Delving into the Latest Updates on Nintedanib esylate with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

CYNEDIV, Intedanib, NDNB

+ [29]

Target

CSF-1R x FGFRs x FLT3

Action

antagonists, inhibitors

Mechanism

CSF-1R antagonists(Colony stimulating factor 1 receptor antagonists), FGFRs antagonists(Fibroblast growth factor receptors antagonists), FLT3 inhibitors(Tyrosine-protein kinase receptor FLT3 inhibitors)

Therapeutic Areas

NeoplasmsRespiratory DiseasesOther Diseases+ [6]

Active Indication

Locally Advanced Lung Non-Small Cell Carcinomametastatic non-small cell lung cancerRecurrent Non-Small Cell Lung Cancer+ [21]

Inactive Indication

Acute Erythroblastic LeukemiaAdenocarcinoma of large intestineAdvanced Colorectal Adenocarcinoma+ [59]

Originator Organization

Boehringer Ingelheim International GmbH

Active Organization

Boehringer Ingelheim GmbHBoehringer Ingelheim International GmbHBoehringer Ingelheim Pharma GmbH & Co., KG

+ [16]

Inactive Organization

Boehringer Ingelheim Ltd.

Meilaipu (Beijing) Pharmaceutical Research Co., Ltd.

Boehringer Ingelheim España SA

License Organization

Grand Pharmaceutical (China) Co., Ltd.

Santen Pharmaceutical Co., Ltd.

Mount Sinai Medical Center of Florida, Inc.

+ [3]

Drug Highest PhaseApproved

First Approval Date

United States (15 Oct 2014),

Idiopathic Pulmonary Fibrosis

RegulationBreakthrough Therapy (United States), Fast Track (United States), Orphan Drug (United States), Priority Review (China), Orphan Drug (Japan), Orphan Drug (South Korea), Orphan Drug (Australia), Special Review Project (China)

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Structure/Sequence

Molecular FormulaC33H39N5O7S

InChIKeyMMMVNAGRWOJNMW-FJBFXRHMSA-N

CAS Registry656247-18-6

Pulmonary fibrosis (PF) is a progressive interstitial lung disease driven by excessive fibroblast activation and extracellular matrix (ECM) deposition, for which pirfenidone and nintedanib slow but do not halt disease progression. Extracellular vesicles (EVs)-lipid bilayer-enclosed nanoparticles that shuttle microRNAs (miRNAs), proteins, and lipids between cells-are increasingly recognized as important mediators and potential modulators of fibrotic remodeling. On the pathogenic side, epithelial- and immune-cell-derived EVs can deliver pro-fibrotic miRNAs (e.g., miR-494-3p) that regulate transforming growth factor beta (TGF-β)/Smad and Wnt/β-catenin signaling, promoting fibroblast-to-myofibroblast transition and ECM accumulation. Conversely, selected mesenchymal stem cell-derived EV (MSC-EV) preparations have demonstrated anti-fibrotic effects in preclinical models through modulation of TGF-β/Smad signaling, M2 macrophage polarization, mitochondrial function, and epithelial-mesenchymal transition; a phase I clinical study has provided initial safety evidence for nebulized administration, although therapeutic efficacy in PF has not yet been established. Beyond MSC-EVs, plant-derived and milk-derived EVs have emerged as potential delivery platforms, although their applications remain largely preclinical. Meanwhile, EVs isolated from plasma, bronchoalveolar lavage fluid, sputum, and urine carry disease-associated molecular signatures that may serve as candidate biomarkers for PF detection or monitoring, but require further clinical validation. This review synthesizes recent evidence on the dual roles of EVs in PF pathogenesis and therapy, evaluates their potential diagnostic utility, and discusses translational hurdles-including cargo standardization, targeted delivery, and scalable manufacturing-that must be overcome for clinical adoption.

