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Rapamycin

Idiopathic Pulmonary Fibrosis · mTOR inhibition reduces cellular senescence, autophagy dysfunction, and fibroblast proliferation in lung

Mechanism
mTOR inhibition reduces cellular senescence, autophagy dysfunction, and fibroblast proliferation in lung
Development stage
Phase I/II
Evidence level
Level 2 (Repositioning)
Developer
Multiple

Overview

FDA-approved immunosuppressant. Reduces lung fibrosis in multiple animal models. Inhibits mTORC1 driving fibroblast proliferation and collagen synthesis. Extends lifespan in every model organism tested. Inhaled formulation under development to reduce systemic immunosuppression.

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Treatment profilemTOR inhibition reduces cellular senescence, autophagy dysfunction, and fibroblast proliferation in lungAll trialsResearch
Medical disclaimer. This page summarizes research about Rapamycin for information only. It is not medical advice. Verify approval status and evidence with the FDA and a pulmonologist.