The company is taking this action because of a potential risk to patients of developing progressive multifocal leukoencephalopathy (PML), a rare, serious, progressive neurologic disease caused by a virus that affects the central nervous system. By June 8, 2009, Raptiva will no longer be available in the United States.

Prescribers are being asked not to initiate Raptiva treatment for any new patients. Prescribers should immediately begin discussing with patients currently using Raptiva on how to transition to alternative therapies. The FDA strongly recommends that patients work with their health care professional to transition to other alternative therapies for psoriasis.

The risk that an individual patient taking Raptiva will develop PML is rare and is generally associated with long-term use. Generally, PML occurs in people whose immune systems have been severely weakened and often leads to an irreversible decline in neurologic function and death. There is no known effective treatment for PML. On Oct. 16, 2008, FDA updated the FDA-approved labeling for Raptiva to warn of the risk of life-threatening infections, including PML. On Feb. 19, 2009, the FDA issued a Public Health Advisory informing patients and prescribers of the risk of PML in patients taking Raptiva, after receiving reports of four patients with PML, three of whom died. On March 13, 2009, the FDA approved a Medication Guide for Raptiva and included additional information in Raptiva's labeling regarding PML.

Raptiva was approved by the FDA in 2003. It is a once-weekly injection for adults with moderate to severe plaque psoriasis.

Prescribers should continue to monitor patients on Raptiva for neurologic symptoms that might represent PML. Prescribers and patients may report adverse events to the FDA's MedWatch program at 800-FDA-1088, by mail at MedWatch, HF-2, FDA, 5600 Fishers Lane, Rockville, MD 20852-9787, or online at www.fda/medwatch/report.htm.

More information about the withdrawal of Raptiva is available on the Genentech Web site: www.gene/gene/products. Prescribers with questions about Raptiva may contact Genentech Medical Communications at (800) 821-8590.

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In the study, astrocytes whose KBBP was high bloomed with transporters. This didn't occur if neurons in the chamber were poisoned. It also didn't occur if production of KBBP was blocked.

The researchers next wanted to see if the pathway they'd uncovered was important in real injuries to the spinal cord or brain. They showed, in rodent models, that injuring the spinal cord neurons that control movement, whether by trauma (like spinal cord injury) or poison, plays havoc with nearby astrocytes. When astrocytes lose the connection with neurons, KBBP drops, they don't make transporters, there's a flood of glutamate and they themselves begin to sicken.

This accelerates the ongoing injury to neighboring neurons.

And last, animal models of familial ALS proved the principle of neuron-directs-astrocyte-to-mop-up-glutamate. The models carry a gene that causes the disease, and as the neurons deterioriate, the astrocytes follow. "The loss of the glutamate transporter in these animal models follows the path of neuron injury; it spreads through the spinal cord," says Rothstein.

"Understanding this biology gives us new clues to the ways a neuron's "neighborhood" forces disease to accelerate," says Rothstein. "Fortunately, it also gives us ideas for roadblocks to slow the process down."

This study was supported by The Robert Packard Center for ALS Research, the National Institutes of Health and the Muscular Dystrophy Association.

The research team includes first author Yongjie Yang, Oguz Gozen, Andrew Watkins, Ileana Lorenzini, Angelo Lepore, Yuanzheng Gao, Svetlana Vidensky and Jean Brennan, with the Johns Hopkins School of Medicine, as well as David Poulsen, from the University of Montana, Missoula, Jeong Won Park and Noo Li Jeon with the University of California, Irvine, and Michael B. Robinson, with the University of Pennsylvania.

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