01 Dec 2026·Cells & Development

Macrophage-fibroblast communication driven by biomechanical stress in the pulmonary profibrotic niche: From signalling transduction to clinical translation

Review

Author: Ye, Liya ; Yang, Hong ; Tao, Xia ; Hou, Xingyun ; He, Yuqiong ; Chen, Wansheng

Pulmonary (interstitial) fibrosis, the terminal pathological stage of various interstitial lung diseases, remains a major therapeutic challenge. The three approved antifibrotic agents - pirfenidone, nintedanib, and nerandomilast - receive only moderate endorsements in current guidelines, as they decelerate rather than arrest or reverse fibrotic remodelling, and none directly engages the mechanical dysregulation of the extracellular matrix (ECM) that underlies fibrogenesis. Macrophages and fibroblasts, two highly plastic cell populations, are the principal orchestrators of the pulmonary profibrotic niche: fibroblasts undergo profibrotic activation to become the dominant extracellular matrix (ECM) producers, while macrophages acquire profibrotic states that sense and amplify microenvironmental signals. Because the lung is an inherently mechanosensitive organ, biomechanical stress within the fibrotic niche emerges as a critical - yet therapeutically underexploited - dimension of their interaction. This review consolidates recent progress in understanding how biomechanical stress drives macrophage-fibroblast communication during pulmonary fibrogenesis. We first delineate the profibrotic activation of each cell type and their biomechanical interplay within the stiffening niche; we then examine the core mechanosensitive signalling mechanisms operating in fibroblasts and macrophages individually, their shared cell-state changes, and the direct and indirect crosstalk - encompassing membrane mechanosensors, integrin-FAK and Piezo1-YAP/TAZ pathways, secreted factors and extracellular vesicles - that closes a self-reinforcing mechano-chemical loop. Finally, we discuss the clinical translation of mechanosignalling-targeted antifibrotic therapies, from the limited mechanosensing engagement of approved drugs to current pipeline advances and the preclinical and clinical hurdles ahead. By framing fibrosis as a druggable biomechanical circuit, this review aims to inform strategies that halt - and potentially reverse - pulmonary fibrosis.

01 Dec 2026·INTERNATIONAL JOURNAL OF PHARMACEUTICS

Mechanofusion-assisted magnesium stearate surface modification enhances dispersion and aerodynamic performance of carrier-based nintedanib inhalable dry powder formulations

Article

Author: Han, Chang-Soo ; Kim, Seungsu ; Jung, Woong-Young ; Choi, Yu-Rim ; Kang, Ji-Hyun ; Jeong, So-Jeong ; Park, Chun-Woong ; Jeong, Jin-Hyuk ; Kim, Dong-Wook

Oral administration of nintedanib, a multi-receptor tyrosine kinase inhibitor for idiopathic pulmonary fibrosis, is associated with gastrointestinal side effects and limited lung targeting. Pulmonary delivery using dry powder inhalers (DPIs) offers a promising alternative, but the strong cohesiveness of drug microparticles hinders aerosolization and deep lung deposition. This study developed carrier-based DPI systems using mechanofusion with magnesium stearate (MgSt) at 0%, 1%, and 5% (w/w) and compared their physicochemical and aerodynamic performance with physical mixtures. Respirable nintedanib particles produced by jet milling were combined with lactose and MgSt to prepare six blends. Solid-state analyses by differential scanning calorimetry, powder X-ray diffraction, and Fourier transform infrared spectroscopy showed that mechanofusion enhanced drug-excipient interactions, with attenuated nintedanib peaks and modified thermal responses, while jet milling largely preserved the crystalline structure of nintedanib. Scanning electron microscopy, energy-dispersive X-ray spectroscopy, and Raman imaging confirmed more uniform adhesion and distribution of nintedanib and MgSt on the carrier surface. Bulk-density-derived flowability indices were numerically lower at higher MgSt contents. Aerodynamic evaluation using a next-generation impactor showed that mechanofusion, particularly with 5% MgSt, achieved higher fine and extra-fine particle fractions, confirming its synergistic role with MgSt in improving pulmonary delivery efficiency. These findings suggest that mechanofusion, particularly when combined with MgSt, is an effective strategy for improving the aerodynamic performance of carrier-based DPI formulations. By reducing particle cohesion and enhancing dispersion, this approach may facilitate more efficient pulmonary delivery of highly cohesive drugs such as nintedanib.

