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Fibrosis Drug Pipeline Across Indications — PatSnap Eureka

Fibrosis Drug Pipeline Across Indications — PatSnap Eureka
Fibrosis Drug Pipeline

Fibrosis Drug Pipeline Across Liver, Lung, Kidney, Heart & Skin

Organ fibrosis collectively accounts for an estimated 45% of deaths in the developed world. Despite decades of preclinical advances, only pirfenidone and nintedanib carry regulatory approval — both solely for IPF. Discover the shared pathway strategies reshaping cross-indication drug discovery.

Target coverage by organ — retrieved dataset
Fibrosis Shared Pathway Target Coverage by Organ: Liver 13 targets, Lung 12 targets, Kidney 11 targets, Heart 8 targets, Skin 6 targets Horizontal bar chart showing the number of shared pro-fibrotic molecular targets identified per organ indication in the PatSnap Eureka patent and literature dataset. Liver and lung have the broadest target coverage, reflecting the density of retrieved results for those indications. Liver Lung Kidney Heart Skin 13 12 11 8 6 Shared molecular targets identified in dataset
Source: PatSnap Eureka · Patent & literature analysis
45%
of deaths in the developed world linked to organ fibrosis
5
organ indications sharing convergent fibrotic pathophysiology
2
approved drugs (pirfenidone & nintedanib) — both IPF only
13+
conserved cross-organ molecular targets identified in dataset
Cross-Indication Mechanisms

One Convergent Pathophysiology Across Five Organs

Regardless of the organ affected, retrieved patent filings and academic literature converge on a shared mechanistic framework. The central cellular effector is the myofibroblast — generated through activation of hepatic stellate cells (HSCs) in the liver, portal fibroblasts, and analogous resident fibroblast populations in lung, kidney, heart, and skin. Once activated, myofibroblasts synthesize excess extracellular matrix (ECM) — predominantly collagens I, III, and fibronectin — driving progressive architectural disruption and organ failure.

At the molecular level, TGF-β/Smad signaling is identified as the dominant pro-fibrotic cytokine axis across all five indications. TGF-β1 activates Smad2/3 transcriptional programs, driving collagen synthesis and myofibroblast persistence. Researchers at NIH-affiliated institutions and multiple academic centres have consistently identified this axis as the master regulator of fibrogenesis. Importantly, indiscriminate inhibition of TGF-β carries systemic risk given its pleiotropic biology — creating demand for pathway-selective or tissue-targeted interventions.

Beyond TGF-β, retrieved results highlight conserved roles for PPAR pathways (negative regulators of myofibroblast transdifferentiation across liver, lung, kidney, and cardiac fibrosis), NOX4/Nrf2 oxidative stress axes, and HDAC isoforms governing epigenetic reprogramming of fibroblast populations. PatSnap's life sciences intelligence platform enables researchers to map these overlapping pathway clusters across indication-specific patent families and literature simultaneously.

A bioinformatics drug repurposing pipeline applied across nine fibrotic diseases — published by the Cyprus Institute of Neurology and Genetics — identified unique and shared genes, biological pathways, and candidate repurposed substances, underscoring the cross-indication opportunity. Transcriptomic analysis from Johns Hopkins University identified conserved signaling networks shared between lung and liver fibrosis specifically.

Core conserved drivers
  • TGF-β1 / Smad2/3 — all 5 organ indications
  • PPAR-γ / pan-PPAR — liver, lung, kidney, heart
  • NOX4 / Nrf2 oxidative stress — lung & cross-organ
  • HDAC isoforms — heart, lung, liver, conjunctiva
  • IL-11 / IL-11RA — cardiac & renal fibroblasts
  • LOX / LOXL2 collagen crosslinking — skin, lung
  • miR-29b / miR-132 — liver, kidney
  • BMP-7 signaling — kidney, cardiovascular
7+
therapeutic modality classes in the fibrosis pipeline
13
cross-organ targets identified in retrieved dataset
IPF
only indication with approved drugs to date
45%
of developed-world deaths attributable to organ fibrosis
Pipeline Intelligence

Key Data Signals from the Fibrosis Patent & Literature Dataset

Visualising the distribution of therapeutic modalities and cross-organ target breadth identified across retrieved patent filings and academic publications.

