What Medication is Used to Reduce Fibrosis?: Understanding Antifibrotic Treatments

October 11, 2025 •

4 min read

Finding an effective what medication is used to reduce fibrosis has been a major focus of medical research, particularly since diseases involving progressive scarring, such as Idiopathic Pulmonary Fibrosis (IPF), significantly impact millions of individuals worldwide. The answer depends heavily on the specific organ affected and the underlying cause. While there are no universal cures, targeted antifibrotic drugs can slow disease progression and improve patient outcomes.

Quick Summary

Antifibrotic medications, including nintedanib and pirfenidone, can slow the progression of scarring in specific conditions like pulmonary fibrosis and SSc-related lung disease. Treatment options vary by affected organ.

Key Points

Specific Organ, Specific Treatment: There is no single medication for all types of fibrosis; treatment depends on the affected organ (e.g., lungs, liver, kidneys) and the underlying cause.
Key Lung Medications: Nintedanib (Ofev®) and pirfenidone (Esbriet®) are FDA-approved antifibrotic drugs used to slow the progression of Idiopathic Pulmonary Fibrosis (IPF) and other interstitial lung diseases (ILD).
Differing Mechanisms: Nintedanib is a tyrosine kinase inhibitor, blocking multiple growth factor receptors, while pirfenidone is an anti-inflammatory and antifibrotic agent that targets TGF-β signaling.
Focus on Underlying Cause for Other Organs: For liver and renal fibrosis, the primary treatment strategy is to manage the root cause of the scarring, such as hepatitis or chronic kidney disease, as specific antifibrotic medications are not yet approved.
Active Research and Emerging Therapies: Many new drugs and investigational therapies are in development or clinical trials for various forms of fibrosis, focusing on different signaling pathways to inhibit or reverse scarring.
Progression vs. Reversal: Most current treatments primarily focus on slowing the progression of fibrosis and do not reverse existing scar tissue, though some emerging therapies show potential for reversal.
Personalized Approach is Key: The choice of treatment, management of side effects, and monitoring requires a personalized approach in consultation with a medical professional.

The Core of Antifibrotic Therapy: Targeting Pulmonary Fibrosis

Currently, the most established medications used to reduce fibrosis are aimed at treating Idiopathic Pulmonary Fibrosis (IPF), a progressive and fatal lung disease. Two key drugs, nintedanib and pirfenidone, are FDA-approved specifically for this purpose and have demonstrated the ability to slow the rate of lung function decline.

Nintedanib (Ofev®)

Nintedanib is a small molecule tyrosine kinase inhibitor that targets multiple signaling pathways involved in the development of fibrosis. Its mechanism involves blocking specific growth factor receptors, thereby inhibiting the proliferation and migration of fibroblasts, the cells responsible for producing scar tissue.

Key actions of nintedanib:

Targets multiple receptors: Inhibits platelet-derived growth factor receptors (PDGFR), fibroblast growth factor receptors (FGFR), and vascular endothelial growth factor receptors (VEGFR).
Reduces fibroblast activity: Prevents fibroblasts from differentiating into myofibroblasts, which are potent scar-producing cells.
Reduces extracellular matrix (ECM) deposition: Decreases the overproduction and accumulation of collagen and other ECM proteins that form the scar tissue.

Initially approved for IPF, nintedanib has also been approved for treating other chronic fibrosing interstitial lung diseases (ILD) that have a progressive phenotype, including Scleroderma-related ILD. This expanded indication highlights its broad antifibrotic potential.

Pirfenidone (Esbriet®)

Pirfenidone is another antifibrotic medication that has anti-inflammatory and antioxidant properties. It works by downregulating the production of growth factors and procollagens, thereby disrupting the fibrotic process.

Key actions of pirfenidone:

Inhibits fibrogenic mediators: Suppresses the activity of growth factors like transforming growth factor-beta (TGF-β), a central driver of fibrosis.
Reduces fibroblast proliferation: Directly curbs the growth of fibroblasts, limiting the cellular source of scar tissue.
Modulates the immune system: Decreases the production of inflammatory cytokines, which contributes to the fibrotic cascade.

Pirfenidone has proven effective in slowing disease progression in clinical trials for IPF, leading to its global approval for this condition.

Comparison of Nintedanib and Pirfenidone

While both drugs are used for IPF, their mechanisms differ slightly, and patient tolerance can vary. The choice between them is a personalized decision made by a medical provider based on the patient's specific health profile.


Feature	Nintedanib (Ofev®)	Pirfenidone (Esbriet®)
Mechanism	Triple kinase inhibitor, blocking growth factor receptors (PDGF, FGF, VEGF).	Anti-inflammatory and antifibrotic properties, primarily targeting TGF-β signaling.
Approved Indications	Idiopathic Pulmonary Fibrosis (IPF), progressive fibrosing interstitial lung diseases, Scleroderma-related ILD.	Idiopathic Pulmonary Fibrosis (IPF).
Administration	Oral capsule, typically taken twice daily with food.	Oral capsule, taken three times daily with food.
Common Side Effects	Diarrhea, nausea, abdominal pain, liver enzyme elevations.	Nausea, fatigue, indigestion, photosensitivity rash, liver enzyme elevations.

