Roche drug Esbriet (pirfenidone) approved in Switzerland for the treatment of idiopathic pulmonary fibrosis (IPF)

23 September 2015

Analysis of large phase III studies in IPF patients showed enhanced preservation of lung function and a 48-percent reduction in mortality with Esbriet after one year.

Roche (SIX: RO, ROG; OTCQX: RHHBY) announced today that the Swiss licensing and supervisory authority for therapeutic products (Swissmedic) has approved the drug Esbriet (pirfenidone) for the treatment of idiopathic pulmonary fibrosis (IPF). IPF is an ultimately fatal disease in which progressive scarring (fibrosis) of the lungs makes breathing difficult and prevents the heart, muscles and other vital organs from receiving enough oxygen. Idiopathic means something like “without known cause”. The disease can advance quickly or slowly, but after a time the lungs will harden and finally stop working altogether.1

“This is an important day for patients who have to live with this insidious disease,” said Prof. Malcolm Kohler MD, Head of the Department of Pulmonology at Zurich University Hospital. “With the approval of Esbriet in Switzerland, patients with IPF have a medicine that may slow the progression of the disease.”

The approval of Esbriet is based on data from a large, placebo-controlled phase III study (ASCEND) and is supported by two other large phase III trials (known as CAPACITY 1 and 2). In the ASCEND study, significantly more patients who received Esbriet showed delayed progression of the disease – corresponding to preservation of lung function – than those who received placebo. Disease progression was defined by the primary endpoint of percent change in forced vital capacity (FVC), a measure of how well the lungs work based on the amount of air one can exhale with force after inhaling as deeply as possible.

Pooled analysis of the ASCEND and both CAPACITY phase III trials also showed a 48-percent reduction in all-cause mortality at one year, as well as a 68-percent reduction in IPF-related mortality in the Esbriet group compared to placebo.

The commonest side effects observed in patients treated with Esbriet compared to placebo were reversible (meaning that they disappear once the medicine is stopped). They include: sensitivity to light, or rash and gastrointestinal (GI) side effects.

Esbriet was granted marketing authorisation in the European Union (EU) in 2011 for the treatment of adults with mild to moderate IPF in all 28 EU member countries, and has since also been approved in Norway, Iceland and Canada. On 15 October 2014, the United States Food and Drug Administration (FDA) approved Esbriet under the Breakthrough Therapy Designation programme. In the same month, the EU Committee for Medicinal Products for Human Use (CHMP) recommended an update to Esbriet’s European product information in idiopathic pulmonary fibrosis, confirming the benefit of the product in terms of mortality rate and its favourable safety profile. Esbriet is already well established in foreign markets.

About idiopathic pulmonary fibrosis (IPF)

110,000 people in Europe and, based on this estimate, almost 2000 in Switzerland have idiopathic pulmonary fibrosis, an irreversible and ultimately fatal disease characterised by progressive loss of the ability of the lungs to absorb oxygen due to scarring.1-2 The cause is unknown and there is no cure. IPF inevitably causes shortness of breath and destruction of healthy lung tissue, although some patients may experience temporary periods of clinical stability.1-5 The median survival time from diagnosis is two to five years, and the five-year survival rate is approximately 20 to 40 percent.1,6 IPF typically occurs in people over the age of 45, and tends to affect slightly more men than women.2

About Esbriet

Esbriet is an oral medicine for the treatment of idiopathic pulmonary fibrosis. It displays antifibrotic activity, and studies in animal models and cell cultures suggest that the drug affects the production of two proteins, transforming growth factor (TGF)-beta, which is involved in cell growth, and tumour necrosis factor (TNF)-alpha, which plays an important role in inflammation.

About Roche

Headquartered in Basel, Switzerland, Roche is a leader in research-focused healthcare with combined strengths in pharmaceuticals and diagnostics. Roche is the world’s largest biotech company, with truly differentiated medicines in oncology, immunology, infectious diseases, ophthalmology and neuroscience. Roche is also the world leader in in vitro diagnostics and tissue-based cancer diagnostics, and a frontrunner in diabetes management. Roche’s personalised healthcare strategy aims at providing medicines and diagnostics that enable tangible improvements in the health, quality of life and survival of patients. Founded in 1896, Roche has been making important contributions to global health for more than a century. Twenty-nine medicines developed by Roche are included in the World Health Organisation Model Lists of Essential Medicines, among them life-saving antibiotics, antimalarials and chemotherapy.

In 2014 the Roche Group employed over 88,500 people worldwide, invested 8.9 billion Swiss francs in R&D and posted sales of 47.5 billion Swiss francs. Genentech, in the United States, is a wholly owned member of the Roche Group. Roche is the majority shareholder in Chugai Pharmaceutical, Japan. For more information, please visit www.roche.com.

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References
1. Website of the National Institutes for Health. “Idiopathic Pulmonary Fibrosis” http://www.nhlbi.nih.gov/health/health-topics/topics/ipf/. Accessed 2 October 2014.
2. Website of the United States National Library of Medicine. “Idiopathic Pulmonary Fibrosis” http://ghr.nlm.nih.gov/condition/idiopathic-pulmonary-fibrosis. Accessed 7 October 2014.
3. Coalition for Pulmonary Fibrosis. Facts About Idiopathic Pulmonary Fibrosis. http://www.coalitionforpf.org/facts-about-idiopathic-pulmonary-fibrosis. Accessed 14 August 2014.
4. Kim DS, et al. Proc Am Thorac Soc. 2006;3:285-292.
5. Raghu G, et al. Am J Respir Crit Care Med. 2011;183:788-824
6. King TE Jr et al., Proc Am Thorac Soc. 2006 ; 4: 285-292.