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

Structure/Sequence

Molecular FormulaC20H25ClN6O2S

InChIKeyUHYCLWAANUGUMN-SSEXGKCCSA-N

CAS Registry1423719-30-5

Clinical Trials associated with Nerandomilast

NCT07321860

/ Not yet recruitingPhase 2/3

Randomized, Double-Blind, Placebo-Controlled Phase 2a Study of Partial TGF-βR1 (ALK5) Inhibition With Galunisertib Combined With PDE4 Inhibition With Nerandomilast in GREM2-Positive ALS

Amyotrophic lateral sclerosis (ALS) is a relentlessly progressive neurodegenerative disorder characterized by loss of upper and lower motor neurons, leading to muscle weakness, respiratory decline, and eventual mortality. A growing body of translational and clinical evidence implicates neuroinflammation, reactive astrocytosis, and maladaptive TGF-β signaling as central contributors to disease progression. Elevated levels of Gremlin-2 (GREM2) have been identified as a marker of dysregulated TGF-β-linked astrocytic activity and fibrotic gene programs in some ALS patients, and preclinical data suggest that attenuating these pathways may mitigate glial toxicity and improve neuronal survival.
Galunisertib, a selective ATP-competitive TGF-β receptor type I (TGF-βR1/ALK5) inhibitor, has been developed to block SMAD2/3 phosphorylation and TGF-β-mediated transcriptional programs. Meanwhile, nerandomilast, a selective PDE4B inhibitor, elevates intracellular cAMP in immune and glial cells, shifting pro-inflammatory signaling toward resolution and antagonizing secondary fibrotic and inflammatory cascades. Preclinical models show that PDE4 inhibition and TGF-β pathway blockade concurrently reduce maladaptive glial phenotypes and fibrotic mediators.
This study investigates the combination of galunisertib + nerandomilast in ALS patients with elevated GREM2, hypothesizing that dual targeting of TGF-β-mediated astrocytic reactivity and PDE4B-regulated inflammatory signaling will translate into slowing of disease progression and favorable pharmacodynamic effects on central biomarkers of neuroinflammation and neurodegeneration.

Start Date30 Jun 2026

Sponsor / Collaborator-

NCT07366034

/ Not yet recruitingPhase 3

A Study to Evaluate the Dose-exposure, Safety, and Exploratory Efficacy of Nerandomilast in Children and Adolescents From 2 Years to Less Than 18 Years of Age With Fibrosing Interstitial Lung Disease (Part A: Double-blind, Placebo-controlled in Children From 6 to Less Than 18 Years of Age and Open-label Active Treatment in Children From 2 to Less Than 6 Years of Age), Followed by an Open-label Phase With Active Treatment (Part B)

This study is open to children and adolescents aged 2 to 17 years with interstitial lung disease (ILD). Nerandomilast has just been approved in some countries to help adults with a lung condition called idiopathic pulmonary fibrosis. The purpose of this study is to understand how nerandomilast is tolerated and handled by the body and whether nerandomilast also helps children and adolescents with ILD.
For participants aged 6 to 17 years when joining, the study has 2 parts. In the first part, participants are put into 1 of 2 groups randomly, which means by chance. One group gets nerandomilast and the other group placebo. Placebo looks like nerandomilast but does not contain any medicine.
Participants are twice as likely to be in the nerandomilast group. They take tablets twice a day for 6 months. After these 6 months, in the second part of this study, they get nerandomilast for at least 2 years regardless of what they got in the first part.
Young participants aged 2 to 5 years when joining get nerandomilast from the start. They receive tablets twice a day for at least 2 and a half years.
Depending on when a person joins, the study lasts between 2 and a half years and up to 5 years. During this time, participants may visit the study site about 18 to 30 times. Study doctors collect blood samples to check participants' health and to find out how their body handles the study medicine. Doctors also check the function of the lungs, body growth, and how participants feel. The study doctors also regularly check participants' health and take note of any changes. For participants aged 6 to 17 years, the results are compared between the groups to see whether nerandomilast treatment helps children and adolescents.

