What drugs reverse lung fibrosis? A look at current and future treatments

October 11, 2025 •

4 min read

Unfortunately, no drug has been proven to reverse established lung fibrosis completely. Current FDA-approved medications focus on slowing disease progression, but a wave of emerging therapies is now investigating ways to halt or even repair lung scarring in the ongoing search for what drugs reverse lung fibrosis.

Quick Summary

Current medications for lung fibrosis aim to slow disease progression, not reverse existing scarring. Researchers are actively developing new therapies, including some showing preclinical potential for reversal.

Key Points

No definitive reversal: Currently, no FDA-approved medication can fully reverse established lung fibrosis; therapies primarily aim to slow disease progression.
Standard care options: Nintedanib (Ofev) and pirfenidone (Esbriet) are established antifibrotic drugs that slow lung function decline.
New FDA approval: Jascayd (nerandomilast) is a new FDA-approved PDE4B inhibitor that also slows lung function decline in IPF patients.
Emerging reversal therapies: Promising investigational treatments include anti-IL-11 antibodies, the cancer drug saracatinib, stem cell therapies, and gene therapy approaches.
Clinical research is ongoing: These emerging therapies are largely still in clinical trials, and their ability to reverse fibrosis in humans has not yet been proven.
Focus on early intervention: Early diagnosis and management with existing medications are critical to preserve lung function, as established fibrosis is difficult to treat.

Idiopathic pulmonary fibrosis (IPF) and other forms of lung fibrosis are serious, progressive, and often fatal conditions characterized by irreversible scarring of the lung tissue. This scarring, or fibrosis, makes breathing progressively more difficult and significantly shortens a person's life expectancy. While the question of whether drugs can reverse this scarring is a primary focus of research, the current medical consensus is that available therapies only slow the rate of decline rather than restore lost lung function. However, recent and ongoing advancements offer new hope.

Established Medications for Slowing Lung Fibrosis

Ofev (Nintedanib)

Nintedanib is a tyrosine kinase inhibitor approved for use in Idiopathic Pulmonary Fibrosis (IPF) and other progressive fibrosing interstitial lung diseases (PF-ILD). It works by blocking multiple signaling pathways involved in the formation of scar tissue, specifically targeting the receptors for fibroblast growth factor (FGFR), platelet-derived growth factor (PDGFR), and vascular endothelial growth factor (VEGFR).

Mechanism of action: By inhibiting these tyrosine kinases, nintedanib reduces fibroblast proliferation and migration, which are key processes in fibrosis.
Effect on fibrosis: The drug slows the annual rate of lung function decline (measured by forced vital capacity) and is designed to manage the disease, not reverse it.
Side effects: Common side effects include diarrhea, nausea, vomiting, abdominal pain, and elevated liver enzymes.

Esbriet (Pirfenidone)

Pirfenidone is another antifibrotic agent that works through a different mechanism than nintedanib. It is approved for the treatment of IPF and has anti-inflammatory and antioxidant properties.

Mechanism of action: Pirfenidone inhibits the production of pro-fibrotic cytokines, including transforming growth factor-beta (TGF-β) and tumor necrosis factor-alpha (TNF-α), which play a central role in stimulating fibroblast activity and collagen synthesis.
Effect on fibrosis: It slows the progression of lung function decline, but like nintedanib, does not reverse existing scarring.
Side effects: Common adverse effects include nausea, rash, gastrointestinal issues, and photosensitivity.

Jascayd (Nerandomilast)

A significant new development, Jascayd (nerandomilast), was approved by the FDA in October 2025 as the first new oral treatment option for IPF in over a decade. It represents a novel mechanism of action.

Mechanism of action: Jascayd is a preferential inhibitor of phosphodiesterase 4B (PDE4B), an enzyme involved in inflammation and fibrosis. It exerts both antifibrotic and immunomodulatory effects.
Effect on fibrosis: Clinical trials demonstrated a significantly smaller decline in forced vital capacity (FVC) compared to placebo. It slows lung function decline but does not reverse scarring.
Side effects: Reported side effects include diarrhea, COVID-19, upper respiratory tract infection, depression, weight and appetite loss, and nausea.

Emerging Therapies Aiming for Reversal

Beyond managing the disease, scientists are exploring therapies that could potentially repair or reverse fibrotic damage. These are largely in clinical trials or earlier stages of development.

