Nerandomilast

Table of Contents

1. What Nerandomilast Is
2. How Blocking Phosphodiesterase 4B Is Thought to Slow Scarring
3. How It Differs From Nintedanib and Pirfenidone
4. Laboratory Work and the First Studies in People
5. The Phase 2 Trial, Twelve Weeks
6. FIBRONEER-IPF, the Trial in Idiopathic Pulmonary Fibrosis
7. FIBRONEER-ILD, the Trial in Progressive Pulmonary Fibrosis
8. Deaths, the Key Secondary Endpoint and the Pooled Survival Analysis
9. Lung Scarring Linked to Autoimmune Disease
10. Diarrhea and the Other Side Effects in the Trials
11. Weight Loss and Mood Changes Reported for the Drug Family
12. Case Reports Since Approval
13. The United States Approvals
14. What Is Not Yet Known
15. Key Research Papers
16. Connections
17. Featured Videos

What Nerandomilast Is

Nerandomilast is a small chemical medicine, not an antibody or an injection. The trial reports describe it as an orally administered “preferential” inhibitor of phosphodiesterase 4B. “Preferential” means it blocks the 4B form of the enzyme more strongly than the other forms of phosphodiesterase 4, although it is not perfectly limited to one form.

It is used for two groups of people. The first is idiopathic pulmonary fibrosis, a scarring disease of the lungs with no known cause, in which the scar tissue slowly replaces the thin, stretchy tissue where oxygen passes into the blood. The second is progressive pulmonary fibrosis: lung scarring from another cause, such as an autoimmune disease or a reaction to something breathed in, that keeps getting worse despite treatment. The Pulmonary Fibrosis and Interstitial Lung Disease pages describe that wider group.

Like the two older medicines, nerandomilast does not repair scar tissue that is already there. In the trials, its effect was measured as a slower loss of lung capacity, not a gain. A 2026 review of the medicine describes its role as keeping the disease steadier rather than reversing established scarring.

How Blocking Phosphodiesterase 4B Is Thought to Slow Scarring

Inside many cells, a small molecule called cyclic adenosine monophosphate (cyclic AMP) carries signals from the cell surface to the inside. It was discovered by Earl Sutherland, who received a Nobel Prize for the work. Phosphodiesterase 4 enzymes break cyclic AMP down and so end its signal. When the enzyme is blocked, cyclic AMP stays higher for longer.

In lung scarring, a key step is the change of ordinary connective-tissue cells, called fibroblasts, into myofibroblasts. Myofibroblasts are tough, contracting cells that lay down large amounts of scar protein. A signal protein called transforming growth factor beta (TGF-beta) is one of the main drivers of that change. Laboratory studies of nerandomilast report the following:

• In fibroblasts taken from the lungs of people with idiopathic pulmonary fibrosis, grown in dishes, nerandomilast blocked the change into myofibroblasts driven by transforming growth factor beta and lowered the production of several scar-tissue proteins (Herrmann 2022).
• In the same kind of cells, a 2025 study reported that it reduced myofibroblast contraction and markers, turned on cyclic AMP pathways and damped transforming growth factor beta signalling. In human lung blood-vessel cells grown on a chip, it made the vessel lining less leaky (Reininger 2025).
• In human blood cells in the laboratory, it lowered the release of the inflammatory signal tumour necrosis factor alpha (Herrmann 2022).
• In mice with lung scarring caused by the drug bleomycin or by silica dust, it improved several measures of the scarring, and in rats with bleomycin scarring it slowed the decline in lung function and reversed most of the gene changes the scarring had caused (Herrmann 2022; Reininger 2024).

Put together, the laboratory picture is of a medicine that acts on several cell types at once: scar-making cells, immune cells and the lining of the small blood vessels. These results come from cells and animals. They explain why the medicine was tested in people; they are not, by themselves, proof of how it works inside a human lung.

How It Differs From Nintedanib and Pirfenidone

Before nerandomilast, two antifibrotic medicines were in use for idiopathic pulmonary fibrosis. Nintedanib is described in its main trial report as an inhibitor inside the cell that targets several tyrosine kinases, enzymes that pass on growth signals. Pirfenidone is described in its main trial report as an oral antifibrotic therapy. Both slowed the loss of lung capacity in their 2014 trials:

• In the two INPULSIS trials of nintedanib (1,066 patients), the yearly fall in forced vital capacity (the amount of air a person can blow out after a full breath) was about 114 milliliters on nintedanib against 207 to 240 milliliters on placebo. Diarrhea affected 61.5% and 63.2% of patients on nintedanib, against about 18% on placebo (Richeldi 2014).
• In the ASCEND trial of pirfenidone (555 patients), the proportion of people whose lung capacity fell by 10 percentage points or more, or who died, was 47.9% lower than on placebo. Stomach and skin side effects were more common on pirfenidone (King 2014).

