Prima in high-level licensing talks
Prima BioMed has commenced preliminary talks with several major drug companies over potential licensing options for its new anti-inflammatory compound,VIB 153.
CEO Marcus Clark said the listed Melbourne company would consider raising up to $8 million in order to take the compound through to human trials, although this would depend on several milestones being achieved.
On February 7, Prima BioMed announced that its subsidiary, Arthron, had successfully prevented rheumatoid arthritis in mouse models.
Clark said Arthron's research was now six months ahead of schedule, with clinical trials pegged to begin in 2003.
"This is a major announcement because it is the first we have made since we committed funding to Arthron and importantly these compounds are showing quite exceptional activity," he said.
"At the moment we are just exploring options and looking for collaborations. We have had talks with several major pharmas in this area, and they're ongoing ? and they're very interested in this as a third generation compound."
Clark declined to name the drug companies involved in the talks.
He said Prima BioMed was also talking with several overseas investors who he hoped would form the core of the company's future capital-raising efforts.
The global rheumatoid arthritis drug market is estimated at $US10 billion, with up to two per cent of Australians ? mostly women in their 30s ? suffering from the disease.
Current treatments involve either killing off white blood cells with anti-cancer drugs, or soaking up inflammatory chemicals, both of which are used once symptoms appear.
Arthron's chief scientific officer, Professor Mark Hogarth, said one of the main benefits of VIB 153 was that it appeared to work in the very early stages of disease before symptoms surfaced.
"It is a very complex disease, and it is difficult to predict the onset initially, so treating the early phases of inflammation would be ideal," he said.
For the past 15 years, Arthron's target has been the human Fc receptor, which sits on the outside of white blood cells and acts as a lock and key system to keep damaging inflammatory cells locked away.
But Hogarth said aberrant proteins, called immune complexes, sometimes entered the lock, releasing inflammatory cells into joints.
He said that by using x-ray crystallography to determine the chemical shape of the lock, the group had designed a drug to plug the keyhole.
While they will continue to test other similar compounds in vitro, VIB 153 is the first to be tested in animals.
The team induced rheumatoid arthritis in transgenic rodents engineered to contain the human Fc receptor. Three weeks after induction, before any symptoms had surfaced, the mice received the drug.
"Of all the mice tested, only two got the disease and that was in a very mild form, so we consider that essentially all the mice remained arthritis-free," Hogarth said.
"We have been watching them for over two months now, which is a long time for this model."
More than 70 mice, including controls, were used in the research, which is yet to be submitted to a scientific journal.
Hogarth said the small size of the compound meant it would likely be developed into an oral medication.
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