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

NCT07540988

/ 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)

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 Date28 Aug 2026

Sponsor / Collaborator

Boehringer Ingelheim GmbH

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 Date27 Jul 2026

Sponsor / Collaborator

Boehringer Ingelheim GmbH

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-

100 Clinical Results associated with Nerandomilast

100 Translational Medicine associated with Nerandomilast

100 Patents (Medical) associated with Nerandomilast

Literatures (Medical) associated with Nerandomilast

01 Apr 2026·DRUGS

Nerandomilast: First Approval

Review

Author: Brown, Michael B

Nerandomilast (JASCAYD^®) is an oral selective phosphodiesterase (PDE) 4B inhibitor developed by Boehringer Ingelheim Pharmaceuticals, Inc. for the treatment of lung fibrosis. It received its first approval on 7 October 2025 in the USA for the treatment of adults with idiopathic pulmonary fibrosis (IPF). Subsequently, nerandomilast was approved on 22 October 2025 in China for the treatment of adults with IPF, and on 10 and 19 December 2025 for treatment of adults with progressive pulmonary fibrosis (PPF) in China and the USA, respectively. Additional global filings and several phase II and III trials are underway. This article summarizes the milestones in the development of nerandomilast leading to this first approval for IPF.

01 Apr 2026·British Journal of Pharmacology

Nerandomilast, a PDE4B inhibitor, alleviates silica‐induced lung inflammation and fibrosis by inhibition of NLRP3 inflammasome and TGF‐β/Smad signalling

Article

Author: Yawen Song ; Di Sun ; Dongmei Wang ; Qiao Ye ; Yuanying Wang ; Nafeisa Dilixiati

Background and Purpose:

Silicosis is a major cause of occupational disease‐related morbidity and mortality worldwide, yet effective pharmacological treatments remain limited. Nerandomilast, a novel inhibitor of phosphodiesterase‐4B (PDE4B), has demonstrated anti‐fibrotic potential in idiopathic pulmonary fibrosis (IPF); however, its efficacy and mechanisms in silicosis have not been investigated.

Experimental Approach:

The therapeutic effects (and their underlying mechanisms) of PDE4B inhibition was evaluated in in models of silicosis, both in vivo (male C57BL/6N mice) and in vitro (THP‐1 macrophages and MRC‐5 cells). Single‐cell RNA sequencing, using lung tissue, was first performed to identify PDE4B as a key regulatory target in the pathogenesis of silicosis. Based on this finding, the therapeutic effects and underlying mechanisms of PDE4B inhibition were assessed using nerandomilast. Pulmonary function tests, inflammatory marker analyses and fibrosis evaluations were conducted to determine treatment efficacy. In addition, bulk RNA sequencing and transcriptomic analyses were performed to explore the molecular pathways modulated by nerandomilast.

Key Results:

PDE4B inhibition effectively prevented and attenuated silica‐induced lung inflammation in the mouse model by suppressing both canonical and non‐canonical NLRP3 inflammasome pathways in lung macrophages. Furthermore, PDE4B inhibition down‐regulated TGF‐β/Smad signalling in lung fibroblasts of silicosis, leading to a significant reduction in fibrosis‐related gene expression.

Conclusions and Implications:

These findings suggest that nerandomilast, a PDE4B inhibitor, may be a promising treatment for silicosis, which currently lacks effective therapies.

01 Apr 2026·Tuberculosis and Respiratory Diseases

Tweaking the Complex Fibrogenic Role of Lymphocytes in Idiopathic Pulmonary Fibrosis

Article

Author: Saba, Julie D ; Bhattacharyya, Aritra

Idiopathic pulmonary fibrosis is a deadly lung disease primarily affecting aged individuals. Even though there are two U.S. Food and Drug Administration-approved drugs, nintedanib and pirfenidone, with a recent addition of another drug, nerandomilast, yet they only reduce the progress of the disease. The mean survival rate is between 5 and 7 years even after treatment with antifibrotics. Cells of lymphoid lineage have been long reported to modulate the outcome of pulmonary fibrosis. In this review, we discuss how the cell of lymphoid lineage regulates the inflammatory niche within the lungs, leading to the development and progress of pulmonary fibrosis. The review also addresses possible therapeutic strategies that can be leveraged by specifically targeting the lymphoid cells in the pulmonary fibrotic niche.

