conditions.
• The team notes potential implications for combining TOR-targeting drugs with dietary or microbial interventions and urges caution about agmatine supplements, which lack validation for anti-aging in animals or humans.