RegulationPriority Review (United States), Breakthrough Therapy (United States), Orphan Drug (United States), Orphan Drug (European Union), Priority Review (China), Orphan Drug (Japan)

Structure/Sequence

Molecular FormulaC20H25ClN6O2S

InChIKeyUHYCLWAANUGUMN-SSEXGKCCSA-N

CAS Registry1423719-30-5

Clinical Trials associated with Nerandomilast

NCT07789015

/ Not yet recruitingPhase 3

A Phase III, Parallel Design, Double-blind, Randomised, Placebo-controlled, Multi-centre Trial to Evaluate the Efficacy and Safety of Nerandomilast Oral Therapy Added to Standard Background Therapy Over 52 Weeks in Adult Trial Participants With Active Idiopathic Inflammatory Myopathies (VERANDA™-IIM)

This study is open to adults aged 18 and older who have a condition known as active idiopathic inflammatory myopathy (IIM) or myositis. People can participate if they have a specific type of myositis. The purpose of this study is to find out whether a medicine called nerandomilast improves IIM symptoms.
Participants are put into 2 groups randomly, which means by chance. One group takes nerandomilast tablets and the other group takes placebo tablets. Placebo tablets look like nerandomilast tablets but do not contain any medicine. Participants take nerandomilast or placebo twice a day for 1 year.
Participants are in the study for about 1 year and 2 months. During this time, they visit the study site at least 16 times. During this time, doctors regularly check the participant's health, IIM symptoms, and take note of any unwanted effects. Participants fill in questionnaires about their IIM symptoms and how IIM impacts their quality of life. The results are compared between the 2 groups to see whether the treatment works.

Start Date14 Dec 2026

Sponsor / Collaborator

Boehringer Ingelheim GmbH

NCT07540988

/ RecruitingPhase 3

A Double-blind, Randomized, Placebo-controlled Trial Investigating the Efficacy and Safety of Nerandomilast Over at Least 52 Weeks in Patients With Fibrosing Interstitial Lung Disease at Risk for Disease Progression (FIBRONEER-ACT)

This study is open to adults with fibrosing interstitial lung disease (ILD) other than idiopathic pulmonary fibrosis (IPF). People can join the study if they have been diagnosed with this condition within the last 3 years and are at risk of developing progressive pulmonary fibrosis (PPF). The purpose of this study is to find out whether a medicine called nerandomilast helps people with fibrosing interstitial lung disease who may be at risk for their disease getting worse.
Participants are put into 2 groups randomly, which means by chance. One group takes nerandomilast tablets, and the other group takes placebo tablets. Placebo tablets look like nerandomilast tablets but do not contain any medicine. Nerandomilast is a type of medicine that may help reduce lung function decline and slow disease progression.
Participants are in the study for up to about 2 years and 4 months. During this time, they visit the study site regularly. Doctors regularly test lung function using methods like spirometry to measure forced vital capacity (FVC, maximum amount of air a participant can blow out after taking a deep breath) and DLCO (diffusing capacity of the lungs for carbon monoxide; it estimates how well oxygen moves from the lungs into the blood). Additionally, high-resolution computed tomography (HRCT) is performed to monitor how the lung condition is changing over time. The results are compared between the groups to see whether the treatment works. The doctors also regularly check participants' health and take note of any unwanted effects.

Start Date17 Sep 2026

Sponsor / Collaborator

Boehringer Ingelheim GmbH

JPRN-jRCT2030260406

/ Not yet recruitingPhase 3

A double-blind, randomized, placebo-controlled trial investigating the efficacy and safety of nerandomilast over at least 52 weeks in patients with fibrosing interstitial lung disease at risk for disease progression (FIBRONEER-ACT)

Start Date01 Sep 2026

Sponsor / Collaborator

Nippon Boehringer Ingelheim Co., Ltd.