Start Date15 Jun 2026

Sponsor / Collaborator

Boehringer Ingelheim GmbH

NCT06241560

/ Not yet recruitingPhase 2

An Open-label, Single-group Trial to Evaluate the Effect of Pirfenidone on the Pharmacokinetics of a Single Oral Dose of BI 1015550

This study is open to adults with idiopathic pulmonary fibrosis (IPF) who are 40 years and older. The purpose of this study is to find out whether a medicine called pirfenidone changes the amount of a medicine called BI 1015550 in the blood. Some people may take more than one medicine at a time. Therefore, it is important to understand how different medicines influence one another.
Participants take one dose of BI 1015550 as a tablet. Participants then take one tablet of pirfenidone 3 times a day for one week. The dose is then increased to 2 tablets 3 times a day for the second week. In the third week the dose is increased further to 3 tablets 3 times a day. Participants then take another dose of BI 1015550 as a tablet.
Participants are in the study for a little over 1 month. During this time, they visit the study site 15 times. Two of the visits include overnight stays at the study site. The study staff also contacts the participants by phone. During the visits, the doctors collect information about participants' health and take blood samples from the participants. They compare the amount of pirfenidone and BI 1015550 in the blood. Doctors also regularly check participants' health and take note of any unwanted effects.

Start Date13 Mar 2026

Sponsor / Collaborator

Boehringer Ingelheim GmbH

100 Clinical Results associated with Nerandomilast

100 Translational Medicine associated with Nerandomilast

100 Patents (Medical) associated with Nerandomilast

Literatures (Medical) associated with Nerandomilast

01 Jan 2026·Annals of Medicine and Surgery

Jascayd (nerandomilast): a novel PDE4B inhibitor for idiopathic pulmonary fibrosis

Author: Hujjat, Syeda Fadak Zahra ; Chandani, Devya Khaim ; Khan, Muhammad Saad ; Chandani, Harshika Khaim ; Mahmoud, Abubakr

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial pneumonia with poor prognosis and limited therapeutic options. Despite the introduction of pirfenidone and nintedanib, treatment discontinuation due to adverse effects remains common, highlighting the need for better-tolerated, mechanistically distinct agents. Jascayd (nerandomilast), a first-in-class selective phosphodiesterase-4B inhibitor developed by Boehringer Ingelheim, was approved by the FDA in October 2025 for adults with IPF. By elevating intracellular cyclic adenosine monophosphate (cAMP) in inflammatory and structural lung cells, nerandomilast suppresses pro-inflammatory cytokines and fibroblast activation, producing anti-inflammatory and antifibrotic effects with improved tolerability over nonselective PDE4 inhibitors. In phase 3 FIBRONEER-IPF and FIBRONEER-ILD trials, nerandomilast significantly reduced the annual rate of forced vital capacity decline versus placebo, regardless of concomitant antifibrotic use. Common adverse effects included mild diarrhea, nausea, and fatigue, with low discontinuation rates. Long-term extension data demonstrate sustained safety and lung function preservation. Offering both monotherapy and combination potential, Jascayd establishes a new therapeutic class that targets inflammation and fibrosis concurrently, representing a pivotal advancement toward personalized, multi-pathway treatment in IPF.

01 Jan 2026·TRENDS IN PHARMACOLOGICAL SCIENCES

Nerandomilast as the first PDE4B-selective therapy in idiopathic pulmonary fibrosis

Article

Author: Ibrahim, Md ; Piazza, Gary A ; Ahsan, Fakhrul

01 Nov 2025·AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY

Insights into the Cellular and Molecular Mechanisms behind the Antifibrotic Effects of Nerandomilast

Article

Author: Herrmann, Franziska E. ; Geillinger-Kästle, Kerstin ; Wolf, Felix ; Mayr, Christoph H. ; Reininger, Dennis ; Wespel, Susanne L. ; Dick, Alec ; Laufhaeger, Nadine ; Gantner, Florian ; Nickolaus, Peter