Therapeutic Modality Distribution — Fibrosis Pipeline Dataset

Small molecules are the most densely represented class; cell-based therapies are the only modality with ongoing clinical trials (liver fibrosis/cirrhosis).

Fibrosis Therapeutic Modality Distribution: Small Molecules (most dense), Biologics (preclinical), Oligonucleotides (emerging), Epigenetic (preclinical), Cell-Based (clinical trials for liver), Delivery Systems (preclinical), Natural Products (preclinical) Horizontal bar chart illustrating the relative representation of seven therapeutic modality classes in the fibrosis drug pipeline dataset, derived from patent and literature analysis via PatSnap Eureka. Small molecules have the broadest coverage; cell-based therapies are the only class with active clinical trials. Small Molecules Biologics Oligonucleotides Epigenetic Cell-Based Delivery Systems ★★★ ★★ ★★ Clinical Relative dataset representation →

Cross-Organ Molecular Target Coverage

TGF-β/Smad is the only target implicated across all five organ indications; PPAR and HDAC cover four each.

Cross-Organ Fibrosis Target Coverage: TGF-β/Smad 5 organs, PPAR-γ/pan-PPAR 4 organs, HDAC isoforms 4 organs, NOX4/Nrf2 3 organs, BMP-7 2 organs, IL-11/IL-11RA 2 organs, LOX/LOXL2 2 organs, HIPK2 1 organ Horizontal bar chart showing the number of organ indications (out of 5: liver, lung, kidney, heart, skin) in which each key molecular target has been implicated in fibrosis, based on patent and literature analysis via PatSnap Eureka. TGF-β/Smad signaling is the only target present across all five indications. TGF-β/Smad PPAR-γ/pan-PPAR HDAC isoforms NOX4 / Nrf2 BMP-7 signaling IL-11 / IL-11RA LOX / LOXL2 HIPK2 5/5 4/5 4/5 3/5 2/5 2/5 2/5 1/5 Number of organ indications implicated (out of 5)

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Therapeutic Modalities

Seven Drug Classes Targeting Shared Fibrotic Pathways

From approved small molecules to emerging oligonucleotide therapies, the fibrosis pipeline spans a diverse range of modalities — many explicitly designed to address cross-indication targets. Explore the PatSnap analytics platform to map competitive landscapes across each class.

Modality 01 — Small Molecules

Kinase Inhibitors, PPAR Agonists & Novel Scaffolds

Small molecules are the most densely represented class in this dataset. Pirfenidone (approved IPF) shows preclinical evidence for NASH-associated liver fibrosis via inhibition of TNF-α-induced apoptosis. Nintedanib (tyrosine kinase inhibitor) is approved for IPF and systemic sclerosis-associated ILD. PXS-5505, a pan-lysyl oxidase inhibitor targeting LOX/LOXL2-mediated collagen crosslinking, demonstrated activity in skin and lung in systemic sclerosis rodent models and is in early clinical development for myelofibrosis. Pan-PPAR agonist lanifibranor reduced lung fibrosis in a TGFβ-overexpressing transgenic mouse model of scleroderma. The California Institute for Biomedical Research has filed patents covering small molecule libraries explicitly spanning IPF, liver cirrhosis, kidney fibrosis, cardiac fibrosis, and keloid formation.

Pirfenidone & nintedanib approved (IPF); PXS-5505 early clinical
Modality 02 — Biologics

IL-11 Antibodies, BMP-7, END55 & Collagen-Targeting Constructs

IL-11 neutralizing antibodies targeting IL-11 or IL-11RA show anti-fibrotic activity in human fibroblasts and murine cardiac and renal fibrosis models. BMP-7 is retrieved as a multi-organ anti-fibrotic biologic with beneficial effects in renal, pulmonary, and cardiovascular fibrosis models; Thrasos Innovation has filed patents on BMP agonist peptides for renal fibrosis and diabetic nephropathy. END55, an endostatin-derived recombinant fusion protein produced in plants, demonstrated anti-fibrotic effects in murine skin and lung fibrosis models and in human organ cultures. Collagen-binding peptide-conjugated micelles (CBP-micelles) and VWF-A3 domain constructs have been engineered to preferentially accumulate at fibrotic sites in lung and kidney.