100 Clinical Results associated with Nerandomilast

100 Translational Medicine associated with Nerandomilast

100 Patents (Medical) associated with Nerandomilast

Literatures (Medical) associated with Nerandomilast

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 Nov 2026·GENES TO CELLS

Nerandomilast is Associated With Altered Alveolar Epithelial Cell State Dynamics While Attenuating Fibrotic Remodeling in Pulmonary Fibrosis

Article

Author: Motooka, Daisuke ; Akira, Shizuo ; Kuwahara, Atsushi ; Hamada, Nanako ; Hayashi, Yoshiaki ; Fukushima, Kiyoharu

ABSTRACT:

Pulmonary fibrosis is a progressive and life‐threatening lung disorder characterized by excessive fibrogenesis and impaired respiratory function. Nerandomilast, a preferential phosphodiesterase 4B inhibitor, is currently approved for the treatment of idiopathic pulmonary fibrosis and progressive pulmonary fibrosis in several countries following its demonstrated clinical efficacy in Phase III trials. However, its cellular mechanisms of action remain incompletely understood. In this study, we investigated the effects of nerandomilast on a bleomycin‐induced mouse model of lung fibrosis. Nerandomilast treatment attenuates fibrotic remodeling and preserves alveolar epithelial architecture. Single‐cell transcriptomic analyses revealed altered alveolar epithelial cell state dynamics accompanied by increased cell cycle‐associated pathways in alveolar type 2 cells and an increased relative abundance of alveolar type 2 cells. Consistent with the single‐cell findings, nerandomilast was associated with an increased SFTPC‐positive area and the preservation of alveolar epithelial architecture in vivo. Collectively, our findings suggest that nerandomilast attenuates fibrotic remodeling while modulating alveolar epithelial cell state dynamics, which may provide a possible cellular explanation for its clinical efficacy in patients with pulmonary fibrosis.

01 Nov 2026·PHARMACOLOGICAL RESEARCH

Reconfiguring the macrophage-centric intercellular network in pulmonary fibrosis: Emerging perspectives and therapeutic opportunities

Review

Author: Zhang, Aoxin ; Wang, Shangxuan ; Zhu, Zhongbo ; Yang, Yujie ; Zhang, Xuhui ; Liu, Xiping ; Wang, Wenjuan ; Liu, Senyu

Pulmonary fibrosis (PF) encompasses a spectrum of progressive and irreversible interstitial lung diseases characterized by a notably poor prognosis. The principal pathological features of PF include recurrent injury to the alveolar epithelium, aberrant accumulation of extracellular matrix (ECM) components, and disruption of the structural integrity of lung tissue. Clinically, effective therapeutic options for PF remain severely limited. Existing studies have demonstrated that the imbalance in macrophage polarization and the heterogeneous functional remodeling of these cells constitute central mechanisms driving the fibrotic cascade. Macrophages exhibit dynamic plasticity, transitioning between the M1 pro-inflammatory phenotype and the M2 pro-fibrotic phenotype. Additionally, they can differentiate into novel subpopulations, including triggering receptor expressed on myeloid cells 2-positive (TREM2⁺) lipid-associated macrophages and SPP1^hipro-fibrotic macrophages, which significantly contribute to the remodeling of the pro-fibrotic pathological microenvironment within the lungs. At the same time, as a critical node in intercellular communication, establishing a bidirectional regulatory network with alveolar epithelial cells, fibroblasts, endothelial cells, and various immune cells. Through signaling mediators such as cytokines, exosomes, and apoptotic bodies, macrophages contribute to the regulation of epithelial-mesenchymal transition (EMT), fibroblast activation, endothelial-to-mesenchymal transition (EndMT), and the disruption of immune homeostasis. Collectively, these interactions play a pivotal role in the initiation and progression of diseases. Currently, only nintedanib, pirfenidone, and the novel phosphodiesterase 4B (PDE4B) inhibitor nerandomilast have received regulatory approval for clinical use. While these agents can slow the progression of lung function decline, they are unable to reverse established fibrotic lesions. Furthermore, numerous candidate drugs targeting single molecular pathways have failed to advance beyond phase II/III clinical trials due to inadequate efficacy or safety concerns. The emerging generation of investigational therapies primarily targets macrophage function remodeling, epithelial repair, and fibroblast inhibition; however, most remain in early clinical trial phases without significant breakthroughs to date. Consequently, there is an urgent clinical demand for more effective and safer therapeutic alternatives. In this context, natural plant-derived active ingredients, due to their ability to target multiple molecular pathways, offer a promising strategy for intervening in this complex network. Existing preclinical studies suggest that certain active compounds (such as quercetin, brusatol, licochalcone B, and salvianolic acid B) can regulate macrophage-associated processes, such as polarization, autophagy, or inflammatory responses, depending on the specific compound and experimental context. These compounds also improve the microenvironment of experimental fibrosis by attenuating pro-fibrotic signaling between macrophages and epithelial cells, fibroblasts, endothelial cells, and immune cells. However, it is important to note that most of this evidence is derived from in vitro and animal studies, and the precise molecular targets, multi-component synergistic mechanisms, and clinical translational potential of these compounds still require systematic validation. Therefore, this article provides a systematic review of the biological characteristics and subgroup heterogeneity of lung macrophages. It elucidates the underlying mechanisms by which the macrophage-centered multicellular interaction network contributes to the progression of PF. Additionally, the article summarizes currently approved Western medications, clinical failures, and the challenges associated with the development of novel targeted agents. Emphasis is placed on reviewing the pharmacological mechanisms and recent advances in natural active compounds targeting this core cellular network to intervene in PF. The objective is to offer a theoretical foundation for a more comprehensive understanding of PF pathogenesis and to facilitate the optimization and innovation of anti-fibrotic therapeutic strategies.