Nerandomilast works on a different target, the cyclic AMP pathway, rather than on growth-factor kinases. That difference is why it was tested both on its own and on top of the older drugs. In the main idiopathic pulmonary fibrosis trial, 77.7% of patients were already taking nintedanib or pirfenidone when they joined, and the medicine was compared with placebo in both groups.

It also differs from earlier phosphodiesterase 4 blockers. Roflumilast, which blocks the enzyme family more broadly, is used for chronic obstructive pulmonary disease (see COPD), and apremilast is used for psoriasis and psoriatic arthritis (see Psoriasis). Nausea and vomiting have limited the use of phosphodiesterase 4 blockers. In the house musk shrew, an animal used because it can vomit, nerandomilast’s gap between the dose that calmed inflammation and the dose that caused vomiting appeared substantially wider than roflumilast’s (Herrmann 2022).

Laboratory Work and the First Studies in People

Two phase 1 studies tested safety. In the first, 42 healthy men received single doses of 36 or 48 milligrams, or repeated doses of 6 or 12 milligrams twice daily for 14 days, or placebo. Side effects judged to be related to the drug were reported in 50.0% of men after a single dose and 37.5% after repeated doses, against 16.7% and 12.5% on placebo. The most common were nervous-system complaints, mainly headache (Maher 2022).

In the second, 15 patients with idiopathic pulmonary fibrosis received 18 milligrams twice daily or placebo for up to 12 weeks. Drug-related side effects were reported in 90.0% of patients on the medicine against 60.0% on placebo, and stomach and bowel complaints were the most common (Maher 2022).

Studies in healthy volunteers of how the body handles the medicine found that it is absorbed quickly, reaching its highest level in the blood 0.5 to 1.25 hours after a dose. With twice-daily dosing, levels settled by day 7. In a study with a radioactively labelled dose, 58.0% of the label left the body in the stool and 36.4% in the urine (Jappar 2026).

The Phase 2 Trial, Twelve Weeks

The phase 2 trial enrolled 147 patients with idiopathic pulmonary fibrosis and assigned them, two to one, to 18 milligrams twice daily or to placebo for 12 weeks. Results were analysed separately for people already taking nintedanib or pirfenidone and for people who were not (Richeldi 2022).

• Without an older antifibrotic: forced vital capacity changed by +5.7 milliliters on the medicine and −81.7 milliliters on placebo, a median difference of 88.4 milliliters.
• With an older antifibrotic: +2.7 milliliters on the medicine and −59.2 milliliters on placebo, a median difference of 62.4 milliliters.

The trial reported that, in both groups, the medicine prevented a fall in lung function over the 12 weeks. Diarrhea was the most common side effect, 13 patients stopped the medicine because of side effects, and serious or severe side effects were in similar proportions in the two groups. A 2023 review described this as the largest effect size reported for an investigational drug in a phase 2 trial in idiopathic pulmonary fibrosis, over the shortest duration (Sgalla 2023).

FIBRONEER-IPF, the Trial in Idiopathic Pulmonary Fibrosis

The phase 3 FIBRONEER-IPF trial assigned 1,177 patients with idiopathic pulmonary fibrosis, in equal thirds, to 18 milligrams twice daily, 9 milligrams twice daily or placebo. Of these, 77.7% were taking nintedanib or pirfenidone at the start. The main measure was the change in forced vital capacity at 52 weeks (Richeldi 2025).

• 18 milligrams twice daily: −114.7 milliliters at 52 weeks, a difference from placebo of 68.8 milliliters (P<0.001).
• 9 milligrams twice daily: −138.6 milliliters at 52 weeks, a difference from placebo of 44.9 milliliters (P = 0.02).
• Placebo: −183.5 milliliters at 52 weeks.

So lung capacity still fell on the medicine, but by less than on placebo. Diarrhea was the most frequent side effect: 41.3% on 18 milligrams and 31.1% on 9 milligrams, against 16.0% on placebo. Serious side effects were balanced across the groups.