Anti-IL-11 inhibitors: Interleukin-11 (IL-11) is a pro-fibrotic cytokine involved in driving fibrosis in multiple organs. Preclinical animal studies have shown that neutralizing antibodies targeting IL-11 can block and even reverse lung fibrosis. However, conflicting evidence exists, and clinical trials are ongoing.
Saracatinib: Originally an anticancer drug, preclinical research showed that saracatinib could reverse the disease signature of IPF in human lung cells and reduce fibrosis in lung slices from IPF patients. Phase 1b/2a clinical trials (STOP-IPF) are evaluating its safety and effectiveness in patients.
Stem cell therapy: Mesenchymal stem cells (MSCs) are being investigated for their potential to modulate inflammation, secrete anti-fibrotic factors, and aid tissue repair. Clinical research is ongoing, with some trials suggesting high-dose MSCs may reduce disease progression, but not yet demonstrating definitive reversal in human lungs. Concerns remain about safety and long-term efficacy.
Gene therapy: Experimental approaches involve using non-viral vectors, such as nanoparticles, to deliver genetic material that can interfere with fibrotic pathways or promote repair. For instance, AAV1.SERCA2a gene therapy in animal models reversed pulmonary fibrosis by blocking specific signaling pathways. Clinical testing is still in the early stages, focusing on delivery methods and targets.
Zinc and nicotinamide riboside: A feasibility trial (NCT06567717) is testing whether a combination of these supplements can improve symptoms or lung function in people with IPF, based on preclinical findings suggesting zinc may help reverse lung damage by restoring the lung's ability to heal.

Comparison of Current FDA-Approved Therapies


Feature	Ofev (Nintedanib)	Esbriet (Pirfenidone)	Jascayd (Nerandomilast)
Mechanism of Action	Inhibits multiple tyrosine kinases (FGFR, PDGFR, VEGFR) to reduce fibroblast proliferation.	Inhibits pro-fibrotic cytokines (TGF-β, TNF-α) and has anti-inflammatory and antioxidant effects.	Preferential inhibitor of phosphodiesterase 4B (PDE4B) to exert antifibrotic and immunomodulatory effects.
Availability	Oral capsule, available for over a decade.	Oral tablet, available for over a decade.	Oral tablet, recently approved (October 2025).
Effect on Fibrosis	Slows decline in lung function; does not reverse scarring.	Slows decline in lung function; does not reverse scarring.	Slows decline in lung function; does not reverse scarring.
Common Side Effects	Diarrhea, nausea, vomiting, abdominal pain, liver enzyme elevations.	Nausea, rash, gastrointestinal upset, photosensitivity.	Diarrhea, respiratory infections, depression, weight loss, nausea.
Approved Population	Adults with IPF and other PF-ILDs.	Adults with IPF.	Adults with IPF.

Conclusion: The Horizon of Reversal

The definitive answer to the question, "What drugs reverse lung fibrosis?" remains that none currently do. However, this is a rapidly evolving area of pharmacology and medicine. The approval of Jascayd provides a new option for patients, adding to the therapeutic toolkit alongside nintedanib and pirfenidone to manage this devastating disease. The true game-changers will be the investigational therapies now in clinical development. Approaches like anti-IL-11 antibodies, saracatinib, stem cell therapy, and targeted gene delivery hold the potential to go beyond merely slowing progression and finally offer a way to repair scarred lung tissue. Until that happens, the focus remains on early diagnosis and proactive management with existing antifibrotic drugs, highlighting the urgent need for continued research in this field.

Visit the Pulmonary Fibrosis Foundation for more information on therapies and support.

Frequently Asked Questions

No, lung fibrosis cannot be cured. While medications can slow the disease's progression, they do not repair the existing lung scarring. Lung transplantation is the only curative option for patients with end-stage fibrosis.

No, there are no natural remedies or supplements proven to reverse lung fibrosis. Some, like a zinc and nicotinamide riboside combination, are being studied for potential benefits, but they are not approved treatments and should be discussed with a healthcare provider.

In October 2025, the FDA approved Jascayd (nerandomilast) for Idiopathic Pulmonary Fibrosis (IPF). It is a PDE4B inhibitor that helps slow the decline in lung function.

Nintedanib and pirfenidone are antifibrotic drugs that slow the progression of lung scarring by interfering with the signaling pathways that cause fibrosis. Nintedanib is a tyrosine kinase inhibitor, while pirfenidone has anti-inflammatory and antioxidant properties.

Common side effects vary by medication but can include gastrointestinal issues like diarrhea and nausea for nintedanib and pirfenidone. Jascayd also lists diarrhea and respiratory infections as common side effects.

Stem cell therapy is a promising area of research but is not yet a proven treatment for lung fibrosis. It is being studied in clinical trials, but definitive evidence of its ability to reverse fibrosis in humans is lacking.

Reversing lung fibrosis means restoring scarred lung tissue, which no current drug can do. Slowing fibrosis means decelerating the rate at which scarring worsens, which is the goal of currently approved medications like nintedanib, pirfenidone, and nerandomilast.