Idiopathic Pulmonary Fibrosis Clinical Trials

Browse current & upcoming clinical research / studies on Idiopathic Pulmonary Fibrosis. There are a total of 83 clinical trials for Idiopathic Pulmonary Fibrosis in 28 countries with 20 trials currently in the United States. 34 are either active and/or recruiting patients or have not yet been completed. Click the title of each study to get the complete details on eligibility, location & other facts about the study.

Other clinical trials

Interventional trials
Determine whether experimental treatments or new ways of using known therapies are safe and effective under controlled environments.
Observational trials
Address health issues in large groups of people or populations in natural settings.
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Recruiting or enrolling participants has halted prematurely and will not resume; participants are no longer being examined or treated.
April 2014 - June 2019
This registry will collect data on the strategies used to achieve a diagnosis of Idiopathic Pulmonary Fibrosis (IPF) and the treatment and management efforts applied throughout study follow-up, clinical outcome events and patient reported outcome data. Blood samples will be collected periodically throughout the study for use in future research efforts.
Sponsor: Duke University
Study type: Observational [P
March 2014 - May 2015
The investigator has recently studied markers of platelet activation in idiopathic pulmonary fibrosis (IPF) and found that in IPF patients there is a significantly increased platelet reactivity when compared with controls which is demonstrated by a concentration dependent increase in platelet-monocyte complex formation, platelet P-selectin expression and platelet fibrinogen binding in the presence of` the platelet agonists Adenosine diphosphate and L-?Threonyl-?L-?phenylalanyl-?L-?leucyl-?L-?leucyl- L-argininamide (TFLLR). During platelet activation the platelets degranulate releasing numerous profibrotic cytokines including Transforming growth factor beta and Platelet derived growth factor that are recognised to be important in the pathogenesis of IPF. It is therefore plausible that the observed increased platelet reactivity in IPF contributes to the fibrotic process through local activation and degranulation with release of proinflammatory and profibrotic mediators within the pulmonary circulation. There is evidence that corticosteroid treatment may alter platelet adhesion, in a study of spontaneously hypertensive rat (SHR) increased circulating glucocorticoid, suppressed p-selectin expression. p selectin is a transmembrane protein present in the a granules of platelets. P selectin has a crucial role in platelet aggregation and platelet-leukocyte interactions, which are both potentially important mechanisms in the initiation and/or progression of tissue injury and development of thrombosis. In a study of patients with chronic obstructive pulmonary disease (COPD) exacerbation these were treated with either ß agonists alone or ß agonist and 40mg prednisolone and compared with a control group. At presentation the COPD patients had higher pulmonary artery pressure (PAP) higher p selectin and fibrinogen levels but lower Antithrombin III levels (AT III). The pulmonary artery pressure and fibrinogen levels were found to be significantly decreased in the steroid treated group whilst the p-selectin levels further increased in the non steroidal therapy patients. Rationale for the Current Study There is a significant unmet medical need for the treatment of IPF; the only medication approved for treatment of IPF in the United Kingdom (UK) is Pirfenidone and outside the UK there is none. The main goal of the current study is to evaluate the effect of Fostair on the biomarkers of platelet activation in IPF disease which the investigator believes play a pivotal role in the pathogenesis of IPF and whether this translates in to a clinically beneficial effect of Fostair on IPF disease.
Sponsor: Hull and East Yorkshire Hospitals NHS Trust
Study type: Interventional
February 2014 - August 2015
Idiopathic pulmonary fibrosis (IPF) is a disease of unknown cause in which areas of normal lung tissue are replaced by scars. As a result it becomes harder for the lungs to extract oxygen from the air. IPF is commonly progressive, and around 50% of patients diagnosed with the disease die after approximately 3 years. The most common, troublesome symptoms of IPF are breathlessness on exertion, and cough. No drug treatments have been unequivocally shown to improve the death rate, or to significantly impact upon symptoms, in IPF. In recent years it has been recognised that cough can be caused by small amounts of liquid coming up from the stomach and "going down the wrong way" into the lungs, a process commonly known as "reflux". As liquid in the stomach is usually acidic, patients' lungs may repeatedly be exposed to small amounts of acid. Reflux is unusually common in IPF and could potentially contribute to the debilitating cough found with the disease. However there are many potential causes for cough in IPF. Stomach acid