Patients stayed on their assigned treatment after week 52 until the trial ended, for an average of about 15 months. Over that whole period, the trial’s key secondary measure, the time to a first sudden flare of the disease, a hospital stay for a breathing cause, or death, did not differ from placebo: the hazard ratios were 0.92 for 9 milligrams and 0.99 for 18 milligrams. For death alone, the hazard ratio was 0.66 on 18 milligrams, a numerically lower risk whose range (0.41 to 1.08) included no difference. Side effects led to stopping treatment in 13.0% on placebo, 13.5% on 9 milligrams and 16.1% on 18 milligrams (Oldham, Am J Respir Crit Care Med 2026).

FIBRONEER-ILD, the Trial in Progressive Pulmonary Fibrosis

The companion phase 3 FIBRONEER-ILD trial took the same design to people with progressive pulmonary fibrosis from causes other than idiopathic pulmonary fibrosis. In all, 1,176 patients received the medicine or placebo, and 43.5% were taking nintedanib at the start. Patients were grouped at the start by whether or not they were taking nintedanib (Maher 2025).

• 18 milligrams twice daily: −98.6 milliliters at 52 weeks, a difference from placebo of 67.2 milliliters (P<0.001).
• 9 milligrams twice daily: −84.6 milliliters at 52 weeks, a difference from placebo of 81.1 milliliters (P<0.001).
• Placebo: −165.8 milliliters at 52 weeks.

In this trial the lower dose did at least as well as the higher one on lung capacity. Diarrhea was again the most frequent side effect, in 36.6% on 18 milligrams, 29.5% on 9 milligrams and 24.7% on placebo, and serious side effects were in similar proportions across the groups.

Over the whole follow-up (an average of 17.0 months of observation), the hazard ratio for the key secondary measure, a first sudden flare, a hospital stay for a breathing cause, or death, was 0.78 (range 0.61 to 1.00) on 9 milligrams and 0.77 (0.60 to 0.99) on 18 milligrams. The effect was clearer in people not taking nintedanib (0.69 and 0.65) than in those taking it (0.90 and 0.93). For death, the hazard ratio was 0.51 for both doses. Side effects led to stopping treatment in about 12% of every group, placebo included (Wijsenbeek 2026).

Deaths, the Key Secondary Endpoint and the Pooled Survival Analysis

Each trial had one main measure, lung capacity at 52 weeks, and one key secondary measure, the combined time to a flare, a breathing-related hospital stay or death. A 2026 pooled analysis by the trial investigators states plainly that in FIBRONEER-IPF and FIBRONEER-ILD the key secondary endpoint was not met. A 2026 review of the medicine likewise reports that the secondary time-to-event results were not statistically significant (Bui 2026). Time to death was a separate secondary measure, and there the trials showed numerical benefits.

The pooled analysis then looked at death more closely, combining both trials over the whole follow-up, an average of 16.7 months (Oldham, Eur Respir J 2026):

• 9 milligrams twice daily: risk of death 33% lower than placebo (hazard ratio 0.67; range 0.49 to 0.90).
• 18 milligrams twice daily: risk of death 43% lower than placebo (hazard ratio 0.57; range 0.41 to 0.78).

The authors reported that several checks, including tests of how much missing data could have changed the result, were consistent with the main survival result, and that people with higher blood levels of the medicine had a lower risk of death.

A 2026 meta-analysis of four randomized trials with 2,515 patients found a pooled slowing of lung-capacity loss of 69.25 milliliters, no improvement in a second lung test (the diffusing capacity for carbon monoxide, which measures how well oxygen crosses into the blood), and a lower pooled risk of death from any cause (risk ratio 0.68). Its authors note that the individual trials were not designed to measure deaths and that death rates were low, so they describe the survival finding as one to read with caution (Shahzad 2026).

Lung Scarring Linked to Autoimmune Disease

Lung scarring is a known complication of several autoimmune diseases, among them rheumatoid arthritis and systemic sclerosis. FIBRONEER-ILD included 325 people whose progressive scarring was linked to an autoimmune disease, and a 2026 report looked at them separately (Hoffmann-Vold 2026).

At 52 weeks, lung capacity fell by 107.1 milliliters on placebo, 61.2 milliliters on 9 milligrams and 64.9 milliliters on 18 milligrams. The differences from placebo, 45.9 and 42.2 milliliters, had ranges that crossed zero, so in this smaller group the lung-capacity result on its own was not clear. Over the whole trial, the hazard ratio for the combined flare, hospital or death measure was 0.66 on 9 milligrams and 0.56 on 18 milligrams, and for death alone 0.40 and 0.28. Side effects led to stopping treatment in 13.0% on placebo, 8.0% on 9 milligrams and 10.6% on 18 milligrams. The authors describe the results as consistent with the whole trial.

