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Sirolimus (Rapamycin)

Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.

IDDRUG-SIROLIMUS
TypeDrug
Aliases
RapamuneSirolimusСіролімус (Рапаміцин)
Statusreviewed 2026-05-04 | pending_clinical_signoff
DiseasesDIS-LAM
SourcesSRC-MILES-MCCORMACK-2011

Drug Facts

ClassmTOR inhibitor (mTORC1 — rapamycin analog, first-generation)
MechanismSirolimus (rapamycin) binds FKBP-12 and the sirolimus-FKBP12 complex inhibits mTORC1, blocking downstream S6K1 and 4E-BP1 signaling → reduced cell proliferation, protein synthesis, and autophagy suppression. In LAM, TSC1/TSC2 loss leads to mTORC1 hyperactivation → excessive LAM cell proliferation. MILES trial: sirolimus stabilized FEV1, improved functional performance, and reduced VEGF-D. FDA-approved for LAM 2015.
Typical dosingLAM (MILES trial dosing): target trough level 5–15 ng/mL; start 2 mg PO once daily and titrate. Monitor trough levels at 1–2 weeks after each dose change. VEGF-D ≥800 pg/mL at baseline predicts response.
Ukraine registeredTrue
NSZU reimbursedFalse
Ukraine last verified2026-05-04

Warnings

Notes

MILES trial (McCormack 2011 NEJM): sirolimus vs placebo in LAM with FEV1 <70% predicted or declining lung function (n=89). Primary endpoint: FEV1 rate of change — sirolimus arm stable (±1.0 mL/mo) vs placebo declining (−12 mL/mo, p<0.001). Secondary: improved DLCO, 6MWD, VEGF-D reduction. FDA approved sirolimus for LAM 2015. Note: benefits are stabilizing (not curative) and may not persist after stopping. Serum VEGF-D ≥800 pg/mL identifies patients most likely to respond and can also confirm LAM diagnosis (avoiding biopsy). Everolimus (another mTORC1 inhibitor) is used for TSC-related SEGA and renal AML; sirolimus is preferred for LAM-specific indication based on MILES data.

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