113

News (Medical) associated with Nerandomilast

14 Oct 2026

·www.biospace.com

JASCAYD™ receives Health Canada authorization for a new, well-tolerated oral treatment for adults with IPF and PPF

This marks the first new treatment approved for IPF in Canada in over a decade and for PPF in more than five years. 1 , 2 BURLINGTON, ON , Oct. 13, 2026 /CNW/ -- Boehringer Ingelheim Canada announced that JASCAYD ™ (nerandomilast) has received authorization from Health Canada for the treatment of adults with idiopathic pulmonary fibrosis (IPF) and adults with progressive pulmonary fibrosis (PPF). JASCAYD™ is the first phosphodiesterase 4B (PDE4B) inhibitor authorized in Canada for these indications and represents an important new treatment option for Canadians living with these progressive and life-limiting fibrosing lung diseases. 3 JASCAYD™ is the first treatment in over a decade to demonstrate efficacy in IPF and the first alternative treatment option for PPF in more than five years. 1 , 2 It also shows a favorable tolerability and safety pro low discontinuation rates across both conditions in the phase III clinical trials. 1 , 2 The authorization is supported by results from the Phase III FIBRONEER™-IPF and FIBRONEER™-ILD trials, the largest Phase III clinical program conducted across IPF and PPF to date. 1 , 2 In both the FIBRONEER™-IPF and FIBRONEER™-ILD trials, the primary endpoint was met: nerandomilast successfully slowed lung function decline, measured by absolute change in forced vital capacity (FVC) from baseline to week 52 compared to placebo. 1 , 2 While the key secondary endpoint was not met in either trial, a numerical reduction in mortality was observed across both trials, reaching nominal significance in FIBRONEER™-ILD. 1 , 2 Nerandomilast demonstrated a favorable safety and tolerability pro no requirement for liver monitoring. As monotherapy, it showed similar discontinuation rates to placebo. 1 , 2 Canadian prevalence estimates suggest that more than 17,000 people may be living with IPF. 4 IPF and PPF are rare, progressive lung diseases, causing irreversible lung scarring that severely restricts breathing. 5 , 6 Despite the life-threatening nature of these conditions that have a prognosis worse than many cancers, 7 , 8 , 9 many people delay initiating therapy or discontinue therapy due to gastrointestinal side effects and/or photosensitivity. 10 , 11 , 13 In IPF specifically, approximately half of those who stop therapy do so within six months. 12 Dr. Martin Kolb, MD, PhD, Professor of Medicine, Division of Respirology, McMaster University "Idiopathic pulmonary fibrosis and progressive pulmonary fibrosis are rare, progressive diseases with limited treatment options. In IPF, we have seen little clinical trial success over the past decade. The authorization of JASCAYD™ is welcome news and provides an important new and better tolerated treatment option for patients living with IPF and PPF." Sharon Lee, CEO, Canadian Pulmonary Fibrosis Foundation (CPFF) "People living with pulmonary fibrosis have waited more than a decade for a new treatment option. During that time, patients and families have faced the daily challenges of a disease that affects their independence, quality of life and plans for the future. The authorization of JASCAYD™ brings renewed hope to our community. We are grateful to the researchers and clinical trial participants who made this advancement possible, and we will continue working toward equitable access for Canadians who need it." Dr. Rasha Eldesouky Abouelabbas, Vice President, Medical and Regulatory