Diarrhea and the Other Side Effects in the Trials

Diarrhea is the side effect that runs through every trial of nerandomilast:

• Phase 2: diarrhea was the most frequent side effect (Richeldi 2022).
• FIBRONEER-IPF: 41.3% on 18 milligrams and 31.1% on 9 milligrams, against 16.0% on placebo (Richeldi 2025).
• FIBRONEER-ILD: 36.6% on 18 milligrams and 29.5% on 9 milligrams, against 24.7% on placebo (Maher 2025).

Nintedanib, which many trial patients were also taking, causes diarrhea on its own: in its 2014 trials about six in ten people on nintedanib had it (Richeldi 2014). The higher placebo rate in FIBRONEER-ILD, where 43.5% of patients took nintedanib, is in line with that. The main trial abstracts do not give the diarrhea rate split by whether people were taking nintedanib, so this page does not give a figure for the combination.

Beyond diarrhea, the trial abstracts report that serious side effects occurred in similar proportions on the medicine and on placebo, and that over the long follow-up of the two main trials, stopping treatment because of side effects was in the range of about 12% to 16% in every group, placebo included. The 2026 meta-analysis found no increase in side effects overall (risk ratio 1.00) or in serious side effects (risk ratio 0.93) (Shahzad 2026). In the phase 1 studies, headache was the most common complaint in healthy men (Maher 2022).

The United States liver-injury reference of the National Institutes of Health reports that nerandomilast has not been associated with rises in liver enzymes during therapy or with clinically apparent liver injury (Hoofnagle, LiverTox).

Weight Loss and Mood Changes Reported for the Drug Family

Nerandomilast belongs to the phosphodiesterase 4 inhibitor family, and the older members of that family carry two well-documented signals besides stomach upset: weight loss and psychiatric effects.

• A 2020 Cochrane review of phosphodiesterase 4 inhibitors in chronic obstructive pulmonary disease (42 trials) found that roflumilast in particular was associated with weight loss and with more insomnia and depressed mood. Psychiatric side effects were about twice as likely with roflumilast 500 micrograms as with placebo (odds ratio 2.13) (Janjua 2020).
• A 2025 study of 3,140 reports to the United States Food and Drug Administration (FDA) adverse event reporting system found that diarrhea, weight decrease, nausea, insomnia and headache were frequent signals for roflumilast, with depression and suicidal thoughts among the psychiatric signals (Huang 2025). Reporting-system data show signals, not rates.

The nerandomilast trial abstracts read for this page do not give figures for weight loss, depression or suicidal thoughts, so this page does not state a rate for them. Whether the preferential action on the 4B form changes the size of these family-wide signals has not been reported in those abstracts.

Case Reports Since Approval

Once a medicine is in wide use, rarer events appear in case reports. Two had been published by October 2026:

• A case series described 5 patients with idiopathic or progressive pulmonary fibrosis who had a sudden flare of their lung disease within 2 weeks of starting nerandomilast. All flares were confirmed by worse breathlessness or cough, a higher oxygen need and new hazy areas on the scan, and all needed a hospital stay. The author proposes a possible mechanism through cyclic AMP and the immune signal interleukin-17 and states that the findings need to be tested prospectively (Adams 2026).
• A case report described a 33-year-old woman with advanced lung scarring who developed fever, breathlessness, low oxygen and new shadows on both lungs 9 days after starting the medicine. She improved after it was stopped, worsened again the day after it was restarted at a lower dose, and improved again when it was stopped. The authors judged this to strongly support pneumonitis (lung inflammation) caused by the medicine (Yanagihara 2026).

Case reports cannot show how often an event happens or prove cause on their own. In the large trials, the combined flare, hospital or death measure was not higher on the medicine than on placebo.

The United States Approvals

According to a 2026 summary of the medicine’s development (Brown 2026):

• 7 October 2025: first approval anywhere, in the United States, for adults with idiopathic pulmonary fibrosis.
• 22 October 2025: approval in China for adults with idiopathic pulmonary fibrosis.
• 10 December 2025: approval in China for adults with progressive pulmonary fibrosis.
• 19 December 2025: approval in the United States for adults with progressive pulmonary fibrosis.