can be efficiently "switched off" by drugs called "proton pump inhibitors", one of which is called omeprazole. If reflux of stomach acid does contribute to cough in IPF, omeprazole might be expected to reduce cough. The purpose of this study is therefore to test whether omeprazole does reduce cough in patients with IPF. Sixty patients with IPF will be randomly allocated to have 3 months of omeprazole or a placebo. Neither the patient nor the doctor will be aware which treatment has been given, ie this is a randomised "double-blind", placebo--controlled trial. Patients' cough frequency will be measured before and after treatment and the change in cough frequency compared in those receiving omeprazole and those receiving placebo. Change in cough frequency is the main thing we aim to compare, but a range of other measurements will be assessed such as the numbers of patients eligible to take part, agreeing to randomisation and providing outcome data, patients' lung function, symptom scores, the amount of reflux, and the amount of inflammation in the lungs.
Sponsor: Newcastle-upon-Tyne Hospitals NHS Trust
Study type: Interventional
January 2014 - December 2014
This is a methodology study to examine the quantification of GSK2634673F binding in humans, with the aim of characterising a robust, non-invasive method to quantify the specific binding signal for the alpha(V)beta6 protein in human tissues. This will be the first time that this micro-dose ligand is administered to humans. The study will consist of three parts; Part A, Part B and Part C. Healthy subjects will be recruited into Parts A and B of the study in order to gain experience with the GSK2634673F positron emission tomography (PET) ligand and to optimise the scanning procedures prior to administration to IPF patients in Part C.
Sponsor: GlaxoSmithKline
Study type: Interventional
January 2014 - November 2015
The purpose of the study is to evaluate the safety and tolerability of multiple-doses of tralokinumab in Japanese patients with Idiopathic Pulmonary Fibrosis.
Sponsor: AstraZeneca
Study type: Interventional
December 2013 - June 2015
In this study we evaluate the effect of Pirfenidone on cough and quality of life in patients with idiopathic pulmonary fibrosis (IPF) that are treated with Pirfenidone in daily practice. The hypothesis is that Pirfenidone will decrease cough and increase quality of life.
Sponsor: Erasmus Medical Center
Study type: Observational
December 2013 - December 2016
This study will test the hypothesis that treatment with laparoscopic anti-reflux surgery in subjects with idiopathic pulmonary fibrosis (IPF) and abnormal gastroesophageal reflux (GER) will slow the decline of forced vital capacity (FVC) over 48 weeks.
Sponsor: University of California, San Francisco
Study type: Interventional
December 2013 - August 2014
This is a clinical study to characterise the lung function, airway morphometry, pharyngometry and inhalation profiles in patients with mild to severe Idiopathic Pulmonary Fibrosis (IPF) over a period of up to 6 months. Inhalation profiles will be recorded from patients with IPF as they inhale during tidal breathing, and following two sets of instructions (maximal effort and 'long, steady and deep' inhalation), across a range of airflow resistances that reflect those of typical inhalers used to deliver medication to the lungs. Mouth and throat dimensions will be measured using an acoustic reflectance Pharyngometer. Measurements of lung function will be made using conventional sprirometry, plethysmography and diffusion, whilst Low Dose High Resolution Computed Tomography (HRCT) will be used to scan the airways at two lung volumes; functional residual capacity (FRC) and total lung capacity (TLC). Data from HRCT will be used to reconstruct airway morphometry, and model inhaled particle deposition within the lung. Overall, the study allows a further understanding of the IPF patient population, using the data to assist in the development of new inhaled products for this disease. Following up the patients with additional HRCT scans at 3 and 6 months will enable the sensitivity of CT based criteria of disease progression to be compared with lung function criteria. No investigational product will be used in this study.
Sponsor: GlaxoSmithKline
Study type: Interventional
November 2013 - February 2016
This is an 12 month multi-centre, prospective, randomized, placebo controlled, double blind clinical trial designed to assess the effect of nintedanib 150mg BID on the progression of IPF measured by using HRCT, lung function, 6MWT, biomarkers, and PROs with continued treatment and assessments for up to 18 months.
Sponsor: Boehringer Ingelheim
Study type: Interventional
October 2013 - August 2016
This randomized, multicenter, double-blind, placebo-controlled, parallel-group study will evaluate the efficacy and safety of lebrikizumab in patients with idiopathic pulmonary fibrosis. Patients will be randomized to receive either lebrikizumab or placebo subcutaneously every 4 weeks.
Sponsor: Hoffmann-La Roche
Study type: Interventional
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