Affairs, Boehringer Ingelheim (Canada) Ltd . "The authorization of JASCAYD™ marks an important milestone for patients, caregivers and healthcare professionals. We are proud to bring a new treatment option to Canadians living with IPF and PPF and remain committed to advancing lung health innovation for people affected by serious lung diseases." About nerandomilast JASCAYD ™ (nerandomilast) is an oral PDE4B inhibitor with antifibrotic and immunomodulatory effects authorized in multiple countries worldwide for the treatment of adults with IPF and adults with PPF. Boehringer Ingelheim is also exploring the potential of nerandomilast in two rheumatic diseases: systemic sclerosis (SSc) and myositis (IIM). About IPF and PPF Idiopathic pulmonary fibrosis (IPF) and progressive pulmonary fibrosis (PPF) are both conditions with irreversible build-up of scar tissue in the lungs, affecting the lungs' ability to take in and transfer oxygen into the bloodstream. 6 , 7 , 13 Signs and symptoms of IPF and PPF include a persistent dry cough and shortness of breath on exertion. 7 , 14 In IPF, the root cause of pulmonary fibrosis is not known. 14 In PPF, the scarring of the lungs may be linked to an existing condition (e.g. rheumatoid arthritis or systemic sclerosis), result from exposure to inhaled substances (e.g. asbestos or mold), or due to an unknown cause (idiopathic). 6 About Boehringer Ingelheim (Canada) Ltd. Boehringer Ingelheim is a biopharmaceutical company active in both human and animal health. As one of the industry's top investors in research and development, the company focuses on developing innovative therapies that can improve and extend lives in areas of high unmet medical need. Independent since its foundation in 1885, Boehringer takes a long-term perspective, embedding sustainability along the entire value chain. Our approximately 54,300 employees serve over 130 markets to build a healthier and more sustainable tomorrow. The Canadian headquarters of Boehringer Ingelheim was established in 1972 in Montreal, Quebec and is now located in Burlington, Ontario. Boehringer Ingelheim employs approximately 500 people across Canada. Learn more at . References ___________________________________ 1 Maher T et al. Nerandomilast in Patients with Progressive Pulmonary Fibrosis. N Engl J Med. 2025;392(22):2203-2214. 2 Richeldi L, et al. Nerandomilast in Patients with Idiopathic Pulmonary Fibrosis. N Engl J Med . 2025;392(22):2193-2202. 3 JASCAYD™ (nerandomilast) Product Monograph. Canada. (Last updated: Oct 2026). 4 Hopkins, Robert & Burke, Natasha & Fell, Charlene & Dion, Genevieve & Kolb, Martin. (2016). Epidemiology and survival of idiopathic pulmonary fibrosis from national data in Canada. European Respiratory Journal. 48. ERJ-01504. 10.1183/13993003.01504-2015. 5 Kondoh Y, Inoue Y. Progressive Pulmonary Fibrosis: Current Status in Terminology and Future Directions. Adv Ther . 2025;42(7):2988–3001. 6 van Cleemput, J, et al. Idiopathic Pulmonary Fibrosis for Cardiologists: Differential Diagnosis, Cardiovascular Comorbidities, and Patient Management. Adv Ther . 2019;36, 298–317. 7 Cen Z, et al . Ann Med . 2024;56(1):2406439. 8 Siegel RL, et al. A Cancer Journal for Clinicians . 2024;74(1):12–49. 9 Vancheri C, et al. Eur Respir J . 2010;35(3):496–504. 10 Esbriet SmPC -- Roche, 2014. 11 Ofev SmPC -- Boehringer Ingelheim, 2025 (Last updated: Oct 2025). 12 Levra S et al. Biomedicine s. 2022;10(12):3229. 13 Upagupta C, et al. Eur Respir Rev . 2018;27:180033. 14 Grant-Orser A, et al. BMJ Open Respir Res. 2024;11:e002333. SOURCE Boehringer Ingelheim Canada Ltd.