The trials gave 18 milligrams twice daily or 9 milligrams twice daily by mouth. Further filings in other countries and more phase 2 and phase 3 trials were under way at the time of that summary.

The United States drug and breastfeeding database of the National Institutes of Health (LactMed) reports that no information is available on the use of nerandomilast during breastfeeding.

What Is Not Yet Known

• Whether the slower loss of lung capacity turns into fewer flares and hospital stays: the key secondary measure was not met in the trial reports as first published.
• Whether the lower death rate seen in the pooled analysis holds up: death was a secondary measure, and the trials were not designed to measure it.
• How the medicine performs over many years: the trials followed people for an average of about 15 to 17 months.
• How often weight loss, mood changes and lung reactions occur outside trials, among people who are older or sicker than trial patients.
• How nerandomilast compares directly with nintedanib or pirfenidone: the trials compared it with placebo, not with the other drugs head to head.
• Whether the cell and animal findings on how it works match what happens in human lungs.

Decisions about prescription medicines belong with a clinician who knows the person’s whole history.

Key Research Papers

1. Richeldi L, Azuma A, Cottin V, Hesslinger C, Stowasser S, Valenzuela C, et al. Trial of a Preferential Phosphodiesterase 4B Inhibitor for Idiopathic Pulmonary Fibrosis. N Engl J Med. 2022;386(23):2178-2187. PubMed PMID: 35569036
2. Richeldi L, Azuma A, Cottin V, Kreuter M, Maher TM, Martinez FJ, et al. Nerandomilast in Patients with Idiopathic Pulmonary Fibrosis. N Engl J Med. 2025;392(22):2193-2202. PubMed PMID: 40387033
3. Maher TM, Assassi S, Azuma A, Cottin V, Hoffmann-Vold AM, Kreuter M, et al. Nerandomilast in Patients with Progressive Pulmonary Fibrosis. N Engl J Med. 2025;392(22):2203-2214. PubMed PMID: 40388329
4. Oldham JM, Assassi S, Azuma A, Cottin V, Hoffmann-Vold AM, Kreuter M, et al. Effect of nerandomilast on survival in patients with pulmonary fibrosis. Eur Respir J. 2026:2600338. PubMed PMID: 42532543
5. Oldham JM, Azuma A, Kreuter M, Maher TM, Martinez FJ, Richeldi L, et al. Nerandomilast in idiopathic pulmonary fibrosis: data from the whole follow-up period of the FIBRONEER-IPF trial. Am J Respir Crit Care Med. 2026;212(5):972-980. PubMed PMID: 41738262
6. Wijsenbeek MS, Assassi S, Azuma A, Cottin V, Hoffmann-Vold AM, Maher TM, et al. Nerandomilast in progressive pulmonary fibrosis: data from the whole follow-up period of the FIBRONEER-ILD trial. Eur Respir J. 2026;68(1):2501899. PubMed PMID: 41887669
7. Hoffmann-Vold AM, Assassi S, Cottin V, Kreuter M, Valenzuela C, Wijsenbeek MS, et al. Efficacy and safety of nerandomilast in patients with autoimmune disease-related progressive pulmonary fibrosis in the FIBRONEER-ILD trial. Ann Rheum Dis. 2026;85(10):2004-2013. PubMed PMID: 42062162
8. Shahzad H, Afzaal U, Saleem F, Gul AH, Thummar F, Murtaza HN, et al. Safety and Efficacy of Nerandomilast in Patients With Pulmonary Fibrosis: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Clin Respir J. 2026;20(3):e70181. PubMed PMID: 41810560
9. Bui PT, St Onge E, Sotolongo-Miranda H, Trabulsi T. Nerandomilast for Idiopathic Pulmonary Fibrosis and Progressive Pulmonary Fibrosis: Clinical Efficacy, Safety, and Place in Therapy. Ann Pharmacother. 2026;60(12):1220-1226. PubMed PMID: 42145068
10. Brown MB. Nerandomilast: First Approval. Drugs. 2026;86(4):557-563. PubMed PMID: 41746571
11. Herrmann FE, Hesslinger C, Wollin L, Nickolaus P. BI 1015550 is a PDE4B Inhibitor and a Clinical Drug Candidate for the Oral Treatment of Idiopathic Pulmonary Fibrosis. Front Pharmacol. 2022;13:838449. PubMed PMID: 35517783
