Table 2. Potential alternative therapeutic drugs against PF.

Drugs	Mechanism	Evidence stage	Ref.
Abbreviations: FGFR, fibroblast growth factor receptor; PDGFR, platelet-derived growth factor receptor; ROS, reactive oxygen species; VEGFR, vascular endothelial growth factor receptor.
Deferoxamine (iron chelator)	By chelating intracellular iron, deferoxamine suppresses iron-dependent lipid peroxidation and inhibits ferroptosis, thereby attenuating PF progression.	Preclinical	[128–129]
Ferrostatin-1 (ferroptosis inhibitor)	By inhibiting ferroptosis through ROS scavenging, ferrostatin-1 reduces lipid peroxidation and prevents iron-dependent cell death, thereby attenuating ECM deposition and PF.	Preclinical	[130–131]
Liproxstatin-1 (ferroptosis inhibitor)	By inhibiting ferroptosis through suppression of lipid peroxidation, liproxstatin-1 reduces inflammation and ECM deposition, thereby alleviating PF.	Preclinical	[132–133]
Nintedanib	Through multi-target inhibition of PDGFR/FGFR/VEGFR and disruption of TGF-β/SMAD3 signaling, nintedanib reduces fibroblast activation, ECM deposition, and collagen production.	Specific clinical trial for PF	[134–135]
Pirfenidone	Pirfenidone combats PF through TGF-β1/Smad3 inhibition, antioxidant activity, anti-inflammatory activity, and suppression of ECM deposition, collectively suppressing PF.	Specific clinical trial for PF	[136–137]
Metformin (AMPK activator)	Metformin activates AMPK to suppress myofibroblast fibrogenic activity and inhibits the TGF-β1 signaling pathway, collectively attenuating PF.	Clinical investigation	[138–139]
Rapamycin (mTORC1 inhibitor)	Rapamycin attenuates PF by inhibiting mTOR to suppress cell proliferation, and blocking TGF-β/Smad signaling and EMT, synergistically reducing ECM synthesis.	Preclinical	[140–141]
Berberine (autophagy activator)	Through dual activation of autophagy and suppression of ferroptosis, complemented by antioxidant and anti-inflammatory effects, Berberine reduces ECM deposition to alleviate PF.	Preclinical	[142–143]