Phase 3Drug ApprovalClinical Result

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 Nerandomilast

External Link

KEGG	Wiki	ATC	Drug Bank
D12975	-	-	-

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Progressive fibrotic interstitial lung disease	European Union	Boehringer Ingelheim GmbH	15 Jul 2026
Progressive fibrotic interstitial lung disease	Iceland	Boehringer Ingelheim GmbH	15 Jul 2026
Progressive fibrotic interstitial lung disease	Liechtenstein	Boehringer Ingelheim GmbH	15 Jul 2026
Progressive fibrotic interstitial lung disease	Norway	Boehringer Ingelheim GmbH	15 Jul 2026
Progressive pulmonary fibrosis	China	Boehringer Ingelheim International GmbH	09 Dec 2025
Idiopathic Pulmonary Fibrosis	United States	Boehringer Ingelheim Pharmaceuticals, Inc.	07 Oct 2025

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Idiopathic Inflammatory Myopathies	Phase 3	United States	Boehringer Ingelheim GmbH	14 Dec 2026
Idiopathic Inflammatory Myopathies	Phase 3	China	Boehringer Ingelheim GmbH	14 Dec 2026
Idiopathic Inflammatory Myopathies	Phase 3	Japan	Boehringer Ingelheim GmbH	14 Dec 2026
Idiopathic Inflammatory Myopathies	Phase 3	Argentina	Boehringer Ingelheim GmbH	14 Dec 2026
Idiopathic Inflammatory Myopathies	Phase 3	Australia	Boehringer Ingelheim GmbH	14 Dec 2026
Idiopathic Inflammatory Myopathies	Phase 3	Belgium	Boehringer Ingelheim GmbH	14 Dec 2026
Idiopathic Inflammatory Myopathies	Phase 3	Brazil	Boehringer Ingelheim GmbH	14 Dec 2026
Idiopathic Inflammatory Myopathies	Phase 3	Bulgaria	Boehringer Ingelheim GmbH	14 Dec 2026
Idiopathic Inflammatory Myopathies	Phase 3	Canada	Boehringer Ingelheim GmbH	14 Dec 2026
Idiopathic Inflammatory Myopathies	Phase 3	France	Boehringer Ingelheim GmbH	14 Dec 2026