Predominantly preclinical; IL-11 antibodies in early translation
Modality 03 — Oligonucleotide Therapies

ASOs, siRNA Lipid Nanoparticles & miRNA Delivery

ONTs offer distinct advantages for targeting otherwise undruggable fibrotic pathways. ASOs targeting TGF-β pathway components are validated by the Royal Holloway group, citing recent ASO approvals in Duchenne muscular dystrophy and SMA as platform validation. Biogen researchers used siRNA-formulated lipid nanoparticles to silence genes upregulated in liver and kidney fibrosis, identifying five novel modifiers: Egr2, Atp1a2, Fkbp10, Fstl1, and Has2 — all reducing Col1a1 expression. Co-delivery of miR-29b and germacrone via cyclic RGD-modified PEG-PLGA nanoparticles demonstrated HSC targeting and collagen suppression in CCl4-induced liver fibrosis models. Eli Lilly researchers reviewed direct lung ONT delivery strategies, noting reduced systemic side effects.

Preclinical proof-of-concept in murine models
Modality 04 — Epigenetic Approaches

HDAC Inhibitors & the miR-132/PPARγ Epigenetic Relay

HDAC inhibitors are documented to suppress myofibroblast differentiation in cardiac, pulmonary, hepatic, and conjunctival fibrosis, establishing epigenetic regulation as a cross-organ mechanism. A University of Georgia Research Foundation patent describes an epigenetic relay in which loss of miR-132 leads to transcriptional silencing of PPARγ, driving hepatic stellate cell activation — with nucleoside compounds and conjugated antibodies claimed as interventions. PatSnap analytics can be used to map patent families covering HDAC isoform-selective inhibitors across organ indications.

Preclinical stage
Modality 05 — Cell-Based & Stem Cell Therapies

Muse Cells, hFSSC Secretome & Clinical Liver Trials

Stem and progenitor cell therapies are under active clinical investigation in liver fibrosis/cirrhosis, encompassing different cell sources, dosing, and delivery methods. Life Science Institute, Inc. (Japan) has filed a patent for SSEA-3-positive pluripotent stem cells (Muse cells) derived from mesenchymal tissue as a cell product for organ fibrosis including liver. Human fetal skin-derived stem cell (hFSSC) secretome demonstrated anti-fibrotic effects via HSC suppression and liver regeneration in CCl4-induced rat models. According to ClinicalTrials.gov, multiple stem cell trials in liver cirrhosis are registered globally.

Clinical trials ongoing (liver); earlier stage for other organs
Modality 06 — Targeted Delivery & Natural Products

Nanoparticles, Collagen-Binding Platforms & Herbal Derivatives

A dedicated literature stream addresses poor bioavailability and off-target effects via organ-targeted delivery: HSC-targeted nanoparticles loaded with drugs and nucleic acids for liver fibrosis; collagen-binding micelles and VWF-A3 domain constructs exploiting leaky vasculature for lung/kidney targeting; and machine perfusion supplementation with anti-fibrotic drugs proposed for kidney transplant interstitial fibrosis prevention. A substantial body of retrieved academic literature — predominantly from Chinese institutions — covers natural product compounds including naringenin, artemisinin, germacrone, epoxyeicosatrienoic acids, and pyrroloquinoline quinone (PQQ) evaluated across multiple organ fibrosis models at the preclinical stage. The PatSnap chemicals & materials platform supports structure-activity relationship analysis for natural product scaffolds.

Preclinical; machine perfusion approach novel for transplant setting
PatSnap Eureka

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Molecular Target Intelligence

Key Targets Appearing Across Multiple Organ Indications

The following targets appear across multiple retrieved results and multiple organ indications, signaling their relevance to cross-indication strategies. Data derived from patent filings and academic literature retrieved via PatSnap Eureka.

