PR Newswire
10/04/04, 9:08a
(Copyright © 2004, PR Newswire)

Research Presented at the 128th Annual Meeting of the American Neurological Association

TORONTO, Oct 4, 2004 /PRNewswire-FirstCall via COMTEX/ -- Vasogen Inc. (NASDAQ:VSGN; TSX:VAS), a research and development company focused on immune modulation therapies targeting the chronic inflammation underlying cardiovascular and neurological disorders, today announced the presentation of preclinical research demonstrating the ability of VP025 to significantly delay the onset of disease and increase survival in a model of amyotrophic lateral sclerosis (ALS) -- also referred to as Lou Gehrig's disease. This research, presented today at the 128th Annual Meeting of the American Neurological Association in Toronto by Dr. David Beers, was conducted under the direction of Dr. Stan Appel, Chief of Neurology at the Methodist Hospital, Professor of Neurology at Baylor College of Medicine, and member of Vasogen's Scientific Advisory Board.

"Vasogen has previously shown, in a number of different preclinical models, that VP025 has the ability to significantly inhibit neuro-inflammation, which is now implicated as an underlying pathology in ALS," commented Dr. Appel. "These findings suggest that the anti-inflammatory effects of VP025 may be useful in slowing the progression of ALS. There is a desperate need for more effective therapies in ALS and this research could lead to a new approach for the treatment of this devastating disease."

In ALS, thg immune system actively contributes to motor neuron injury through inflammatory processes. Prominent pathological features of ALS are the presence of dendritic cells and activated microglia in spinal cord tissue. In this preclinical model of ALS, intramuscular injection of VP025 significantly delayed disease onset (p (equal sign) 0.009) and prolonged survival (p (equal sign) 0.004). Examination of spinal cord sections also revealed a suppression of microglial cell activation when compared with controls. These findings suggest that VP025 has the potential to inhibit immune system activation and protect motor neurons from injury.

Amyotrophic lateral sclerosis (ALS) is one of the most common neuromuscular diseases worldwide. It is a rapidly progressive neurodegenerative disease that attacks nerve cells in the brain and the spinal cord. The progressive degeneration of the motor neurons in ALS causes the muscles under their control to weaken and waste away, leading to paralysis and eventual death. As many as 30,000 Americans have ALS, and an estimated 5,000 people in the United States are diagnosed with the disease each year. ALS most commonly strikes people between 40 and 60 years of age, but younger and older people can also develop the disease.

VP025, the lead product candidate from a new class of structurally related drugs, is being developed for the treatment chronic neuro-inflammatory disorders. VP025 is designed to interact with immune cells leading to the modulation of cytokines -- potent chemical messengers that regulate and control inflammation.

Neurological conditions that are associated with an inflammatory response in the nervous system include Alzheimer's disease, Parkinson's disease, multiple sclerosis, and ALS. These indications are characterized by increased levels of inflammatory mediators, including cytokines, leading to the death of nerve cells and the eventual loss of functional activity. Due to the prevalence, morbidity and mortality associated with neuro-inflammatory diseases, they represent a significant medical, social, and financial burden.