297

News (Medical) associated with Nintedanib esylate

13 Oct 2026

·www.biospace.com

aTyr Pharma Announces Publication Demonstrating Anti-Fibrotic Effects of ATYR0101 in the Journal of Biological Chemistry

Findings highlight ATYR0101’s potential as a transformative therapy for disrupting the process of chronic tissue fibrosis. ATYR0101 is currently undergoing IND-enabling studies and expects to be advanced into the clinic in 2027. SAN DIEGO, Oct. 13, 2026 (GLOBE NEWSWIRE) -- aTyr Pharma, Inc. (Nasdaq: ATYR) (“aTyr” or the “Company”), a clinical stage biotechnology company engaged in the discovery and development of first-in-class medicines from its proprietary tRNA synthetase platform, today announced a publication demonstrating the anti-fibrotic effects of ATYR0101 in the Journal of Biological Chemistry . The publication, entitled, “Natural Asp-tRNA Synthetase Fragment Targets Myofibroblasts to Abrogate Tissue Fibrosis,” is available on the journal’s website and at: (26)02458-0/fulltext . ATYR0101 is a fusion protein derived from a proprietary extracellular domain of aspartyl-tRNA synthetase (DARS) that binds to latent transforming growth factor beta binding protein 1 (LTBP-1) to induce myofibroblast apoptosis. “Fibrosis remains a major global health challenge across multiple organ and tissue systems with limited therapies that only slow disease progression,” said Leslie A. Nangle, Ph.D., Vice President, Research at aTyr Pharma. “This publication highlights the novel mechanism by which ATYR0101 disrupts fibrosis through a unique molecular program that facilitates a transition towards a restorative phenotype thus fundamentally altering the underlying fibrotic cellular landscape. These findings suggest that ATYR0101 does not merely stop disease progression but may also facilitate a reversal of fibrotic pathology, providing a differentiated approach to current anti-fibrotic therapies in conditions such as idiopathic pulmonary fibrosis, where more effective treatment options are greatly needed.” The publication describes the mechanism by which ATYR0101 selectively triggers apoptosis in myofibroblasts by targeting LTBP-1 on the extracellular matrix, with ATY0101 induced myofibroblast apoptosis shown to be dependent on active transforming growth factor beta (TGF-β), a central player in the pathogenesis of fibrotic diseases. Furthermore, the pharmacologic activity of ATYR0101 was demonstrated in an in vivo bleomycin lung model of fibrosis, where ATYR0101 showed a significant reduction in both collagen content and Ashcroft score leading to a marked decline in pulmonary fibrosis compared to the use of nintedanib, a known anti-fibrotic, as a control. About ATYR0101 ATYR0101 is a fusion protein derived from a proprietary extracellular domain of aspartyl-tRNA synthetase (DARS) that binds to latent transforming growth factor beta binding protein 1 (LTBP-1) to induce myofibroblast apoptosis. ATYR0101 interacts with LTBP-1 through a unique way that presents a differentiated approach to targeting fibrosis. ATYR0101 has demonstrated anti-fibrotic effects in models of lung and kidney fibrosis suggesting it may have broad therapeutic potential in multiple fibrotic diseases. ATYR0101 is currently undergoing IND-enabling studies. About aTyr aTyr is a clinical stage biotechnology company leveraging evolutionary intelligence to translate tRNA synthetase biology into new therapies for fibrosis and inflammation. tRNA synthetases are ancient, essential proteins that have evolved novel domains that regulate diverse pathways extracellularly in humans. aTyr’s discovery platform is focused on unlocking hidden therapeutic intervention points by uncovering signaling pathways driven by its proprietary library of domains derived from all 20 tRNA synthetases. aTyr’s lead therapeutic candidate is efzofitimod, a novel biologic immunomodulator in clinical development for the treatment of interstitial lung disease, a group of immune-mediated disorders that can cause inflammation and progressive fibrosis, or scarring, of the lungs. For more information, please visit . Forward-Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements are usually identified by the use of words such as "anticipate," “believes,” “can,” “could,” “designed,” “expects,” “intends,” “may,” “plans,” “potential,” “upcoming,” “will,” and variations of such words or similar expressions. We intend these forward-looking statements to be covered by such safe harbor provisions for forward-looking statements and are making this statement for purposes of complying with those safe harbor provisions. These forward-looking statements include, among others, statements regarding the potential therapeutic benefits and applications of ATYR0101, including the potential for ATYR0101 to provide a differentiated approach to current anti-fibrotic therapies in conditions such as idiopathic pulmonary fibrosis; timelines, plans and expected results with respect to certain research and development activities and development goals, including IND-enabling studies and our expectation that ATYR0101 will be advanced into the clinic in 2027. These forward-looking statements also reflect our current views about our plans, intentions, expectations, strategies and prospects, which are based on the information currently available to us and on assumptions we have made. Although we believe that our plans, intentions, expectations, strategies and prospects, as reflected in or suggested by these forward-looking statements, are reasonable, we can give no assurance that the plans, intentions, expectations, strategies or prospects will be attained or achieved. All forward-looking statements are based on estimates and assumptions by our management that, although we believe to be reasonable, are inherently uncertain. Furthermore, actual results may differ materially from those described in these forward-looking statements and will be affected by a variety of risks and factors that are beyond our control including, without limitation, uncertainty regarding geopolitical and macroeconomic events, risks associated with the discovery, development and regulation of our product candidates, the risks inherent in studies of potential medical therapies, the risk that we or future partners may cease or delay preclinical or clinical development activities for any of our existing or future product candidates for a variety of reasons (including difficulties or delays in patient enrollment in planned clinical trials), the possibility that future collaborations could be terminated early, and the risk that we may not be able to raise the additional funding required for our business and product development plans, as well as those risks set forth in our most recent Annual Report on Form 10-K, Quarterly Reports on Form 10-Q and in our other SEC filings. Except as required by law, we assume no obligation to update publicly any forward-looking statements, whether as a result of new information, future events or otherwise. Contact: Ashlee Dunston Investor Relations and Public Affairs adunston@atyrpharma.com