Abstract:

The quest for innovative pharmacologic interventions in idiopathic pulmonary fibrosis (IPF) is a challenging journey. The complexity of the disease demands a comprehensive approach that targets multiple cell types and pathways. This study examined the antifibrotic properties of nerandomilast, a preferential phosphodiesterase 4B inhibitor, focusing on its effects on myofibroblasts (MFs) and endothelial cells. Using cytokine-stimulated human IPF lung fibroblasts and RNA sequencing, we assessed the effects of nerandomilast on MF contractility, MF markers, and differentiation mechanisms. In addition, using human microvascular endothelial cells, we assessed endothelial barrier integrity and monocyte adhesion in a three-dimensional microfluidic chip. Our results show that nerandomilast significantly inhibited MF contractility and marker expression in cytokine-stimulated human IPF lung fibroblast cells. Treatment with nerandomilast significantly activated cAMP-associated pathways and G-protein–coupled receptor signaling events while inhibiting mitogen-activated protein kinase signaling pathways and transforming growth factor β signaling. Nerandomilast also significantly reduced microvascular permeability in cytokine-stimulated human lung microvascular endothelial cells. Finally, in an adeno-associated virus–human diphtheria toxin receptor/diphtheria toxin mouse model of acute lung injury, nerandomilast significantly inhibited total protein in lavage, total macrophages, neutrophils, cell count, and VCAM-1 expression. In summary, our results demonstrate that nerandomilast induces the dedifferentiation of human IPF lung MFs and diminishes their contractility in vitro by interfering with transforming growth factor β, mitogen-activated protein kinase phosphatase-1, and G-protein–coupled receptor signaling pathways. It also mitigates vascular dysfunction by strengthening endothelial junctions and inhibiting adhesion protein expression. These findings highlight nerandomilast’s potential therapeutic use in IPF by providing insights into its cellular and molecular actions.

News (Medical) associated with Nerandomilast

02 Feb 2026

·www.fiercebiotech.com

China\'s Newsoara pens $135M deal for remaining rights to vTv\'s inflammation drug

Newsoara CEO Benny Li touted HPP737 as “highly differentiated oral PDE4 inhibitor with the potential to address unmet needs in inflammation-mediated disease.”\n Having already secured regional rights to vTv Therapeutics’ inflammation drug, China’s Newsoara is fronting $20 million to take ownership of the clinical-stage asset across the rest of the world.The therapy in question is HPP737, a phosphodiesterase type 4 (PDE4) inhibitor that vTv has taken into phase 1 development to treat psoriasis. Newsoara originally secured the rights for the drug in China and various other Pacific Rim countries in 2018 for an undisclosed price.Targeting PDE4 drives anti-inflammatory and antifibrotic effects and has been put to good use with Arcutis’ psoriasis cream Zoryve and Amgen’s oral psoriasis drug Otezla.According to vTv Therapeutics, the preclinical and clinical data for HPP737 suggest the oral drug “may be able to expand the therapeutic use for [the PDE4] target, which has been limited by the side effects of currently available PDE4 inhibitors,” such as nausea, vomiting and diarrhea.Now, Newsoara is willing to hand over $20 million for the global rights to HPP737. The new deal means North Carolina-based vTv could also be in line for up to $50 million in development milestones, $65 million in sales milestones and tiered royalties on sales should Newsoara manage to get HPP737 to market.“Over the last several years, vTv and Newsoara have enjoyed a productive and collaborative relationship, and this exciting expansion of the relationship will help accelerate the clinical development of our highly differentiated and potential best-in-class PDE4 inhibitor HPP737,” vTv’s chief business officer Rich Nelson said in the release. The company’s CEO, Paul Sekhri, said vTv “remain[s] opportunistic in exploring potential collaborations” for its in-house pipeline while it continues to push to get its lead candidate, the Type 1 diabetes drug cadisegliatin, through phase 3 development. The FDA placed a hold on a trial of the liver-selective glucokinase activator in 2024, but the hold was lifted last year.In this morning\'s release, Newsoara CEO Benny Li touted HPP737 as a “highly differentiated oral PDE4 inhibitor with the potential to address unmet needs in inflammation-mediated disease.”“With this expanded license, we plan to leverage our development and commercialization capabilities to advance HPP737’s progress and, if approved, bring it to patients worldwide,” Li added.There was a continued buzz of activity in the PDE4 inhibitor space last year, especially around respiratory conditions. This included the approval of Boehringer Ingelheim’s idiopathic pulmonary fibrosis (IPF) drug Jascayd as well as Merck & Co.’s $10 billion acquisition of Verona Pharma for its approved PDE3 and PED4 inhibitor Ohtuvayre for chronic obstructive pulmonary disorder (COPD).GSK secured its own PED3/4 inhibitor for COPD as part of a $12 billion biobucks, 12-asset deal with Hengrui Pharma, while Transpire Bio licensed an inhaled PDE4 inhibitor for IPF from China’s Intragrand Pharma.

