Elan Corp. said Wednesday that its third-quarter net loss widened to $117 million, from $67.1 million a year ago, after taking a $10.9 million stock based compensation charge and paying a $15 million license fee to Transition Therapeutics. Elan said it's encouraged by the initial results from the relaunch of its Tysabri drug for multiple scleroris. Elan added its confident that revenue, excluding Tysarbi, will exceed $500 million in 2006 and that its EBITDA loss will less than previous guidance.
ELN closed up at 15.70 on tuesday in after hours trading ( on a volume of 1700 LOL)
Natalizumab [earlier post note the suffix] is being marketed under the name of Tysabri. In early news releases, the company had proposed the name of Antegren, but changed the name before launch.
This is a compound of several antibodies in the pipeline targeting different steps in the immune dysfunction that leads to the clinical condition we call MS.
The exact mechanism of action by which natalizumab exerts its effects is not fully defined. MS is believed to develop when activated inflammatory cells, including T cells, cross the blood brain barrier. No one is sure how the inflammatory cells are activated, but the result is the presence of highly active inflammatory cells within the CNS causing destruction of the "insulating" myelin sheath around nerves. Once damaged, the nerves cease functioning normally and the neurologic effects become the symptoms of MS.
Before the inflammatory cells can cross into the CNS, they must bind to the lining of the blood vessels, the endothelium. Natalizumab is thought to work by preventing this binding and hence stopping the migration of the damaging cells.
Structurally, natalizumab is a recombinant humanized IgG4κ monoclonal antibody produced in murine myeloma cells (mouse cells but the Fc receptor replaced by human one).
This binding basically disrupts the attachment of leukocytes to the blood vessels and prevents the migration of these activated leukocytes into the inflamed area; in the case of MS this is the central nervous system. Simply put, if the T cells establish a foothold on the endothelium, leukocytes cannot migrate through. Natalizumab prevents the foothold from occurring.
Wednesday, October 25, 2006
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