Actelion obtains option to acquire privately-held Trophos
Please find on this page additional material to help you with your article.
On 20 July 2009, Actelion announced that it has obtained an option to acquire privately-held Trophos
Actelion obtains option to acquire privately-held Trophos
Please find on this page additional material to help you with your article.
On 20 July 2009, Actelion announced that it has obtained an option to acquire privately-held Trophos
Quoted in the press release:
Simon Buckingham, President, Global Corporate and Business Development:
“Trophos has done an excellent job to enroll more than 500 ALS patients into a well-designed pivotal study. Once study results are available, Actelion is ideally positioned to leverage these achievements with our proven global regulatory and marketing expertise in the area of orphan drugs.”
Damian Marron, Chief Executive Officer at Trophos commented:
“Since its inception, Trophos has made significant progress in turning its key expertise in neurodegenerative disorders and orphan diseases into achievements that include advancing our lead compound olesoxime into late stage clinical development. The development of olesoxime has benefited from significant support from patient communities, clinical investigators and the European Union (EU), including Trophos spearheading an EU-funded consortium dedicated to improving the treatment of ALS.”
Damian Marron continued: “We are delighted with the option agreement with Actelion, which will bring additional expertise and competencies to enable Trophos’ compound to rapidly reach patients following a successful study outcome.”
Martine Clozel, MD and Chief Scientific Officer at Actelion commented:
“Trophos has a pioneering approach and proprietary expertise that has enabled the development of high throughput screens using primary neurons as well as the ability to broadly profile more advanced compounds. This is of great value to Actelion as we have developed a large in-house compound library and significant expertise in the field of neurological disorders.”
Damian Marron is Chief Executive Officer of Trophos.
Damian Marron has extensive experience in the biotechnology and international pharmaceutical industry, including corporate development, product and technology licensing, research and development, and sales and marketing. Damian’s last role was Executive Vice President Corporate Development at NicOx SA, where he held responsibility for Commercial, Business Development and Alliances, and Investor and Media Relations.
During his six years at NicOx, Damian was responsible for the establishment of major collaborations with Merck & Co Inc and Pfizer and participated in financing rounds raising in excess of €175 million. Prior to NicOx, Damian held various business development, operational and R&D roles at 3M Pharmaceuticals, Orphan Europe, Rhone-Poulenc-Rorer and Glaxo.
Education: Graduated in pharmacology from the University of Liverpool in 1985, followed by post-graduate research into monoclonal antibodies at the University’s Department
Nerve terminal endplate staining
(green : neurofilament ; red: bungarotoxin-stained post-synaptic AChR)
Nerve terminal endplate loss in a new SMA mouse model developed by Trophos
(diaphragm; green: neurofilament; red: bungarotoxin-stained post-synaptic AChR; blue: pre-synaptic vesicles)
About Amyotrophic Lateral Sclerosis
Amyotrophic Lateral Sclerosis (ALS), often referred to as "Lou Gehrig's Disease", is the most common motor neuron disease with a prevalence of 2-3 per 100,000 (30,000 patients in US; 45,000 in Europe at any given time).
Most people who develop ALS are between the ages of 40 and 70 (average age of 55) and over 80% die three to five years after diagnosis. The most common form of ALS is sporadic, but 5-10% of cases are inherited in a dominant manner (familial ALS).
Early symptoms of ALS include muscle weakness in arms and legs; later difficulties in breathing and swallowing are generally the cause of death. There is no treatment today that halts disease progression in ALS patients.