News Feature | August 7, 2014

FDA Grants Orphan Status To Genoa's IPF Drug

By Estel Grace Masangkay

Orphan drug

The U.S. Food and Drug Administration (FDA) has granted orphan drug status to Genoa Pharmaceutical’s inhaled pirfenidone for the treatment of idiopathic pulmonary fibrosis.

Pirfernidone in its oral form (marketed under the brand name Esbriet) has the potential to slow down IPF progression in patients. However a huge dose is needed for efficacy in lung levels. In aerosol form, inhaled pirfenidone is anticipated to deliver Esbriet-equivalent efficacy in IPF patients. The recommended dose of the drug’s inhaled form remains small to meet safety and tolerability standards, but can be increased to improve efficacy in IPF. This is in contrast to the oral form dosage, which has been established above safety thresholds, but which still remains too low for optimal effect.

IPF is a life-threatening lung disease stemming from both genetic and environmental factors. The disease is characterized by progressive scarring of the lungs and ultimately death due to respiratory failure and/or co-morbidities. Typical symptoms include dry cough, shortness of breath, and reduced exercise capacity. IPF is irreversible at present and requires a treatment that maintains and protects healthy lung tissues against invading fibrosis or that slows down disease progression.

Commenting on the FDA designation, Genoa President and CEO Dr. Mark Surber said, “Acquiring orphan status marks an important regulatory milestone in GP-101’s life cycle to treat people with this devastating disease. We are pleased to continue the development of inhaled GP-101, with clinical trials beginning in early 2015.” Orphan status brings a number of benefits to sponsor companies including a period of market exclusivity upon approval of the drug candidate.

Earlier this year Genoa presented research data regarding inhaled pirfenidone at the American Thoracic Society International Conference (ATS 2014) in San Diego, California. The company has also previously collaborated with Dr. Martin Kolb and fellow researchers at McMaster University to investigate mechanisms of pulmonary fibrosis in conjunction with the development program for pirfenidone.