Treatment of Fibrosis in Other Organs

Fibrosis is not limited to the lungs and can affect the liver, kidneys, and other organs. Treatment approaches for these areas often involve addressing the underlying cause, as FDA-approved antifibrotic drugs like nintedanib and pirfenidone are not indicated for these conditions.

Liver Fibrosis

For liver fibrosis, the primary strategy is to manage the disease causing the scarring, such as viral hepatitis, non-alcoholic steatohepatitis (NASH), or alcohol-related liver disease. While there are no approved drugs specifically for liver fibrosis, several are under investigation:

Targeting inflammation and metabolic pathways: Drugs like cenicriviroc (CCR2/CCR5 dual antagonist) and obeticholic acid (FXR agonist) are being studied for NASH-related fibrosis.
Modulating growth factors: Experimental therapies targeting connective tissue growth factor (CTGF) are also explored.
Antioxidants and herbal remedies: Research is ongoing into the potential benefits of compounds like vitamin E and silymarin.

Renal Fibrosis

Renal fibrosis is a common pathway to chronic kidney disease (CKD) and end-stage renal disease (ESRD). Aside from managing the underlying kidney disease and controlling blood pressure with therapies like RAAS blockers (e.g., Losartan), treatment options for the fibrosis itself are limited and largely experimental. Some promising avenues include:

Targeting signaling pathways: Investigating agents that interfere with pathways such as TGF-β or CTGF.
Stem cell therapy: Studies are exploring the use of mesenchymal stem cells to reduce inflammation and inhibit fibrosis.
Repurposing existing drugs: Testing the antifibrotic effects of drugs like pirfenidone and pentoxifylline in preclinical studies and trials.

Emerging Therapies and Future Directions

Medical research continues to advance with a focus on new antifibrotic compounds and approaches. Promising areas of investigation include:

Tyrosine kinase inhibitors: New inhibitors are in development to target similar pathways to nintedanib, potentially with improved efficacy or side-effect profiles.
LPA1 receptor agonists: Drugs like admilparant are in Phase III trials for IPF, targeting a different pathway involved in fibrosis.
Inhaled treatments: Inhaled therapies like treprostinil are being studied to deliver medication directly to the lungs for conditions like IPF.
Anticancer drug repurposing: Some cancer drugs, such as saracatinib, have shown antifibrotic properties in preclinical studies and are being explored for IPF.

While significant progress has been made in understanding the mechanisms of fibrosis, the challenge lies in translating these findings into effective, safe treatments across different organs. Most current therapies focus on slowing, not reversing, the damage. Future advancements will likely involve combination therapies and more precise targeting of the fibrotic process.

Conclusion

While a single medication to cure all forms of fibrosis does not exist, progress in understanding organ-specific fibrotic diseases has led to targeted treatments. For Idiopathic Pulmonary Fibrosis, nintedanib and pirfenidone represent the current standard of care, successfully slowing disease progression in many patients. For liver and renal fibrosis, treatment remains largely focused on managing the underlying cause, though numerous novel therapies are in various stages of development. Patients with fibrotic conditions should always consult with their healthcare provider to determine the most appropriate and personalized treatment strategy. Research into new and existing compounds offers hope for more effective interventions in the future.

For more in-depth information on fibrosis research and clinical trials, consult resources like the National Institutes of Health.

Frequently Asked Questions

Nintedanib is a multi-targeted tyrosine kinase inhibitor that blocks growth factor receptors (PDGFR, FGFR, VEGFR) involved in fibrosis. Pirfenidone is an antifibrotic agent with anti-inflammatory and antioxidant properties that primarily targets the TGF-β pathway.

Currently approved antifibrotic medications for pulmonary fibrosis are primarily designed to slow the progression of scarring, not reverse existing scar tissue. Research into therapies with potential for reversal is ongoing.

No. While research is ongoing, there are currently no FDA-approved drugs specifically for liver fibrosis. Treatment focuses on addressing the underlying cause, such as viral hepatitis or non-alcoholic steatohepatitis (NASH).

Common side effects of pirfenidone include gastrointestinal issues (nausea, indigestion), photosensitivity (requiring sun protection), fatigue, and elevated liver enzymes.

The most common side effect of nintedanib is diarrhea. Other common side effects include nausea, vomiting, abdominal pain, and abnormal liver enzyme levels.

No, there is currently no cure for fibrosis. Treatment options focus on slowing the progression of the disease and managing symptoms to improve quality of life.

Renal fibrosis treatment mainly involves managing the underlying kidney disease, often with blood pressure medications like RAAS blockers. Specific antifibrotic drugs for the kidneys are still in the experimental stages.