Target / Pathway Organs Implicated in Dataset Modalities Addressing It Key Agent / Finding
TGF-β1 / Smad2/3 Liver, lung, kidney, heart, skin Small moleculesASOsBiologics Dominant pro-fibrotic axis; pleiotropic biology demands tissue-selective targeting
PPAR-γ / pan-PPAR Liver, lung, kidney, heart Small molecules Lanifibranor reduced lung fibrosis in TGFβ-transgenic scleroderma model
LOX / LOXL2 Skin, lung (systemic sclerosis) Small molecules PXS-5505 pan-LOX inhibitor; in clinical development for myelofibrosis
αvβ6 / α3β1 integrins Cross-organ ECM sensing Biologics Integrin-mediated ECM sensing; cadherin-11 co-identified as structural node
IL-11 / IL-11RA Heart, kidney Neutralizing antibodies Il11ra1 genetic deletion protective in mouse models; MRC-LMS, 2020
HDAC isoforms Heart, lung, liver, conjunctiva HDAC inhibitors Cross-organ myofibroblast differentiation suppression; Chonnam National U, 2019
NOX4 / Nrf2 Lung, cross-organ Small molecules Nrf2 activation attenuates pulmonary fibrosis; validated cross-organ ROS target
miR-29b / miR-132 Liver, kidney miRNA mimicsASOs miR-29b suppresses collagen; miR-132 loss drives PPARγ silencing in HSCs
🔒
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See HIPK2, BMP-7, S1P, JNK/Smad3, collagen I targets, and all modality-assignee mappings in PatSnap Eureka.
HIPK2 / kidney BMP-7 signaling S1P / JNK + more targets
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Assignee & Author Landscape

Academic Institutions Lead Discovery; Biotech Drives IP Commercialisation

Retrieved results are overwhelmingly literature-driven (academic papers), with a smaller but strategically significant patent component reflecting growing IP commercialisation activity.

🎓

RWTH Aachen / Bonn University — SFB/TRR57 Consortium

Multiple publications spanning 13 years covering both liver and kidney fibrosis mechanisms and therapeutic modulation, representing one of the most sustained academic research programmes in the retrieved dataset.

🔬

MRC-London Institute of Medical Sciences

Identified IL-11 as an unexpected central mediator of cardiac and renal fibroblast activation. Demonstrated that genetic deletion of IL-11 receptor (Il11ra1) is protective in mouse models — a finding with significant therapeutic implications for neutralizing antibody development.

🏛️

University of Chicago & University of Pittsburgh

Engineered collagen-targeting therapeutics (CBP-micelles, VWF-A3 domain constructs, END55 recombinant fusion protein) demonstrating anti-fibrotic effects in murine skin and lung fibrosis models and in human organ cultures — advancing targeted delivery as a cross-organ platform.

🧬

Biogen, Eli Lilly & Boehringer Ingelheim

Pharmaceutical contributors include Biogen (siRNA LNP identification of five novel fibrosis modifiers: Egr2, Atp1a2, Fkbp10, Fstl1, Has2), Eli Lilly (pulmonary ONT delivery review), and Boehringer Ingelheim (nintedanib clinical development challenges), reflecting industry engagement with both established and emerging modalities.

🔒
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Access Vascular Biogenics, California Institute for Biomedical Research, Thrasos Innovation, and Life Science Institute patent family details in PatSnap Eureka.
Vascular Biogenics patents Thrasos Innovation CALIBR fibrosis library
View Assignee IP Portfolios →
PatSnap Eureka for Drug Discovery

Accelerate Cross-Indication Fibrosis Research with AI-Native Intelligence

The fibrosis drug pipeline challenge is fundamentally a data problem: shared pathway signals are buried across thousands of organ-specific patent families, literature reviews, and clinical records. PatSnap Eureka applies AI to surface cross-indication connections that would take research teams months to identify manually.

For fibrosis specifically, Eureka enables teams to identify which TGF-β pathway inhibitors have been claimed across multiple organ indications, track assignee patent filing velocity for emerging modalities like oligonucleotide therapies, and map the competitive white space between approved agents (pirfenidone, nintedanib) and the preclinical pipeline. The PatSnap customer base includes leading pharmaceutical and biotech organisations leveraging these capabilities for indication expansion decisions.

Bioinformatics approaches have already demonstrated the value of cross-indication analysis: a drug repurposing pipeline applied across nine fibrotic diseases by the Cyprus Institute of Neurology and Genetics identified unique and shared genes and candidate repurposed substances. PatSnap Eureka enables R&D teams to run equivalent analyses against a live, continuously updated database of 2B+ data points — as documented by WHO-aligned global disease burden frameworks and supported by PatSnap's open API for programmatic data access.

