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Clinical Trial Summary

Lung transplantation (TxP) is now a validated treatment of end-stage pulmonary diseases, but long-term graft and patient survival are still hampered by the development of chronic allograft dysfunction (CLAD) affecting > 50% of patients. The investigators propose to conduct a phase III clinical randomized trial that will assess the efficacy of Nintedanib to hamper the lung decline in LTx recipients with BOS. This is the first trial testing this molecule in lung Tx recipients. If case of demonstrated effectiveness of Nintedanib, the benefit for lung transplant patients carrying a BO is high in terms of stabilization of lung function and enhancement of survival.


Clinical Trial Description

Introduction: Lung transplantation (TxP) is now a validated treatment of end-stage pulmonary diseases, but long-term graft and patient survival are still hampered by the development of chronic allograft dysfunction (CLAD) affecting > 50% of patients. Obliterative bronchiolitis (OB), the obstructive CLAD, is the most common manifestation of CLAD, and affects > 50% of recipients who survive the early post-transplant period. OB is thought to arise from repeated injury to graft epithelial cells, leading to fibrous scarring and obliteration of the small airway lumen, as a result of dysregulated fibrotic repair and loss of peribronchial microvasculature. The patchy histopathologic distribution at onset makes it difficult to confirm histopathologically the diagnosis of OB from lung specimens. Hence, bronchiolitis obliterans syndrome (BOS) has become a generally accepted surrogate diagnostic of OB, characterized physiologically by progressive airflow limitation, with a median monthly decline of FEV1 of about 50 ml. Survival after onset of BOS is poor, reported as < 50% at 3 years after onset of disease, due to end-stage respiratory failure. Thus far, there is currently no approved treatment to stabilize BOS disease, and especially no treatment addressing the fibrotic lung graft manifestation of BOS. The crucial role of a dysregulated fibrotic repair has now been demonstrated in BOS, with the following: (i) Architectural remodelling with fibrosis and scarring of airways involving myofibroblasts; (ii) Increased extracellular matrix synthetic; (iii) Epithelial-mesenchymal transition mechanism; (iv) Role of growth factors PDGF, VEGF, FGF, and IGF-1 shown in BO mechanisms (animals and humans studies). These data strongly suggest the potential role of tyrosine kinase inhibitors (TKI) that target these growth factors involved in the post-TxP BO. In this axis, the new TKI Nintedanib, which has recently been demonstrated as effective in the treatment of idiopathic pulmonary fibrosis (IPF) in large-scale randomized studies (8) appears as a candidate molecule capable of stopping the fibroproliferative process and stabilize the development of a CLAD after TxP. Whereas Nintedanib is a validated and available treatment in patients with IPF, paucity of data are currently available in lung-transplant recipients. Primary objective: to assess Nintedanib efficacy in the reduction of the rate of decline of FEV1 (forced expiratory volume in 1 sec) in BOS post-LTx at a dose of 150 mg twice daily (bid) compared to placebo over 6 months. Secondary objectives: to assess Nintedanib efficacy and tolerance in the treatment of BOS grade 0p-1-2 post-lung transplantation. Experimental design: a 2 groups parallel, randomized, prospective multicentric placebo-controlled phase III trial to assess Nintedanib superiority versus placebo. Eligible LTx recipients with BOS are to be randomized in a 1:1 ratio to receive either Nintedanib 150 mg BID or the matching placebo treatment for 6 months. The follow-up of patients with BOS included in the trial will be similar to usual and standard care in both arms of the study (Nintedanib group and placebo group). The intervention group is expected to be beneficial compared to the placebo group. ;


Study Design


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NCT number NCT03283007
Study type Interventional
Source Assistance Publique - Hôpitaux de Paris
Contact Olivier Brugière, MD, PhD
Phone (0)1 46 25 36 01
Email o.brugiere@hopital-foch.com
Status Recruiting
Phase Phase 3
Start date October 30, 2019
Completion date June 2024