Phase 1Drug ApprovalAcquisitionLicense out/inPhase 3

20 Jan 2026

·www.prnewswire.com

Brainomix e-Lung AI Imaging Technology Selected as Co-Primary Endpoint in Boehringer Ingelheim Phase 3 Clinical Trial in Pulmonary Fibrosis

The DROP-FPF trial is the first Phase 3 trial in interstitial lung disease (ILD) to use automated, quantitative high-resolution CT scan (HRCT) imaging biomarkers as a co-primary endpoint OXFORD, England and CHICAGO, Jan. 20, 2026 /PRNewswire/ -- Brainomix, a global leader and pioneer of AI-powered imaging tools in lung fibrosis and stroke, today announced it was selected by Boehringer Ingelheim, the leading biopharmaceutical company providing therapeutic options for interstitial lung disease (ILD), to provide objective, quantitative HRCT imaging biomarkers as a co-primary endpoint in the DROP-FPF Phase 3 study. Continue Reading Brainomix e-Lung is an FDA-cleared, AI-powered imaging software platform that automatically quantifies and segments CT lung scans. DROP-FPF is a Phase 3b double blind, randomized, placebo-controlled study investigating the safety and effectiveness of nerandomilast (Jascayd®) in individuals with interstitial lung abnormalities (ILA's) and a family history of pulmonary fibrosis. Jascayd® received FDA approval for both idiopathic pulmonary fibrosis (IPF) and progressive pulmonary fibrosis (PPF) in late 2025, ushering in a new therapeutic option to help manage these devastating forms of ILD. The study, set to initiate patient enrollment in January and include a two-year follow-up period, will investigate whether early intervention with nerandomilast slows the progression of early signs of pulmonary fibrosis in people with a family history of the condition. Pulmonary fibrosis causes irreversible lung damage and impacts 3-4 million people worldwide1. Yet individuals at elevated risk due to family history currently have no approved treatment options until symptoms emerge, often after substantial lung damage has already occurred. This trial marks the first time that automated, quantitative high-resolution CT (HRCT) imaging biomarkers will serve as a co-primary endpoint in a Phase 3 ILD study. Brainomix's AI-powered e-Lung software will provide objective measurements of fibrosis extent and disease severity by analyzing HRCT scans at baseline and at follow-up timepoints. Martin Beck, Senior VP and Head of Therapeutic Area Inflammation at Boehringer Ingelheim, commented: "IPF and PPF are serious, progressive lung diseases that can be more life-threatening than some forms of cancer. They progress silently, with early symptoms often dismissed as ageing or misdiagnosed. But in a progressive disease, there is no going back. Once fibrosis advances, the damage is irreversible. That's why this study is so important. Our goal is simple but profound: learn whether acting earlier can change outcomes for families facing these devastating diseases. Using Brainomix's advanced HRCT algorithms to define meaningful progression, we aim to generate insights that could transform how and when to intervene." Professor Peter George, Consultant Pulmonologist at the Royal Brompton Hospital, UK and Brainomix Senior Medical Director, added: "Accurate and reliable quantification of subtle but clinically meaningful features of disease progression is essential to achieving the objectives of this study. Brainomix e-Lung enables this through validated, proprietary, AI-driven CT biomarkers that accurately quantify physiologically meaningful features of interstitial lung disease. This information can reveal whether disease biology is changing, even when patients still appear clinically well and have normal lung function, allowing researchers to detect treatment effects far earlier than previously possible. This has the potential to significantly improve clinical trial design." The AI-powered and FDA-cleared e-Lung software has been trained on large, diverse datasets of patients with various forms of ILD and has been validated in the Phase 3 INBUILD study that originally led to the approval of nintedanib (Ofev®) in patients with progressive pulmonary fibrosis. The DROP-FPF study will be delivered in partnership with Voiant – the industry leading AI-based clinical trial imaging solution provider – leveraging Brainomix's advanced imaging biomarkers alongside Voiant's centralized image management and analytics framework. "AI-driven quantitative imaging analysis enables more confident detection of treatment effects while improving efficiency through smarter patient selection and optimized trial design. By combining Brainomix's advanced imaging biomarkers with Voiant's independent imaging and analytics framework, the study will deliver higher-precision respiratory endpoints with greater speed and reliability," Jessica Ataharul, Vice President of Clinical Operations at Voiant. 