What Eureka enables for fibrosis teams
  • Cross-indication target mapping across patent & literature simultaneously
  • Assignee portfolio analysis for emerging modalities (ONTs, cell therapy)
  • Drug repurposing signal identification across nine+ fibrotic diseases
  • Pathway-selective inhibitor candidate identification (TGF-β, PPAR, HDAC)
  • IP white space analysis between approved drugs and preclinical pipeline
  • Natural product scaffold structure-activity relationship analysis
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PatSnap platform coverage
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Frequently asked questions

Fibrosis Drug Pipeline — Key Questions Answered

Still have questions about the fibrosis pipeline? Let PatSnap Eureka answer them for you.

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PatSnap Eureka

Map the Full Fibrosis Drug Pipeline — Across All Five Organ Indications

Join 18,000+ innovators already using PatSnap Eureka to accelerate their R&D. Search 2B+ patent and literature records to identify cross-indication targets, assignee strategies, and pipeline white space.

References

  1. Research progress on drugs targeting the TGF-β signaling pathway in fibrotic diseases — Central South University, 2022
  2. Targeting TGFβ Signaling to Address Fibrosis Using Antisense Oligonucleotides — Royal Holloway, University of London, 2018
  3. Integrins and cadherins as therapeutic targets in fibrosis — Baylor College of Medicine, 2014
  4. Pan-Lysyl Oxidase Inhibitor PXS-5505 Ameliorates Multiple-Organ Fibrosis — McMaster University, 2022
  5. IL-11 in cardiac and renal fibrosis: Late to the party but a central player — MRC-London Institute of Medical Sciences, 2020
  6. The Role of Nrf2 in Pulmonary Fibrosis: Molecular Mechanisms and Treatment Approaches — Tongji University, 2022
  7. HDAC Inhibitors: Therapeutic Potential in Fibrosis-Associated Human Diseases — Chonnam National University, 2019
  8. HIPK2 is a new drug target for anti-fibrosis therapy in kidney disease — James J. Peter Veterans Administration Medical Center, 2015
  9. The pan-PPAR agonist lanifibranor reduces development of lung fibrosis and attenuates cardiorespiratory manifestations — UCL Division of Medicine, 2021
  10. Antifibrotic effect of pirfenidone in a mouse model of human nonalcoholic steatohepatitis — Tokyo Medical and Dental University, 2017
  11. Identification of Novel Fibrosis Modifiers by In Vivo siRNA Silencing — Biogen, Inc., 2017
  12. Co-delivery of miR-29b and germacrone based on cyclic RGD-modified nanoparticles for liver fibrosis therapy — Wenzhou Medical University, 2020
  13. The Promising Therapeutic Potential of Oligonucleotides for Pulmonary Fibrotic Diseases — Eli Lilly and Company, 2022
  14. Engineered collagen-targeting therapeutics reverse lung and kidney fibrosis in mice — University of Chicago, 2022
  15. Ameliorating Fibrosis in Murine and Human Tissues with END55 — University of Pittsburgh, 2022
  16. Stem cells for treatment of liver fibrosis/cirrhosis: clinical progress and therapeutic potential — Lanzhou University First Hospital, 2022
  17. Common pathway signature in lung and liver fibrosis — Johns Hopkins University, 2016
  18. Drug Repurposing Through a Bioinformatics Pipeline Applied on Fibrotic Diseases — Cyprus Institute of Neurology and Genetics, 2020
  19. Pathologic Proteolytic Processing of N-Cadherin as a Marker of Human Fibrotic Disease — Duke University Medical Center, 2022
  20. Naringenin: A Promising Therapeutic Agent against Organ Fibrosis — Southwest Medical University, 2021
  21. Artemisinin and artemisinin derivatives as anti-fibrotic therapeutics — Northwestern University-Feinberg, 2021
  22. National Institutes of Health (NIH) — Fibrosis Research Resources
  23. World Health Organization (WHO) — Global Disease Burden Framework
  24. ClinicalTrials.gov — Registered Fibrosis Clinical Trials

All data and statistics on this page are sourced from the references above and from PatSnap's proprietary innovation intelligence platform. This page is derived from a limited set of patent and literature records retrieved across targeted searches and represents a snapshot of innovation signals within this dataset only.

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