News (Medical) associated with Nerandomilast

05 May 2026

·allsci.com

Insilico’s rentosertib inhalation solution receives China IND clearance for IPF

Insilico Medicine (HKEX: 3696) announced that China’s Center for Drug Evaluation (CDE) has cleared an investigational new drug (IND) application for an inhalation solution formulation of rentosertib (ISM001-055), its small-molecule TNIK inhibitor in development for idiopathic pulmonary fibrosis (IPF). The clearance allows the company to initiate a Phase I study evaluating the inhaled formulation in healthy volunteers and IPF patients, marking a formulation expansion for a molecule that has already generated Phase IIa oral data. IPF is a chronic, progressive fibrotic lung disease affecting approximately 5 million people worldwide. Median survival after diagnosis is three to four years, and the two antifibrotic agents approved by the US FDA in 2014 — Boehringer Ingelheim’s nintedanib (Ofev) and Genentech’s pirfenidone (Esbriet) — slow the rate of lung function decline without reversing or halting the underlying fibrotic process. Boehringer Ingelheim’s nerandomilast (Jascayd), a preferential phosphodiesterase 4B inhibitor, received FDA approval in October 2025, representing the first new mechanism approved for IPF in over a decade. All three approved agents are administered orally and act systemically, carrying tolerability burdens — particularly gastrointestinal toxicity with nintedanib and pirfenidone — that contribute to dose reductions and treatment discontinuations in clinical practice. Rentosertib (formerly ISM001-055) targets TNIK, or TRAF2- and NCK-interacting kinase, a serine/threonine kinase that Insilico identified as a potential antifibrotic target using its generative AI platform, Pharma.AI. The molecule was designed and nominated as a preclinical candidate in approximately 18 months, with fewer than 80 compounds synthesized and tested during the discovery phase. TNIK inhibition is mechanistically distinct from the tyrosine kinase inhibition of nintedanib, the TGF-β pathway modulation of pirfenidone, and the cAMP-elevating mechanism of nerandomilast, placing rentosertib in a class not yet represented among approved IPF therapies. The oral formulation of rentosertib completed a Phase IIa randomized trial, GENESIS-IPF, with results published in Nature Medicine in June 2025. Insilico has described the trial as showing good tolerability, a favorable pharmacokinetic profile, and dose-dependent improvements in forced vital capacity — the standard measure of lung function decline used as the primary endpoint across IPF trials. The US FDA granted rentosertib Orphan Drug Designation for IPF in February 2023, and China’s CDE granted it Breakthrough Therapy Designation in May 2025, a designation that carries expedited review implications under China’s regulatory framework. The newly cleared IND covers a Phase I study structured in two parts. The first is a randomized, double-blind, placebo-controlled evaluation in healthy participants using single ascending dose and multiple ascending dose cohorts. The second is a non-randomized, open-label multiple-dose evaluation in IPF patients. Approximately 80 subjects are expected to enroll across both parts. The study is designed to characterize the safety, tolerability, and pharmacokinetic profile of the inhaled formulation — standard objectives for a first-in-human study of a new route of administration for a compound with an existing clinical safety database from the oral program. The rationale for pursuing an inhalation solution in IPF is rooted in the pharmacological logic of direct pulmonary delivery. Inhaled administration can, in principle, achieve higher local drug concentrations in lung tissue at lower total doses than oral systemic dosing, potentially reducing the systemic exposure that drives off-target side effects. Insilico has reported that in preclinical studies, the inhalation solution of rentosertib achieved higher lung exposure with low systemic exposure and demonstrated antifibrotic and anti-inflammatory activity in animal models, alongside acceptable pharmacokinetic and safety profiles. No inhaled antifibrotic agent is currently approved for IPF, and if the inhaled formulation of rentosertib can reproduce the efficacy signals seen with the oral program while improving the tolerability profile, it would occupy a distinct clinical position relative to all three approved agents. Insilico has also stated that the oral rentosertib program remains on track to initiate Phase III trials in the second half of 2026, meaning the company is advancing two formulations of the same molecule in parallel — a strategy that, if both prove viable, could offer clinicians and patients flexibility in dosing route depending on tolerability and disease stage. The CDE clearance is the 13th IND clearance from Insilico’s AI-driven pipeline, which spans fibrosis, oncology, immunology, and central nervous system disorders. Rentosertib remains its most clinically advanced internal program and the one carrying the most direct evidence for the company’s broader thesis that generative AI can reproducibly identify novel drug targets and design molecules that reach clinical validation. This article was generated with AI assistance and reviewed and edited by the AllSci editorial team Explore more at AllSci News: https://allsci.com/news/ Your email address will not be published. Required fields are marked * Comment * Name * Email * Website