Immunotherapy

12 Oct 2026

·www.biopharmadive.com

Bristol Myers dips on ‘confounding’ lung drug results

Dive Brief:Bristol Myers Squibb said Monday that its experimental lung disease drug admilparant succeeded in a Phase 3 trial in idiopathic pulmonary fibrosis, significantly slowing the decline of study participants breathing capacity when compared to a placebo over the course of a year.However, trial investigators only found a clear benefit among those who received a 60 milligram dose of admilparant. A 120 milligram dose was associated with an impact on disease progression, but the difference didnt meet the threshold for statistical significance, the company said.The failure of the high-dose arm is confounding and requires further explanation, RBC Capital Markets analyst Trung Huynh wrote in a client note. Bristol Myers previously made certain trial revisions that sparked liver-related safety concerns about admilparant, too, although the company said Monday that the drug demonstrated a well-tolerated safety profile and treatment-related study discontinuations were similar between study groups.Dive Insight:Admilparant is the furthest along among a class of idiopathic pulmonary fibrosis, or IPF, drugs called LPA1 receptor antagonists. These treatments work by blocking a signaling molecule that plays an important role in lung scarring. They could emerge as alternatives to marketed drugs like Esbriet, Ofev and Jascayd, each of which has limitations.These admilparant results represent an important advancement as there remains a need for therapies that are both effective and tolerable for patients living with IPF, Fernando Martinez, the trial steering committee chair and a medical professor at the University of Massachusetts, in a statement from Bristol Myers.Earlier LPA1 drugs struggled in clinical testing. Bristol Myers scrapped one because of liver toxicity and Amgen canceled work on another after it fell short in a Phase 2 trial. News last month that Bristol Myers changed safety monitoring protocols in Europe for admilparants trial fueled additional consternation among Wall Street analysts and investors and heightened anticipation for the coming study readout.The announcement Monday that a 60 mg dose helped meaningfully improve forced vital capacity, or the amount of air people can exhale from their lungs at once, when compared to a placebo would ordinarily be taken as positive. However, physicians and drug reviewers frequently look to see whether higher doses perform better than lower ones. The lack of this kind of dose response sparked debate about admilparants prospects.The results could be sufficient to support admilparant regulatory approval, but the lack of dose response raises questions about [admilparants] profile, Leerink Partners analyst David Risinger wrote in a Monday client note. We await detailed results to better understand the drugs efficacy.Others were more positive. While there will be some lingering questions on dose response and the magnitude of benefit for admilparant, the success of the lower dose is likely to open a blockbuster opportunity, William Blair analyst Matt Phipps wrote in a separate note.Bristol Myers shares initially climbed more than 6% in pre-market trading before reversing course and settling into a roughly 4% loss. The data were also taken as bad news by investors of Contineum Therapeutics, which has a different LPA1 drug in Phase 2 testing. Contineums stock price fell about 30% in Monday morning trading.Bristol Myers separately claimed success in a different late-stage study testing a radiopharmaceutical called RYZ-101 against certain neuroendocrine tumors. The drugmaker gained control of RYZ-101 in a $4.1 billion buyout of RayzeBio. '