1. Boehringer Ingelheim, Facts about IPF – Respiratory Disease About Brainomix Brainomix is a global pioneer in AI medical imaging, enabling precision medicine for better treatment decisions in stroke and lung fibrosis. Its flagship product, Brainomix 360 Stroke, is the world's first fully automated AI-imaging platform, designed for acute stroke assessment at all points of the patient pathway, facilitating more confident treatment and transfer decisions for patients in all hospitals, regardless of local resources or expertise. Brainomix 360 e-Lung technology applies AI-driven CT biomarkers to identify, monitor, and predict disease progression in pulmonary fibrosis. Founded as a spinout from the University of Oxford, Brainomix has offices in the UK, Ireland and the USA, and operations in more than 20 countries. To learn more about Brainomix and its technology visit , and follow us on Twitter, LinkedIn, and Facebook. Contacts Jeff Wyrtzen, Chief Marketing Officer [email protected] T +44 (0)1865 582730 Media Enquiries Jason Braco, Ph.D. LifeSci Communications [email protected] UK & Europe Media Enquiries Sue Charles Charles Consultants [email protected] Photo - Logo - SOURCE Brainomix 21% more press release views with Request a Demo

Phase 3

20 Jan 2026

·firstwordpharma.com

Brainomix AI imaging takes centre stage in Boehringer Ingelheim lung disease trial

Medicine rarely gets a second chance with pulmonary fibrosis, a silent disease often discovered only after irreversible damage has set in. But Boehringer Ingelheim is now testing whether earlier treatment, tracked using AI-powered CT scans, can finally put doctors ahead of the disease instead of chasing it.The DROP-FPF study – the first time that automated, quantitative high-resolution CT (HRCT) imaging biomarkers will serve as a co-primary endpoint in a Phase III interstitial lung disease (ILD) trial – will incorporate imaging analysis from Brainomix's e-Lung software alongside conventional measures to assess disease progression. The move reflects a shift in how late-stage pulmonary fibrosis trials define meaningful change, with imaging taking on a role traditionally held by clinical and functional endpoints (see – Spotlight On: What Boehringer Ingelheim's AI imaging endpoint bet signals for pharma).DROP-FPF is evaluating Boehringer's Jascayd (nerandomilast) in people with interstitial lung abnormalities who have a family history of pulmonary fibrosis. Unlike previous late-stage studies that enrolled patients with established idiopathic or progressive pulmonary fibrosis, the trial is focused on earlier disease, when changes can already be seen on CT scans, even though patients may have few symptoms.It will compare CT scans taken at baseline and during follow-up, using Brainomix's e-Lung software to measure changes in fibrosis and overall disease severity. Those imaging results will be assessed alongside lung function tests, which can be slow to change.In 2024, Brainomix reported data showing that its automated CT biomarkers could identify patients with idiopathic pulmonary fibrosis who were more likely to experience lung function decline based on a single baseline scan. The findings, drawn from a discontinued AstraZeneca trial and published in the American Journal of Respiratory and Critical Care Medicine, showed the imaging could distinguish patients with faster-progressing disease from those with more stable patterns.Jascayd recently secured expanded US approval for progressive pulmonary fibrosis, following Phase III data showing a smaller decline in forced vital capacity than placebo.Boehringer said the DROP-FPF trial is intended to assess whether intervening earlier can alter disease trajectory in people at elevated risk, using imaging to define meaningful change in a condition that can progress silently.The study is expected to begin enrolling patients in January and will follow participants for two years. Imaging delivery and analysis will be supported by Voiant, which is providing centralised image management and analytics for the trial.