05 May 2026

·www.biospace.com

IPF draws investor heat as biotechs target fibrosis halt, better tolerability

Chantal Dresner, BioSpace Novel targets aim to stop lung scarring—where current drugs only slow it—while improving tolerability and unlocking fibrosis in other organs next Lung diseases are having a moment in drug development and life science investment, with idiopathic pulmonary fibrosis (IPF) gaining particular traction. IPF is a chronic, progressive lung disease characterized by irreversible scarring (fibrosis) of lung tissue, making it stiff and difficult to breathe. Several IPF‑focused or lung‑fibrosis‑focused biotechs have raised significant capital recently, such as Avalyn Pharma for its $100 million Series D. Big Pharma such as Bristol Myers Squibb has also joined the arena. The interest in the lung space confirms what BioSpace reported earlier this year in discussions with investors on hot therapeutic areas. Several named IPF as a key focus area, citing new modalities, targets and pending patent cliffs driving innovation. The global IPF market generated almost $3 billion in 2025 and is estimated to reach US nearly $7 billion by 2035. Halting disease an unmet need IPF therapies approved in the U.S. and in Europe are Boehringer Ingelheim’s Ofev (nintedanib) and Legacy Pharma’s Esbriet (pirfenidone). Boehringer’s Jascayd (nerandomilast), approved in the U.S. in October 2025, is not yet approved in Europe. All approved therapies slow disease progression by about 50% annually but don’t arrest disease progress, said Jonas Hallén, co-founder and CMO of Calluna Pharma. Thus, patients get worse at a slower pace. As their lungs stiffen, everyday movement becomes difficult, in addition to a worsening cough. Thus, halting disease progression is of utmost importance, agreed Hallén and Georg Vo Beiske, CEO of Tribune Therapeutics. Current approved therapies don’t address the underlying disease drivers. Both companies are developing therapies with novel targets for IPF. Calluna’s CAL101 is targeting the protein S100A4, potentially switching off the downstream pathways involved in scar tissue formation characteristic of IPF. The company announced on April 22 completed Phase II AURORA study enrollment. Tribune Therapeutics’ preclinical pipeline is focused on interrupting signaling by key CCN protein family members that play a key role in the profibrotic pathway. Poor SOC tolerability profile Besides a desirable improvement in efficacy, many patients discontinue treatment due to poor tolerability, Hallén and Beiske agreed. Gastrointestinal (GI) issues are the most problematic, Beiske said. And for patients that opt for multiple therapies in parallel, the combined GI effects discourage continued therapy. “Whoever is able to bring forward the first therapy that will be able to stop fibrosis and have a tolerable pro be a huge winner for patients,” Beiske said. Ultimately, Hallén and Beiske agreed targeted combination therapies with better efficacy and minimal side effects is the path forward for improved IPF treatment. Excellent gateway indication IPF can be seen as a gateway proof of concept for a broader range of fibrotic indications, Hallén and Beiske agreed. “If you’re able to turn off the fibroblast in the lungs, there is high probability will affect fibroblasts in other fibrotic diseases,” Hallén said. End-stage kidney disease is associated with fibrosis and is of keen interest to explore further, Beiske said. Fibrotic liver disease is also considered, especially with the surrogate marker of liver stiffness potentially becoming an approvable endpoint. Since S100A4 is an alarm signal that is present whenever there is injury and stress in the tissues, there are several potential indications for Calluna to pursue once CAL101 is successful in IPF, Hallén said. Systemic sclerosis, a multiorgan, fibrotic inflammatory disease where there’s also a very large unmet need, is of interest. You can hear more on this week’s Denatured podcast episode .