Phase 2AcquisitionPhase 3Clinical ResultClinical Trial Failure

08 Oct 2026

·www.medpace.com

Respiratory Innovation Moves Closer to Disease Modification

Medpace Respiratory Experts Share Highlights from ERS Congress 2026 In September 2026, Medpace respiratory experts attended the ERS Congress in Barcelona, Spain. As the world’s largest respiratory meeting, the ERS Congress brings together delegates from around the world to discuss enhancing the treatment and care of respiratory illness. ERS 2026 showcased a respiratory pipeline increasingly shaped by precision medicine, earlier intervention, and objective biomarkers. Across airway disease, interstitial lung disease (ILD), pulmonary hypertension associated with ILD (PH-ILD), and quantitative imaging, emerging data pointed beyond symptom control towards disease stability, remission, slower progression, and reduced healthcare burden. Continue reading for 4 key insights from Medpace experts. Airway Disease: Biologics Raise the Bar Biologic therapies are reshaping the management of severe asthma and COPD by enabling more targeted treatment, longer dosing intervals, and a greater focus on clinical remission, disease stability, and reduced healthcare burden. For example, depemokimab reduced exacerbations with twice-yearly dosing in the Phase III SWIFT-1 and SWIFT-2 trials, with longer-term outcomes assessed in AGILE. In VESTIGE, dupilumab reduced CT-measured mucus plugging and improved lung function, illustrating benefits beyond exacerbation prevention. Other severe-asthma biologics, including mepolizumab, benralizumab, and tezepelumab, have contributed to increasing rates of symptom control, freedom from exacerbations, and reduced oral corticosteroid use, although continued monitoring remains important because some patients relapse or lose response. In COPD, dupilumab and mepolizumab have shown benefit in selected patients with type 2 inflammation, while tozorakimab reduced moderate and severe exacerbations in the Phase III OBERON and TITANIA trials. Collectively, these studies support earlier biomarker-guided treatment and the development of longer-acting, phenotype-directed anti-inflammatory strategies. Interstitial Lung Disease: A Broader Therapeutic Pipeline The therapeutic landscape in pulmonary fibrosis is expanding beyond established antifibrotic treatment, with emerging therapies targeting lung-function decline, epithelial injury, and broader disease progression. For example, nerandomilast reduced FVC decline across IPF and progressive pulmonary fibrosis in the FIBRONEER-IPF and FIBRONEER-ILD trials, with particularly notable benefit in patients diagnosed within the previous year; reductions in KL-6 and SP-D also suggested effects on epithelial injury and fibrotic pathways. In the TETON-IPF studies, inhaled treprostinil provided an approximately 112 mL FVC benefit versus placebo at week 52, while a greater proportion of patients achieved improvements in DLCO. Further examples illustrate the increasing diversity of mechanisms and development strategies. The selective PDE4B inhibitor HSK44459 improved FVC at higher doses with a manageable safety profile, while the Phase III ALOFT-PPF study is evaluating admilparant, an oral LPA₁ antagonist, in a broad PPF population. Early translational findings also suggest that seralutinib combined with nintedanib may produce synergistic antifibrotic effects, supporting future combination strategies. CT Scanning and AI: From Diagnostic Image to Digital Biomarker AI-powered quantitative CT is transforming how ILD and pulmonary fibrosis are characterized. New approaches can objectively quantify fibrosis, ground-glass opacities, honeycombing, airways and pulmonary vessels—features that may be difficult to assess consistently through visual interpretation alone. Across prospective ILD cohorts, quantitative airway measurements emerged as strong predictors of survival, while quantitative pulmonary vascular measurements have shown potential prognostic value in idiopathic pulmonary fibrosis. By reducing variability between readers and integrating imaging with biomarkers such as KL-6 and SP-D, quantitative CT may enable more reproducible risk stratification, earlier detection of progression, and more precise identification of patients at greatest risk of hospitalization or mortality. For clinical development, these tools could support patient enrichment, objective longitudinal monitoring, and more sensitive assessment of treatment response. PH-ILD: Targeting the Vascular Component PH-ILD, historically an area with limited treatment options, is gaining a more diverse therapeutic pipeline. In the Phase II PHOCUS study of 135 patients, inhaled mosliciguat achieved a robust and statistically significant reduction in pulmonary vascular resistance at week 16: approximately 51% versus a 7% increase with placebo. Secondary endpoints, including six-minute walk distance and NT-proBNP, also showed improvement in the treatment arms compared to placebo. Other programs include novel treprostinil formulations, seralutinib, and vascular-targeted therapies. Preclinical results for NS-863, a highly selective oral PDGFR inhibitor, demonstrated improvements in pulmonary vascular remodeling, right ventricular hypertrophy, and survival in PAH and PH-ILD models, supporting progression into Phase II development. Together, these findings reinforce the concept that endothelial dysfunction, immune activation, fibrosis, and vascular remodeling are interconnected—and may be amenable to multi-pathway treatment strategies. The direction of travel is clear: respiratory medicine is moving toward earlier intervention, biologically targeted therapy, and measurable disease modification. As imaging, biomarkers, and innovative trial designs become more closely integrated, developers will be better positioned to identify responsive populations, track meaningful change, and translate scientific advances into durable patient benefit. Unable to connect with us during the ERS Congress? We welcome the opportunity to collaborate. Contact our respriatory experts to discuss how Medpace can support your upcoming clinical development plans. A Leading Global Respiratory CRO Medpace is a trusted global CRO partner in respiratory clinical trials, leveraging deep therapeutic expertise and operational excellence to streamline complex trial designs and accelerate drug development. With a track record of success across a broad range of respiratory indications, our integrated team of experts ensures high-quality data and efficient trial execution.

