In short
mTOR inhibition is a therapeutic strategy of pharmacologically reducing mTOR pathway signaling, most commonly with rapamycin or its analogs (rapalogs), based on the reproducible finding that this extends lifespan in multiple model organisms.
Rapamycin binds the protein FKBP12, and this complex then inhibits mTORC1. At the high, continuous doses used clinically for organ transplant immunosuppression, this produces significant side effects including impaired wound healing, mouth ulcers, elevated cholesterol and triglycerides, and increased infection risk, because mTORC1 is also important for normal immune function.
The longevity-research interest is in whether lower, intermittent dosing regimens can capture the lifespan-extension signal seen in mice — the NIA Interventions Testing Program has repeatedly shown rapamycin extends median and maximal lifespan in genetically heterogeneous mice, including when started relatively late in life — while avoiding the side-effect burden of transplant-level dosing. Some human research, including a study by Mannick et al. (2014, Science Translational Medicine) using an mTOR-inhibitor combination, found improved influenza vaccine antibody response in older adults, a biomarker suggesting improved immune function rather than impairment at that lower dose.
No human trial has tested whether low-dose, intermittent rapamycin extends human lifespan or meaningfully delays age-related disease onset — the human data that exists covers biomarkers, immune function, and safety at various dosing schedules, mostly in small or short-duration studies, alongside the much larger body of long-term safety data from transplant medicine at higher doses. Off-label longevity prescribing of low-dose rapamycin, which some clinics offer, is therefore built on a strong animal-model rationale and early-stage human safety/biomarker data, not on a completed human efficacy trial for lifespan or healthspan.