Rapamycin (Sirolimus)
Selective inhibitor of mTORC1 at low doses, suppressing the nutrient-sensing pathway that drives cellular growth and proliferation. Periodic inhibition upregulates autophagy, reduces senescent cell burden, and mimics caloric restriction signaling. At higher continuous doses, mTORC2 inhibition causes immunosuppression and metabolic disruption.
Three tiers ordered by aggressiveness. Tier chips on every OPTIMIZE intervention let you filter the catalog by your evidence tolerance.
- fasting-glucose
- hba1c
- fasting-insulin
- lipid-panel
- hdl
- ldl
- triglycerides
- wbc
- creatinine
- egfr
- active-infection
- immunocompromised
- hepatic-impairment
- uncontrolled-diabetes
- organ-transplant-recipient
- PMID:19587680Rapamycin fed late in life extends lifespan in genetically heterogeneous mice — Nature, 2009
- PMID:25540326mTOR inhibition improves immune function in the elderly — Sci Transl Med, 2014
- PMID:31806903Rapamycin for longevity: opinion article — Aging, 2019
Rapamycin is the most interesting molecule in longevity science and the most misunderstood. Discovered in Easter Island soil in 1972. Used for decades to prevent organ rejection at high continuous doses. The longevity application is the opposite paradigm. Low dose. Pulsed. Weekly. The goal is selective mTORC1 inhibition without touching mTORC2. The difference between those two targets is the difference between enhanced autophagy and immunosuppression. Dose, timing, and periodicity are everything. This is not a molecule you eyeball. Tier 2 for longevity because the human RCTs for healthspan extension are still running. The mouse data is the most robust lifespan extension ever recorded in a mammalian model.
This is not medical advice
Discuss with a licensed clinician before starting, stopping, or changing any compound. This page documents what the research literature describes — it is not a prescription.
See Rapamycin (Sirolimus) in a protocol matched to you