Clinical ResultPhase 2Phase 3

100 Deals associated with Nintedanib esylate

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External Link

KEGG	Wiki	ATC	Drug Bank
D10396 D10481	Nintedanib esylate	L01XE31	DB09079

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Locally Advanced Lung Non-Small Cell Carcinoma	Australia	Boehringer Ingelheim Pty Ltd.	01 Sep 2015
metastatic non-small cell lung cancer	Australia	Boehringer Ingelheim Pty Ltd.	01 Sep 2015
Recurrent Non-Small Cell Lung Cancer	Australia	Boehringer Ingelheim Pty Ltd.	01 Sep 2015
Interstitial lung disease due to systemic disease	European Union	Boehringer Ingelheim International GmbH	14 Jan 2015
Interstitial lung disease due to systemic disease	Iceland	Boehringer Ingelheim International GmbH	14 Jan 2015
Interstitial lung disease due to systemic disease	Liechtenstein	Boehringer Ingelheim International GmbH	14 Jan 2015
Interstitial lung disease due to systemic disease	Norway	Boehringer Ingelheim International GmbH	14 Jan 2015
Progressive fibrotic interstitial lung disease	European Union	Boehringer Ingelheim International GmbH	14 Jan 2015
Progressive fibrotic interstitial lung disease	Iceland	Boehringer Ingelheim International GmbH	14 Jan 2015
Progressive fibrotic interstitial lung disease	Liechtenstein	Boehringer Ingelheim International GmbH	14 Jan 2015
Progressive fibrotic interstitial lung disease	Norway	Boehringer Ingelheim International GmbH	14 Jan 2015
Adenocarcinoma of Lung	European Union	Boehringer Ingelheim International GmbH	21 Nov 2014
Adenocarcinoma of Lung	Iceland	Boehringer Ingelheim International GmbH	21 Nov 2014
Adenocarcinoma of Lung	Liechtenstein	Boehringer Ingelheim International GmbH	21 Nov 2014
Adenocarcinoma of Lung	Norway	Boehringer Ingelheim International GmbH	21 Nov 2014
Adenocarcinoma of Lung	United Kingdom	Boehringer Ingelheim GmbH	21 Nov 2014
Idiopathic Pulmonary Fibrosis	United States	Boehringer Ingelheim Pharmaceuticals, Inc.	15 Oct 2014

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Chronic interstitial lung disease	NDA/BLA	European Union	Accord Healthcare SL	22 Feb 2024
Lung Diseases, Interstitial	NDA/BLA	United States	Boehringer Ingelheim GmbH	25 Jul 2023
Pterygium	Phase 3	United States	Cloudbreak Therapeutics LLC	30 Jun 2022
Pterygium	Phase 3	China	Cloudbreak Therapeutics LLC	30 Jun 2022
Pterygium	Phase 3	Australia	Cloudbreak Therapeutics LLC	30 Jun 2022
Pterygium	Phase 3	India	Cloudbreak Therapeutics LLC	30 Jun 2022
Pterygium	Phase 3	New Zealand	Cloudbreak Therapeutics LLC	30 Jun 2022
Scleroderma	Phase 3	United States	Boehringer Ingelheim International GmbH	05 Dec 2017
Scleroderma	Phase 3	Japan	Boehringer Ingelheim International GmbH	05 Dec 2017
Scleroderma	Phase 3	Argentina	Boehringer Ingelheim International GmbH	05 Dec 2017