Phase 3

100 Deals associated with Nerandomilast

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Progressive pulmonary fibrosis	China	Boehringer Ingelheim International GmbH	09 Dec 2025
Idiopathic Pulmonary Fibrosis	United States	Boehringer Ingelheim Pharmaceuticals, Inc.	07 Oct 2025
Idiopathic Pulmonary Fibrosis	United States	Boehringer Ingelheim Norway KS	07 Oct 2025

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Idiopathic Interstitial Pneumonias	Phase 3	United States	Boehringer Ingelheim GmbH	23 Jan 2026
Idiopathic Interstitial Pneumonias	Phase 3	Japan	Boehringer Ingelheim GmbH	23 Jan 2026
Idiopathic Interstitial Pneumonias	Phase 3	Argentina	Boehringer Ingelheim GmbH	23 Jan 2026
Idiopathic Interstitial Pneumonias	Phase 3	Belgium	Boehringer Ingelheim GmbH	23 Jan 2026
Idiopathic Interstitial Pneumonias	Phase 3	Canada	Boehringer Ingelheim GmbH	23 Jan 2026
Idiopathic Interstitial Pneumonias	Phase 3	France	Boehringer Ingelheim GmbH	23 Jan 2026
Idiopathic Interstitial Pneumonias	Phase 3	Germany	Boehringer Ingelheim GmbH	23 Jan 2026
Idiopathic Interstitial Pneumonias	Phase 3	Italy	Boehringer Ingelheim GmbH	23 Jan 2026
Idiopathic Interstitial Pneumonias	Phase 3	Netherlands	Boehringer Ingelheim GmbH	23 Jan 2026
Idiopathic Interstitial Pneumonias	Phase 3	South Korea	Boehringer Ingelheim GmbH	23 Jan 2026