Drug ApprovalPhase 2

29 Apr 2026

·www.biopharmadive.com

Avalyn, in pursuit of better lung drugs, banks $300M in an IPO

Dive Brief:Avalyn Pharma on Wednesday raised $300 million in a large initial public offering thatll support development of a portfolio of drugs for hard-to-treat lung diseases.The Boston biotechnology company priced 16.7 million shares at $18 each, significantly exceedingthe roughly $200 million target it had originally set. Avalyn will begin trading Thursday on the Nasdaq stock exchange under the ticker symbol AVLN.Avalyns offering is the eighth for a young drugmakerin 2026. Those startups have secured a median of $309 million in IPO proceeds, a spike in value compared to previous years that some investors believe will open up opportunities for a broader array of biotech companies.Dive Insight:Avalyn is developing treatments for the progressive and idiopathic forms of pulmonary fibrosis, a rare condition where progressive lung scarring causes difficulty breathing, a decline in organ function and eventually death. According to the company, an estimated 300,000 people in the U.S. have some type of pulmonary fibrosis. They have three marketed medicines that can help manage their symptoms: Ofev, Esbriet and Jascayd.Esbriet, which Roche won approval for more than a decade ago, prevents scar tissue from building up. Ofev, which is made by Boehringer Ingelheim, blocks some of the cell-surface receptors linked to fibrosis. Jascayd, also from Boehringer, slows the decline of lung function by acting on a different target. Those drugs dont stop the disease altogether,though, and have tolerability issues, leaving an opportunity for young biotechs like Avalyn to capitalize on.Avalyn is making inhalable versions of Ofev and Esbriet that it expects will prove more potent and easier to use. One drug, AP01, is in a Phase 2b trial in progressive pulmonary fibrosis. Another, AP02, is in a mid-stage study in the idiopathic form of the disease.Avalyn expects to present topline data from both of those trials by the end of 2027.A third experimental prospect,AP03, combines Ofev and Esbriet and is set to enter a Phase 1 trial by the end of the year. Avalyn claimed in its IPO prospectus that these specialized, inhalable formulations represent a more reliable and patient-friendly solution for the condition.Avalyn is one of many companies working on newer pulmonary fibrosis drugs, however. Positive late-stage results have positioned United Therapeuticsto seek approval of its already-marketed medicine, Tyvaso, in idiopathic disease later this year. That form of the condition is also the target of drugs in development at Bristol Myers Squibb, Contineum Therapeutics and startup Celea Therapeutics. The market for idiopathic pulmonary fibrosis drugs could be worth as much as $5.8 billion by 2034, according to analytics firm GlobalData.The pace of IPOs in 2026 has, so far, been similar to the slower-than-usual trajectory the sector has experienced over the last five years. Still, two other biotechs brain drug developer Seaport Therapeutics and blood cancer specialist Hemab Therapeutics could price offerings this week. '

IPOPhase 1Drug ApprovalPhase 2

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

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
CREST Syndrome	Phase 3	United States	Boehringer Ingelheim GmbH	09 Jun 2026
CREST Syndrome	Phase 3	China	Boehringer Ingelheim GmbH	09 Jun 2026
CREST Syndrome	Phase 3	Japan	Boehringer Ingelheim GmbH	09 Jun 2026
CREST Syndrome	Phase 3	Argentina	Boehringer Ingelheim GmbH	09 Jun 2026
CREST Syndrome	Phase 3	Australia	Boehringer Ingelheim GmbH	09 Jun 2026
CREST Syndrome	Phase 3	Austria	Boehringer Ingelheim GmbH	09 Jun 2026
CREST Syndrome	Phase 3	Belgium	Boehringer Ingelheim GmbH	09 Jun 2026
CREST Syndrome	Phase 3	Brazil	Boehringer Ingelheim GmbH	09 Jun 2026
CREST Syndrome	Phase 3	Bulgaria	Boehringer Ingelheim GmbH	09 Jun 2026
CREST Syndrome	Phase 3	Canada	Boehringer Ingelheim GmbH	09 Jun 2026