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ACR2026	Not Applicable	Interstitial lung disease due to systemic disease	36	Nintedanib with background immunosuppression	eulchtaeif(fepxlrongu) = diarrhea in 18 (50.0%), dose reduction in 23 (63.9%), and permanent discontinuation in only 2 (5.6%). eaddfxjros (kmphtlrdgb )	Positive	06 Nov 2026
ACR2026	Not Applicable	Interstitial lung disease due to systemic disease	20	Nintedanib or pirfenidone	rponutxtcg(lxjkmhrski) = zrvgquuzhl hzjtgzqyom (bnlrwcfjhy ) View more	Positive	06 Nov 2026
NCT05799755 (MINT, ACR2026)	Phase 2	Lung Diseases, Interstitial	49	Nintedanib	lqbqbpbkcd(plrwelgopm) = every component achieved ≥88.9% top-2-box satisfaction, and most components reached ≥93% pwgjvxkbaw (neksvqqrfx )	Positive	06 Nov 2026
ACR2026	Not Applicable	Interstitial lung disease due to systemic disease	1,530	Tocilizumab	cttsvvivds(mqtdfurwul) = vznhjlcawf cskorltlbe (jdnknruhpc ) View more	Positive	06 Nov 2026
ACR2026	Not Applicable	Interstitial lung disease due to systemic disease	1,530	Nintedanib	cttsvvivds(mqtdfurwul) = dbmviirgqq cskorltlbe (jdnknruhpc ) View more	Positive	06 Nov 2026
EULAR2026	Not Applicable	Interstitial lung disease due to connective tissue disease	72	NintedanibPirfenidone + NintedanibPirfenidone (Antifibrotic Therapy)	ewenlpfdqe(cidhsbnywq) = significant improvements were observed in both FVC (p<0.001 at 6 and 12 months) and DLCO (p<0.001 at 6 and 12 months) for the overall cohort hzjcjxizvs (lmanlbdjan ) View more	Positive	11 Jun 2026
EULAR2026	Not Applicable	Lung Diseases, Interstitial	94	Nintedanib + glucocorticoids + cDMARD + bDMARD +/- JAKi	wlmeajwozf(viqndbeged) = eledccivss addzkidyml (swbzoeeriw, 20.9) View more	Positive	11 Jun 2026
EULAR2026	Not Applicable	Lung Diseases, Interstitial	94	Nintedanib	wlmeajwozf(viqndbeged) = qpoakswsec addzkidyml (swbzoeeriw, 20.9) View more	Positive	11 Jun 2026
EULAR2026	Not Applicable	Rheumatic Diseases	135	Nintedanib + Nintedanibressants	goimnoxahf(uddgzgmgse) = betymoejrt rdrbybcpln (oidasxrgte ) View more	Positive	11 Jun 2026
EULAR2026	Not Applicable	Lung Diseases, Interstitial	64	Nintedanib + Mycophenolate mofetil + Rituximab	egglykcrje(ezelfzqmun) = vivbdfwjly ywxmglcpkg (enovawjnoq ) View more	Positive	11 Jun 2026
EULAR2026	Not Applicable	Lung Diseases, Interstitial	64	Nintedanib + Mycophenolate mofetil + Rituximab	-	Positive	11 Jun 2026
EULAR2026	Not Applicable	Lung Diseases, Interstitial	51	Mycophenolate mofetil + Rituximab	bchgzhlrpg(frvgyshapi) = khcgqxjuuy lefkjuivjm (jubconkgoe ) View more	Positive	11 Jun 2026
EULAR2026	Not Applicable	Lung Diseases, Interstitial	51	Mycophenolate mofetil + Rituximab + Nintedanib	bchgzhlrpg(frvgyshapi) = ivthacohgc lefkjuivjm (jubconkgoe ) View more	Positive	11 Jun 2026
EULAR2026	Not Applicable	Interstitial lung disease due to systemic disease	191	immunosuppressive therapy	njdbcrtipv(uhdhwkabyb) = saptjiveel cjtpbytyeg (zljsggxfie ) View more	Positive	11 Jun 2026