Clinical Result

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Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT05321082 (FIBRONEER-ILD, CTgov)	Phase 3	Progressive fibrotic interstitial lung disease	1,178	Placebo (Placebo)	dhzuqzihih(bcyxghcyqn) = zhetbrxohh xiiedfecsw (dowxeytbtm, ktyadeeoap - rpaowbgzby) View more	-	09 Jan 2026
				BI 1015550 (Nerandomilast 9 mg)	dhzuqzihih(bcyxghcyqn) = mefgnlklcy xiiedfecsw (dowxeytbtm, xckrroeidp - chxwliumno) View more
NCT06624072 (CTgov)	Phase 1	-	15	Nerandomilast (Nerandomilast 18 mg Pediatric (Ped) Fasted State (Treatment T1))	rjadjgekoy(gbnabwfazf) = fzczkdiooo txcatmiflv (ghmzpyutzy, NA) View more	-	08 Jan 2026
				Nerandomilast (Nerandomilast 18 mg Adult Fasted State (Reference R))	rjadjgekoy(gbnabwfazf) = fwmdaseujj txcatmiflv (ghmzpyutzy, NA) View more
NCT06070610 (CTgov)	Phase 1	-	14	Pirfenidone+Nintedanib (Pirfenidone/Nintedanib alone (Reference))	wijtcdwnnp(pepixctwmg) = qzvlzhdzlf vpkdzvuvll (ktznpayewl, NA) View more	-	02 Dec 2025
				Pirfenidone+Nerandomilast+Nintedanib (Pirfenidone/Nintedanib in combination with Nerandomilast (Test))	wijtcdwnnp(pepixctwmg) = whmcuibory vpkdzvuvll (ktznpayewl, NA) View more
NCT06139302 (CTgov)	Phase 1	-	12	Nerandomilast (Nerandomilast 9 mg)	sqphsrkypv(rcavxdbdmo) = qqqwlwbtkn jsaiykpxnv (anthxfgjmh, 13.8) View more	-	01 Dec 2025
				Nerandomilast (Nerandomilast 18 mg)	sqphsrkypv(rcavxdbdmo) = jgxhkknyfm jsaiykpxnv (anthxfgjmh, 52.8) View more
NCT06415045 (CTgov)	Phase 1	-	18	Nerandomilast (Nerandomilast fasted state (Reference (R)))	hofkabaugz(zdtkdeqagt) = scftammvvh ubpcxevjqb (hqjcziuerm, NA) View more	-	01 Dec 2025
				Nerandomilast (Nerandomilast fed state (Test (T)))	hofkabaugz(zdtkdeqagt) = lkdgvecebi ubpcxevjqb (hqjcziuerm, NA) View more
NCT06393127 (CTgov)	Phase 1	-	64	nerandomilast (Test treatment (T))	bstvxgvjcs(bvcaeifkyx) = vunityffag cpqdjzjpvv (xuesdgfapk, NA) View more	-	01 Dec 2025
				nerandomilast (Reference treatment (R))	bstvxgvjcs(bvcaeifkyx) = inwijztwfi cpqdjzjpvv (xuesdgfapk, NA) View more
NCT06408870 (CTgov)	Phase 1	-	64	BI 1015550 (BI 1015550 Formulation C1 (Reference, R))	dpupggxoaf(mowbksblvp) = fvjzyvfpjf tzkyzkeoqo (usnrtypqqp, na) View more	-	01 Dec 2025
				BI 1015550 (BI 1015550 Formulation C2 (Test, T))	dpupggxoaf(mowbksblvp) = qqxuiodknu tzkyzkeoqo (usnrtypqqp, na) View more
NCT05550636 (CTgov)	Phase 1	-	15	Midazolam (Midazolam (R))	nymicuwtye(httqjdpoio) = bakrjczdvu aoxpgntoyz (rxdaivckqn, NA) View more	-	01 Dec 2025
				Midazolam (T+BI 1015550 (BI 1015550 + Midazolam (T))	nymicuwtye(httqjdpoio) = rpwzlsatqp aoxpgntoyz (rxdaivckqn, NA) View more
NCT05633862 (CTgov)	Phase 1	-	24	BI 1015550 (BI 1015550 9 mg)	tgavrhtwxm(tltrkccapm) = bukjycbzkk jobbskkkbz (pafcegkfic, 19.1) View more	-	28 Nov 2025
				BI 1015550 (BI 1015550 18 mg)	tgavrhtwxm(tltrkccapm) = noqyaeffkd jobbskkkbz (pafcegkfic, 32.6) View more
NCT05661344 (CTgov)	Phase 1	Hepatic Insufficiency	28	BI 1015550 (BI 1015550 mild hepatic impairment)	bmowsxeclu(uztoiwuuwn) = hrjtmphcei ghvbasrxyv (xybpxfcqgx, NA) View more	-	28 Nov 2025
				BI 1015550 (BI 1015550 moderate hepatic impairment)	bmowsxeclu(uztoiwuuwn) = nfwflrcwan ghvbasrxyv (xybpxfcqgx, NA) View more

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