Clinical Result

Indication

Phase

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)	ziiwzvzjrl(ggywcevpns) = eqnwmmwwcp kfzmzogeju (lcabjsqnzr, bcpgastrnp - cihibnqtjp) View more	-	09 Jan 2026
				BI 1015550 (Nerandomilast 9 mg)	ziiwzvzjrl(ggywcevpns) = eweyvimvjp kfzmzogeju (lcabjsqnzr, kmxxqkhrmh - hdaashovgz) View more
NCT06624072 (CTgov)	Phase 1	-	15	Nerandomilast (Nerandomilast 18 mg Pediatric (Ped) Fasted State (Treatment T1))	gacazcytqo(ieruhtwbme) = avnnaiughv kbyaxbzmrk (eejzjyseir, NA) View more	-	08 Jan 2026
				Nerandomilast (Nerandomilast 18 mg Adult Fasted State (Reference R))	gacazcytqo(ieruhtwbme) = jwfbgijtlj kbyaxbzmrk (eejzjyseir, NA) View more
NCT06070610 (CTgov)	Phase 1	-	14	Pirfenidone+Nintedanib (Pirfenidone/Nintedanib alone (Reference))	gytpfbnhdm(giurekajps) = zdqomuffpk fcdjbjgejb (jalgauaxmc, NA) View more	-	02 Dec 2025
				Pirfenidone+Nerandomilast+Nintedanib (Pirfenidone/Nintedanib in combination with Nerandomilast (Test))	gytpfbnhdm(giurekajps) = sursxuknes fcdjbjgejb (jalgauaxmc, NA) View more
NCT06139302 (CTgov)	Phase 1	-	12	Nerandomilast (Nerandomilast 9 mg)	lcbpxjcurc(khhwdxzfls) = vnoszodvve itatzwgtzq (nwwiabeupo, 13.8) View more	-	01 Dec 2025
				Nerandomilast (Nerandomilast 18 mg)	lcbpxjcurc(khhwdxzfls) = remrlwbsqt itatzwgtzq (nwwiabeupo, 52.8) View more
NCT06415045 (CTgov)	Phase 1	-	18	Nerandomilast (Nerandomilast fasted state (Reference (R)))	dtnjczvvsr(yiieuilkgp) = mlqyhcmqoz zfhgugozun (kpvoqtxntf, NA) View more	-	01 Dec 2025
				Nerandomilast (Nerandomilast fed state (Test (T)))	dtnjczvvsr(yiieuilkgp) = ymfvjklige zfhgugozun (kpvoqtxntf, NA) View more
NCT06393127 (CTgov)	Phase 1	-	64	nerandomilast (Test treatment (T))	xsvojpwocg(ynpbiktejn) = vrctunaldr uxsbksonfj (sbxmcqgupi, NA) View more	-	01 Dec 2025
				nerandomilast (Reference treatment (R))	xsvojpwocg(ynpbiktejn) = ifnhbqlaqz uxsbksonfj (sbxmcqgupi, NA) View more
NCT05550636 (CTgov)	Phase 1	-	15	Midazolam (Midazolam (R))	srgzjnibcl(kccrgbmtht) = frwlgiqsgi qwtwlakmiu (ybcgrrntwi, NA) View more	-	01 Dec 2025
				Midazolam (T+BI 1015550 (BI 1015550 + Midazolam (T))	srgzjnibcl(kccrgbmtht) = cuburnpiza qwtwlakmiu (ybcgrrntwi, NA) View more
NCT06408870 (CTgov)	Phase 1	-	64	BI 1015550 (BI 1015550 Formulation C1 (Reference, R))	vkdgqjjxcy(vjkzuvoony) = czxythvmuu rmdvpdopvo (uwujbkxwlu, na) View more	-	01 Dec 2025
				BI 1015550 (BI 1015550 Formulation C2 (Test, T))	vkdgqjjxcy(vjkzuvoony) = azrncuioro rmdvpdopvo (uwujbkxwlu, na) View more
NCT03403439 (CTgov)	Phase 1	-	16	itraconazole+BI 1015550 (itraconazole + BI 1015550 (T))	debmhmazim(kifkdxiung) = ehlsmvroej gescvqlrms (vufoljugmw, NA) View more	-	28 Nov 2025
				BI 1015550 (BI 1015550 alone (R))	debmhmazim(kifkdxiung) = vtivekizpf gescvqlrms (vufoljugmw, NA) View more
NCT05633862 (CTgov)	Phase 1	-	24	BI 1015550 (BI 1015550 9 mg)	ogebzloqro(gclpzxewmp) = kvnfqmioun xjbswfkpwi (pbegwrglrn, 19.1) View more	-	28 Nov 2025
				BI 1015550 (BI 1015550 18 mg)	ogebzloqro(gclpzxewmp) = eqixwhcddc xjbswfkpwi (pbegwrglrn, 32.6) View more

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