12. Reininger D, Fundel-Clemens K, Mayr CH, Wollin L, Laemmle B, Quast K, et al. PDE4B inhibition by nerandomilast: Effects on lung fibrosis and transcriptome in fibrotic rats and on biomarkers in human lung epithelial cells. Br J Pharmacol. 2024;181(23):4766-4781. PubMed PMID: 39183442
13. Reininger D, Wolf F, Mayr CH, Wespel SL, Laufhaeger N, Geillinger-Kästle K, et al. Insights into the Cellular and Molecular Mechanisms behind the Antifibrotic Effects of Nerandomilast. Am J Respir Cell Mol Biol. 2025;73(5):700-712. PubMed PMID: 40239038
14. Sgalla G, Simonetti J, Cortese S, Richeldi L. BI 1015550: an investigational phosphodiesterase 4B (PDE4B) inhibitor for lung function decline in idiopathic pulmonary fibrosis (IPF). Expert Opin Investig Drugs. 2023;32(1):17-23. PubMed PMID: 36693635
15. Maher TM, Schlecker C, Luedtke D, Bossert S, Zoz DF, Schultz A. Phase I studies of BI 1015550, a preferential phosphodiesterase 4B inhibitor, in healthy males and patients with idiopathic pulmonary fibrosis. ERJ Open Res. 2022;8(4):00240-2022. PubMed PMID: 36299369
16. Jappar D, Wu J, Burkard U, Sharma A, Coeck C, Zoz D, et al. Pharmacokinetics and Safety of Nerandomilast in Healthy Volunteers. Eur J Drug Metab Pharmacokinet. 2026;51(5):661-671. PubMed PMID: 42563128
17. Richeldi L, du Bois RM, Raghu G, Azuma A, Brown KK, Costabel U, et al. Efficacy and safety of nintedanib in idiopathic pulmonary fibrosis. N Engl J Med. 2014;370(22):2071-82. PubMed PMID: 24836310
18. King TE Jr, Bradford WZ, Castro-Bernardini S, Fagan EA, Glaspole I, Glassberg MK, et al. A phase 3 trial of pirfenidone in patients with idiopathic pulmonary fibrosis. N Engl J Med. 2014;370(22):2083-92. PubMed PMID: 24836312
19. Janjua S, Fortescue R, Poole P. Phosphodiesterase-4 inhibitors for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2020;5(5):CD002309. PubMed PMID: 32356609
20. Huang B, Ma Y, Wang W, Gu S, Wang X. A real-world disproportionality analysis of roflumilast using the US food and drug administration adverse event reporting system data. Front Drug Saf Regul. 2025;5:1721656. PubMed PMID: 41458197
21. Adams TN. Interstitial lung disease exacerbations following initiation of nerandomilast: A case series. Respir Med Case Rep. 2026;64:102512. PubMed PMID: 42866541
22. Yanagihara T, Kinoshita E, Sakaki Y, Fujino Y, Fujita M. Nerandomilast-Associated Pneumonitis With a Positive Rechallenge: A Case Report. Respirol Case Rep. 2026;14(10):e70786. PubMed PMID: 42903208
23. Hoofnagle JH. Nerandomilast. In: LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-. PubMed PMID: 42819207
24. Nerandomilast. In: Drugs and Lactation Database (LactMed). Bethesda (MD): National Institute of Child Health and Human Development; 2006-. PubMed PMID: 41855368

PubMed Topic Searches

1. Nerandomilast
2. Nerandomilast and idiopathic pulmonary fibrosis
3. Nerandomilast and progressive pulmonary fibrosis
4. Phosphodiesterase 4B inhibitors and fibrosis
5. Phosphodiesterase 4 inhibitors and psychiatric side effects

Connections

• Drugs — every drug page on the site
• Idiopathic Pulmonary Fibrosis — the disease this medicine was first approved for
• Pulmonary Fibrosis — lung scarring from all causes
• Interstitial Lung Disease — the wider family that includes progressive pulmonary fibrosis
• Interstitial Lung Disease: History and Discovery — how these diseases and their treatments were worked out
• Systemic Sclerosis — an autoimmune disease that can scar the lungs
• Chronic Obstructive Pulmonary Disease (COPD) — where the older phosphodiesterase 4 blocker roflumilast is used
• Psoriasis — where the phosphodiesterase 4 blocker apremilast is used
• Earl Sutherland — the discoverer of cyclic AMP, the messenger this medicine keeps switched on

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