PRAISE, a randomized, placebo-controlled, double-blind Phase 2 clinical trial of pamrevlumab (FG-3019) in IPF patients

Gorina, Eduard; Richeldi, Luca; Raghu, Ganesh; Perez, E. Fernandez; Costabel, Ulrich; Albera, Carlo; Lederer, David J.; Flaherty, Kevin R.; Ettinger, Neil A.; Bercz, Peter A.; Singh, Bhanu; Perez, Rafael L.; Goldin, Jonathan; Kouchakji, Elias; Porter, Seth

doi:10.1183/1393003.congress-2017.oa3400

Cited by 10 publications

(6 citation statements)

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“…The launch of a Phase 3 trial for PRM-151 in IPF has been announced, using FVC as a primary end point and 6MWD as a key secondary end point. Among the anti-connective tissue growth factor antibodies, the antagonist pamrevlumab (FG-3019) in the PRAISE study [432] was established to have a significant effect preventing lung function decline of 160 IPF patients, yet full peer-reviewed data are still awaited [433]. The re-initiation of Phase 3 trials has just been announced.…”

Section: Idiopathic Pulmonary Fibrosis (Ipf)mentioning

confidence: 99%

Airway Redox Homeostasis and Inflammation Gone Awry: From Molecular Pathogenesis to Emerging Therapeutics in Respiratory Pathology

Checa

Aran

2020

IJMS

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As aerobic organisms, we are continuously and throughout our lifetime subjected to an oxidizing atmosphere and, most often, to environmental threats. The lung is the internal organ most highly exposed to this milieu. Therefore, it has evolved to confront both oxidative stress induced by reactive oxygen species (ROS) and a variety of pollutants, pathogens, and allergens that promote inflammation and can harm the airways to different degrees. Indeed, an excess of ROS, generated intrinsically or from external sources, can imprint direct damage to key structural cell components (nucleic acids, sugars, lipids, and proteins) and indirectly perturb ROS-mediated signaling in lung epithelia, impairing its homeostasis. These early events complemented with efficient recognition of pathogen- or damage-associated recognition patterns by the airway resident cells alert the immune system, which mounts an inflammatory response to remove the hazards, including collateral dead cells and cellular debris, in an attempt to return to homeostatic conditions. Thus, any major or chronic dysregulation of the redox balance, the air–liquid interface, or defects in epithelial proteins impairing mucociliary clearance or other defense systems may lead to airway damage. Here, we review our understanding of the key role of oxidative stress and inflammation in respiratory pathology, and extensively report current and future trends in antioxidant and anti-inflammatory treatments focusing on the following major acute and chronic lung diseases: acute lung injury/respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, and cystic fibrosis.

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Section: Idiopathic Pulmonary Fibrosis (Ipf)mentioning

confidence: 99%

Airway Redox Homeostasis and Inflammation Gone Awry: From Molecular Pathogenesis to Emerging Therapeutics in Respiratory Pathology

Checa

Aran

2020

IJMS

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“…FG-3019 (pamrevlumab) is a human monoclonal antibody (mAb) against CTGF that has shown efficacy in a randomized, placebo-controlled phase 2 clinical trial in subjects with idiopathic pulmonary fibrosis (12), as well as in phase 2 clinical trials for treatment of pancreatic cancer and Duchenne muscular dystrophy (NCT02210559 and NCT02606136, respectively). A chimeric antibody, designated FG-3149, has the binding motif of FG-3019 and a mouse IgG2a constant region.…”

mentioning

confidence: 99%

Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction

Vainio

Szabò

Lin

et al. 2019

JACC: Basic to Translational Science

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“…Elevated CTGF levels are measured in the bronchoalveolar lavage (BAL) of IPF patients [97,98]. In the PRAISE study (NCT01890265), the CTGF antagonist pamrevlumab (FG-3019) was determined to have a significant effect on the reduction of the lung function decline of 160 IPF patients, yet full peer-reviewed data are still awaited [99]. The initiation of phase III trials has currently been announced.…”

Section: Novel Therapiesmentioning

confidence: 99%

The therapy of idiopathic pulmonary fibrosis: what is next?

et al. 2019

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Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrosing interstitial lung disease, characterised by progressive scarring of the lung and associated with a high burden of disease and early death. The pathophysiological understanding, clinical diagnostics and therapy of IPF have significantly evolved in recent years. While the recent introduction of the two antifibrotic drugs pirfenidone and nintedanib led to a significant reduction in lung function decline, there is still no cure for IPF; thus, new therapeutic approaches are needed. Currently, several clinical phase I–III trials are focusing on novel therapeutic targets. Furthermore, new approaches in nonpharmacological treatments in palliative care, pulmonary rehabilitation, lung transplantation, management of comorbidities and acute exacerbations aim to improve symptom control and quality of life. Here we summarise new therapeutic attempts and potential future approaches to treat this devastating disease.

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PRAISE, a randomized, placebo-controlled, double-blind Phase 2 clinical trial of pamrevlumab (FG-3019) in IPF patients

Cited by 10 publications

References 0 publications

Airway Redox Homeostasis and Inflammation Gone Awry: From Molecular Pathogenesis to Emerging Therapeutics in Respiratory Pathology

Airway Redox Homeostasis and Inflammation Gone Awry: From Molecular Pathogenesis to Emerging Therapeutics in Respiratory Pathology

Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction

The therapy of idiopathic pulmonary fibrosis: what is next?

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