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04771286 \| NCT01835899 \| NCT01594515 (Pubmed \| Eur J Drug Metab Pharmacokinet)	Phase 1	-	75	Nerandomilast	ilaxdjncay(xdwmdqttyp) = mhuntiqrky iaauqzvcwc (wwmdwrvzmk ) View more	Positive	01 Sep 2026
NCT06195072 (CONQUEST, EULAR2026)	Phase 2	Interstitial lung disease due to systemic disease	127	Amlitelimab	zklzbbhdez(fgsknwibzk) = qslejkzbyn hduvcketei (fmhwwqmprr ) View more	Positive	11 Jun 2026
FIBRONEER-IPF (ATS2026)	Phase 3	Idiopathic Pulmonary Fibrosis \| Progressive fibrotic interstitial lung disease	2,353	Nerandomilast 9 mg bid	pkkwzuzcno(rdwlijextt) = lower with nerandomilast versus placebo hvvsbtbokb (guuwgtuccz ) View more	Positive	15 May 2026
				Nerandomilast 18 mg bid
FIBRONEER-ILD (ATS2026)	Phase 3	Idiopathic Pulmonary Fibrosis \| Progressive pulmonary fibrosis	2,353	Nerandomilast 9 mg bid	bjcpizpmtq(vsanssfqvv): P-Value = 0.88	Positive	15 May 2026
				Nerandomilast 18 mg bid
ATS2026	Not Applicable	Lung Diseases, Interstitial	1,715	Nerandomilast 18 mg	budtvuvgxj(oyzukkprxv): MD = 72.64 (95.0% CI, 49.79 - 95.48), P-Value = < 0.01 View more	Positive	15 May 2026
				Placebo
NCT05321082 (FIBRONEER-ILD, CTgov)	Phase 3	Progressive fibrotic interstitial lung disease	1,178	Placebo (Placebo)	ixowksjilj(vekypfylls) = gzbivfvwvi tjqvdfzfsw (nazntrnlle, ydrggiyksp - vnpogzhnae) View more	-	09 Jan 2026
				BI 1015550 (Nerandomilast 9 mg)	ixowksjilj(vekypfylls) = fjgshrlgmm tjqvdfzfsw (nazntrnlle, vbhlpgwzbc - lwaqcnpkpv) View more
NCT06624072 (CTgov)	Phase 1	-	15	Nerandomilast (Nerandomilast 18 mg Pediatric (Ped) Fasted State (Treatment T1))	whkjcyuqbx(hrnyzhyihx) = rkujfksgzn tbkppvbkoi (chmnfoujlq, NA) View more	-	08 Jan 2026
				Nerandomilast (Nerandomilast 18 mg Adult Fasted State (Reference R))	whkjcyuqbx(hrnyzhyihx) = wiiibyxppe tbkppvbkoi (chmnfoujlq, NA) View more
NCT06070610 (CTgov)	Phase 1	-	14	Pirfenidone+Nintedanib (Pirfenidone/Nintedanib alone (Reference))	pepscavzdu(qqjtowthki) = apsalkqvme nzvhuqhpvt (rugxkfbxze, NA) View more	-	02 Dec 2025
				Pirfenidone+Nerandomilast+Nintedanib (Pirfenidone/Nintedanib in combination with Nerandomilast (Test))	pepscavzdu(qqjtowthki) = iwrideoprr nzvhuqhpvt (rugxkfbxze, NA) View more
NCT06393127 (CTgov)	Phase 1	-	64	nerandomilast (Test treatment (T))	wigmblibgn(ccvmqhvzqq) = aavlajgjzy miaejqmpou (mdwsqcqmip, NA) View more	-	01 Dec 2025
				nerandomilast (Reference treatment (R))	wigmblibgn(ccvmqhvzqq) = byyvavcigm miaejqmpou (mdwsqcqmip, NA) View more
NCT06139302 (CTgov)	Phase 1	-	12	Nerandomilast (Nerandomilast 9 mg)	icgrxpvaru(pnikwlebeh) = rnmzebedyq cupfcnrjyz (udbvihptuj, 13.8) View more	-	01 Dec 2025
				Nerandomilast (Nerandomilast 18 mg)	icgrxpvaru(pnikwlebeh) = vcifjhbqar cupfcnrjyz (udbvihptuj, 52.8) View more

Translational Medicine

Boost your research with our translational medicine data.

view full example data

Deal

Boost your decision using our deal data.

view full example data

Core Patent

Boost your research with our Core Patent data.

view full example data

Clinical Trial

Identify the latest clinical trials across global registries.

view full example data

Approval

Accelerate your research with the latest regulatory approval information.

view full example data

Regulation

Understand key drug designations in just a few clicks with Synapse.

view full example data

Hiro LS Researcher

The AI Search Engine Built to Accelerate Biopharma Decisions

Search across billion-scale life sciences data to uncover signals, validate evidence, and act with confidence.

Ask any biopharma research question→

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, Patsnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Discover Synapse Data Servers

Synapse data is now integrated into the PatSnap LS Model Context Protocol (MCP) service. Customize your LLM agent now using our MCP server!

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis