Acorda Therapeutics Announces Successful Thorough QT Study of Fampridine-SR

Fampridine-SR Not Associated with QT Changes

Company to Host Conference Call at 8:30 am Eastern Time Today

HAWTHORNE, N.Y.--(BUSINESS WIRE)--Jan. 28, 2008--Acorda Therapeutics, Inc. (Nasdaq: ACOR) today announced results from a thorough QT study of Fampridine-SR. This study evaluated the potential to cause an increase in the electrocardiographic QT interval. Fampridine-SR, at both therapeutic and supratherapeutic doses, was found to be no different than placebo. The U.S. Food and Drug Administration requires thorough QT studies for all new drugs seeking regulatory approval, as increases in the QT interval (corrected for changes in heart rate, or QTc) may signify an increased risk of developing malignant cardiac arrhythmias.

This double-blind trial compared the electrocardiographic effects of Fampridine-SR, given at a therapeutic (10 mg twice daily) and supratherapeutic dose (30 mg twice daily), to placebo and moxifloxacin in 208 healthy subjects. Moxifloxacin is a positive control known to increase the QT interval.

The placebo-corrected QTc mean change from baseline (using the individual correction method for heart rate, or QTci) for the therapeutic and supratherapeutic doses of Fampridine-SR were 0 and 1 milliseconds, respectively. Moxifloxacin demonstrated QT prolongation consistent with previous clinical experience. In addition to no changes in the mean QTci interval, none of the subjects in the Fampridine-SR cohort showed increases in the QTci of greater than 30 milliseconds, nor did any of the Fampridine-SR subjects display a QTci interval that exceeded 480 milliseconds at any time.

Ron Cohen, Acorda's President and Chief Executive Officer, commented, "We are delighted with the results of this QT study, and are looking forward to completing our second Phase 3 trial of Fampridine-SR in multiple sclerosis patients in the second quarter of this year."

The company will host a conference call Monday, January 28, 2008 at 8:30 a.m. Eastern Time. To participate, please dial 866-800-8652 (domestic) or 617-614-2705 (international) and reference the access code 87165145. A replay of the call will be available from 11:00 a.m. Eastern Time on January 28, 2008 until February 28, 2008. To access the replay, please dial 888-286-8010 (domestic) or 617-801-6888 (international) and reference the access code 18388394. The archived teleconference will be available for 30 days in the Investor Relations section of the Acorda website at http://www.acorda.com.

About Fampridine-SR

Fampridine-SR is a sustained-release tablet formulation of the investigational drug fampridine

(4-aminopyridine or 4-AP). Laboratory studies have shown that fampridine can improve the communication between damaged nerves, which may result in increased neurological function. Fampridine-SR is currently being studied in a Phase 3 clinical trial to evaluate its safety and efficacy in improving walking ability in people with multiple sclerosis (MS).

About Acorda Therapeutics

Acorda Therapeutics is a biotechnology company developing therapies for spinal cord injury, multiple sclerosis and related nervous system disorders. The Company's marketed products include Zanaflex Capsules(R) (tizanidine hydrochloride), a short-acting drug for the management of spasticity. Acorda's lead clinical product, Fampridine-SR, is in a Phase 3 clinical trial to evaluate its safety and efficacy in improving walking ability in people with MS. The Company's pipeline includes a number of products in development for the treatment, regeneration and repair of the spinal cord and brain.

Forward-Looking Statements

This press release includes forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. All statements, other than statements of historical facts, regarding management's expectations, beliefs, goals, plans or prospects should be considered forward-looking. These statements are subject to risks and uncertainties that could cause actual results to differ materially, including Acorda Therapeutics' ability to successfully market and sell Zanaflex Capsules, the risk of unfavorable results from future studies of Fampridine-SR, delays in obtaining or failure to obtain FDA approval of Fampridine-SR, competition, failure to protect its intellectual property or to defend against the intellectual property claims of others, the ability to obtain additional financing to support Acorda Therapeutics' operations, and unfavorable results from its preclinical programs. These and other risks are described in greater detail in Acorda Therapeutics' filings with the Securities and Exchange Commission. Acorda Therapeutics may not actually achieve the goals or plans described in its forward-looking statements, and investors should not place undue reliance on these statements. Acorda Therapeutics disclaims any intent or obligation to update any forward-looking statements as a result of developments occurring after the date of this press release.

CONTACT: Acorda Therapeutics
MEDIA:
Jeff Macdonald, 914-347-4300 ext. 232
jmacdonald@acorda.com
or
INVESTOR RELATIONS:
Molly Newton, 914-347-4300 ext. 203
mnewton@acorda.com

SOURCE: Acorda Therapeutics, Inc.

Blood Flow May Be Key Player in Neural Processing

January 24, 2008

An M.I.T. scientist believes that if blood flow actually impacts neuronal behavior, the fMRI would be an even more powerful tool for diagnosing disorders such as Alzheimer's and schizophrenia

By Nikhil Swaminathan

Blood racing through a brain region's web of vessels is a sign that nerve cells in that locale have kicked into action. The blood rushes to active areas to supply firing neurons with the oxygen and glucose they need for energy.

It is this blood flow, which can last up to a minute, that scientists track in functional magnetic resonance imaging (fMRI) to determine which brain areas are responding to different stimuli. But a new theory could pave the way for a reinterpretation of fMRI images, elevating their measurements to the evaluation of actual neuronal processing rather than the subsequent blood flow that indirectly indicates it, and thereby enhancing the fMRI's usefulness in diagnosing neurological problems.

Christopher Moore, an assistant neuroscience professor at the Massachusetts Institute of Technology's McGovern Institute for Brain Research, detailed his hypothesis in a recent article published in the Journal of Neurophysiology. In essence, it suggests blood's role in the cortex (a key brain processing center), specifically, is more than just bringing nutrients to the cell, it can also alter the activity of local neuronal circuits. For instance, in experiments in his lab, Moore has seen that there is more blood flow can arrive in an area that processes information from a presented stimulus to a certain sense (e.g. touch, visual, auditory) prior to the appearance of the stimulus, implying that the flow can prime a circuit for activity, as well.

Researchers estimate that blood flow in areas of the brain increases by 40 percent when neurons start to fire (or send out electronic impulses), whereas the corresponding metabolic rate of the cells only increases by 4 percent, meaning the cell only needs a tenth of the blood it is supplied to reenergize. "[Neuroscientists] call this discrepancy an 'uncoupling' between flow and metabolism," says Kenneth Kwong, an associate professor in radiology at Harvard Medical School and the researcher, along with Seiji Ogawa, who is generally credited with developing fMRI.

Moore believes that the reason for the discrepancy could be that blood not only nourishes cells but may be intimately involved in the information processing.

If true, Moore says, blood should be factored into any model of neuronal processing—how nerve cells in the brain are activated, how impulses are transmitted between them, how long activity lasts, and how it is terminated. In addition to changing what fMRI is actually measuring, such models could potentially provide new clues to causes of enigmatic disorders such as Alzheimer's disease, multiple sclerosis and schziophrenia—potentially paving the way for treatments that involve correcting blood flow as well as (or rather than) chemical deficiencies.

"Historically, fMRI researchers have to be a little apologetic because they're not looking [directly] at the neuron," Moore says. "fMRI would stop being a second-class citizen; instead it would make fMRI a much more interesting tool…a Heisenberg sort of thing [referring to how the act of observing a quantum state changes it], where what you're looking at is actually a part of the computation going on." Further, scans taken over a number of years could help predict neurodegeneration, if vasculature in a particular brain region begins to weaken. Preliminary data already suggest this is the case for many neurological disorders such as schizophrenia.

The so-called hemo-neural hypothesis plays out in three tissue types: neurons, the blood vessels that feed them, and astrocytes, the star-shaped nerve cells that support and maintain neurons. (Astrocytes, the feet of which are splayed on blood vessels, also help maintain the endothelial cells that line the vessels as well as make up the semipermeable blood–brain barrier responsible for keeping chemicals in the blood from seeping into the brain unless they are needed for metabolism or some other function.)

According to Moore, the vasculature thus directly or indirectly (via astrocytes) influences neurons. He notes that substances in blood may modulate neuron activity. The most likely candidate, he says, is nitric oxide (NO), which easily crosses the blood–brain barrier and has been shown both in brain slices and in animal models to excite (and in some cases dampen) neuronal action. Blood vessels also affect neurons via thermal and mechanical stress. Increased blood flow can alter the local temperature in a brain region. For instance, a decrease of just one degree Celsius can lead to suppressed firing rates, in some circumstances. As a rule, blood flow changes increase the temperature in outer brain areas, while decreasing the temperature of more central regions. Pressure and volume, meanwhile, within the blood vessels can change the amount that the vessels physically impact the membranes of brain cells. If pressure or volume were to increase, a vessel could bulge, blocking receptors or ion channels and thereby causing a decrease in a neuron's electrical activity.

A change in blood flow could also trigger astrocytes to release certain hormones or neurotransmitters. "If anything is going on in the blood vessel," Moore says, "the glia (astrocytes and other nonneuronal nerve cells) is in a great position to sense it." For instance, astrocytes might secrete the excitatory neurotransmitter glutamate, which binds to neurons and allows ion exchanges that cause cells to fire.

Preliminary data from Moore's lab, involving a drug that selectively binds to receptors on blood vessels (and can open or close them), has shown neurons may become more active when blood flow increases. The M.I.T. group is now trying to develop light-activated ion channels on muscle cells, which they could then selectively control to induce changes in blood flow.

The theory "brings up something that a lot of people have been ignoring—thinking that blood vessels are tubes," says Edith Hamel, a professor of neurology at McGill University in Montreal, who believes that Moore's theory will one day prove true. "But, they are live cells…like neurons." She likens the vasculature interaction within the nervous system to that of the infrastructure of a highway system. "We have always been looking at the highway going out of the city," she says. "We need to look at the one coming into the city, as well."

Rick Buxton, a radiology professor at the University of California, San Diego, finds the idea intriguing, but he is "skeptical that blood flow is really an important modulator." In his interpretation, the rush of blood is necessary to maintain oxygen levels in the tissue, because neurons may take in oxygen at a slower rate than normal when blood is gushing by; therefore, more is needed to properly nourish the cells. Another possible way to account for the excess blood flow, according to some researchers, is that it may help carry away some of the heat generated by neuronal firing. "If there's some low level of neuromodulation in there, [as well], that's good," Buxton adds.

Moore notes that if the blood is responsible for a relatively low level of neuromodulation, it could still be significant. "Let's say that blood flow accounts for 5 percent of the variance of activity in cortical neurons," he supposes. "Five percent of the neuron's work—that's huge, if it's pushing around excitability by that scale."

Moore's theory is supported by research into neurodegenerative and mental disorders. Constantino Iadecola, a professor of neurology and neuroscience at Weill Cornell Medical College in New York City, for instance, has found a link between blood vessels and neurons in his work on Alzheimer's disease.

"We have provided evidence that the vasculature is the first thing that goes," he says, noting that Alzheimer's-associated dementia was previously split into two groups: vascular-induced (in which neurons die due to improper blood flow) and neurodegeneration-induced (with vasculature collapse following nerve cell death). "What's emerging from the literature now is that the [vessel changes occur] at least as early or earlier than the neuronal changes."

Abnormal blood flow has also been linked to epilepsy, which is caused by overactive neurons. And, according to Moore, an impoverished blood supply is usually noted in the areas of schizophrenia sufferers' brains that go awry in the disorder.

Moore envisions that in the future research on treatments for mental disorders will focus on potential drugs designed to maintain proper neuronal function by targeting vasculature. "It would be beneficial to upregulate and downregulate blood flow," he says, "the same way as it's beneficial to upregulate or downregulate [the neurotransmitter] dopamine in schizophrenics."

New Therapeutic Target For Treatment Of Multiple Sclerosis

ScienceDaily (Jan. 24, 2008) — An international research team, led by a scientist from the Centre hospitalier de l'Université de Montréal (CHUM), has identified new therapeutic targets for the treatment of multiple sclerosis (MS). In the February issue of Nature Immunology, the team provides fresh answers concerning the role of novel adhesion molecules in the pathogenesis of MS, a chronic autoimmune disease of the nervous system that affects approximately 55,000 young adults in Canada.

Conducted by Dr. Alexandre Prat, a CHUM neurologist and researcher and a professor at the Université de Montréal's Faculty of Medicine, the study included collaborators from McGill University (Dr. S. David), the Université de Montréal (Dr. N. Arbour), the National Research Council of Canada (Dr. D. Stanimirovic) and University of Zürich (Dr. B. Becher). The team found that the adhesion molecule dubbed ALCAM (Activated Leukocyte Cell Adhesion Molecule), or CD166, plays a major role in the migration of certain types of leukocytes to the brain.

The researchers believe that the molecule, which is expressed by the endothelial cells of the brain, constitutes a novel target to restrict migration of immune cells to the brain, thereby dampening neuroinflammation and decreasing the lesions characteristic of MS. Understanding the molecular mechanisms of brain inflammation is essential in the development of new treatments for MS.

Dr. Prat and his team clearly demonstrate that CD166/ALCAM is involved in the inflammatory process by priming the migration of leukocytes across the blood-brain barrier (BBB). The investigation combined the results of an in vitro human BBB model and an in vivo experimental autoimmune encephalomyelitis mouse model. Normally, a limited number of immune cells are able to cross the BBB and penetrate the central nervous system.

In MS and other neuroinflammatory diseases, the increased permeability of the BBB is associated with an increase in the transmigration of some of these immune cells, which penetrate the central nervous system and cause the demyelinating lesions of MS. A previous study by Dr. Prat's team published in October in Nature Medicine, proved that a certain type of leukocyte, the TH17 lymphocyte, produces two critical products, interleukins 17 and 22 (IL-17 and IL-22), which contribute to infiltrating the blood-brain barrier and causing inflammation of the central nervous system.

"Blocking the migration of immune cells across the BBB has long been considered a promising therapeutic approach to autoimmune diseases of the central nervous system," said Dr. Prat. "This study has given us new insight into the factors involved in the pathogenesis of immune reactions affecting the central nervous system and allowed us to identify potential targets to suppress neuroinflammatory processes."

An attractive therapeutic target

Pharmacological agents exist that reduce the transmigration of immune cells by specifically blocking leukocyte adhesion molecules, which significantly decrease the extent of CNS inflammation. However, they also impede the immune system's ability to provide protection against chronic viral infections of the central nervous system, such as progressive multifocal leukoencephalopathy, a demyelinating disease of the central nervous system caused by the JC virus. Since ALCAM/CD166 blockade does not affect CD8+ T cell migration, whose main function is to destroy cells infected by viruses and neoplastic cells, the study results suggest that CNS immune protection against viruses would not be compromised by ALCAM blockade in vivo. ALCAM/CD166 could be considered as an attractive therapeutic target for multiple sclerosis.

This study was funded by the Multiple Sclerosis Society of Canada and by the Canadian Institutes of Health Research (CIHR).

The blood-brain barrier (BBB)

The BBB is a membranic structure that controls and limits exchanges between the blood and the brain. Composed of endothelial cells packed tightly within brain capillaries, it maintains the composition of the brain's interstitial spaces by its selective and restrictive permeability. It is almost completely impermeable to various molecules, immune cells and substances circulating in the blood. The BBB thus isolates and protects the brain from the rest of the organism.

Multiple Sclerosis

In MS, immune cells penetrate the BBB and attack the myelin, a protective sheath that covers the nerve fibres of the central nervous system. The destruction of myelin causes loss of sensation, paralysis and handicaps. It is believed that genetic, infectious and environmental factors trigger MS, but the exact cause of the disease is still unknown. It affects twice as many women as men.

Adapted from materials provided by University of Montreal.

BioMS Medical Completes Licensing Deal with Lilly

- BioMS receives $87 million upfront payment -

Edmonton, Alberta, January 25, 2008 – BioMS Medical Corp. (TSX: MS) reported today that it has completed the previously-announced licensing and development agreement with Eli Lilly and Company. As part of the agreement, BioMS has received an upfront cash payment of US$87 million. In December, 2007 BioMS Medical entered into a global licensing and development agreement granting Lilly exclusive worldwide rights to BioMS Medical's lead drug, MBP8298, for the treatment of multiple sclerosis (MS).

“We look forward to a productive and successful relationship with Lilly,” said Kevin Giese, President and CEO of BioMS. “With these resources and the support from a world-class pharmaceutical company, we are well positioned to realize our shared goal of developing MBP8298 to bring new hope to patients suffering from MS.”


About BioMS Medical Corp.
BioMS Medical is a biotechnology company engaged in the development and commercialization of novel therapeutic technologies. BioMS Medical's lead technology, MBP8298, is for the treatment of multiple sclerosis and is being evaluated in two pivotal phase III clinical trials for secondary progressive MS patients, MAESTRO-01 in Canada and Europe and MAESTRO-03 in the United States . It additionally is being evaluated for relapsing remitting MS patients in a Phase II trial in Europe entitled MINDSET-01. For further information please visit our website at www.biomsmedical.com .



Ryan Giese
VP Corporate Communications
Phone: 780-413-7152
rgiese@biomsmedical.com

Tony Hesby
Executive VP Corporate Affairs
Phone: 780-413-7152
tony.hesby@biomsmedical.com

Amanda Stadel
Investor Relations Manager
Phone: 780-413-7152
astadel@biomsmedical.com

BIOGEN IDEC AND ELAN PROVIDE UPDATE ON UTILIZATION, SAFETY AND TOTAL PATIENT EXPOSURE OF TYSABRI® IN PATIENTS WITH MULTIPLE SCLEROSIS

More than 21,000 patients on commercial and clinical therapy worldwide

Cambridge, MA and Dublin, Ireland - January 7, 2008 - Biogen Idec (NASDAQ: BIIB) and Elan Corporation, plc (NYSE: ELN) today announced new data on the global utilization, safety and overall patient exposure of TYSABRI® (natalizumab). As of late December 2007, more than 21,000 patients were on commercial and clinical therapy worldwide. To date, the safety data continue to support a favorable benefit-risk profile for TYSABRI. These data will be presented today at 4:00 p.m. PST at the 26th Annual JPMorgan Healthcare Conference in San Francisco.

According to data available to the companies as of late December 2007:

In the US, approximately 12,900 patients were on TYSABRI therapy commercially and approximately 2,500 physicians have prescribed the therapy;
Internationally, approximately 7,500 patients were on TYSABRI therapy commercially;
In global clinical trials, approximately 700 patients were on TYSABRI therapy; and
There have been no cases of progressive multifocal leukoencephalopathy (PML) since re-launch in the US and launch internationally in July 2006.
In addition, as of mid-December 2007:

Cumulatively, in the combined clinical trial and postmarketing settings, up to 30,900 patients have been treated with TYSABRI; and
Of those patients, up to 6,300 have received at least one year of TYSABRI therapy.
TYSABRI is available in the United States through the TOUCH™ Prescribing Program. All US prescribers, infusion sites and patients receiving TYSABRI are required to enroll in TOUCH. Safety information is also collected through ongoing clinical trials and registries, including TYGRIS and the pregnancy registry, making this the largest long-term patient follow-up effort undertaken for any MS therapy.

About TOUCH and TYGRIS
Before initiating treatment, all US patients, prescribers and infusion sites must be enrolled in the TOUCH Prescribing Program (TYSABRI Outreach: Unified Commitment to Health). TOUCH is designed to determine the incidence of and risk factors for serious opportunistic infections (OIs), including PML, and to monitor patients for signs and symptoms of PML while promoting informed benefit-risk discussions prior to initiating TYSABRI treatment. Physicians report on PML, other serious OIs, deaths and discontinuation of therapy on an ongoing basis.

TYGRIS (TYSABRI Global ObseRvation Program In Safety) is expected to enroll 5,000 patients worldwide, including approximately 3,000 patients from TOUCH. Patients in TYGRIS are evaluated at baseline and every six months thereafter for five years. Researchers will evaluate data including medical/MS history; prior TYSABRI use; prior use of immunomodulatory, antineoplastic, or immunosuppressive agents; and all serious adverse events, including PML and other serious OIs, and malignancies.

Adverse event reporting in the post-marketing setting is voluntary. It is possible that not all reactions have been reported, or that some reactions are not reported to Biogen Idec or Elan in a timely manner.

About TYSABRI
TYSABRI is a treatment approved for relapsing forms of MS in the United States and relapsing-remitting MS in the European Union. According to data that have been published in the New England Journal of Medicine, after two years, TYSABRI treatment led to a 68% relative reduction (p<0.001) in the annualized relapse rate compared to placebo and reduced the relative risk of disability progression by 42-54% (p<0.001).

TYSABRI increases the risk of progressive multifocal leukoencephalopathy (PML), an opportunistic viral infection of the brain that usually leads to death or severe disability. Other serious adverse events that have occurred in TYSABRI-treated patients included hypersensitivity reactions (e.g., anaphylaxis) and infections. Serious opportunistic and other atypical infections have been observed in TYSABRI-treated patients, some of whom were receiving concurrent immunosuppressants. Herpes infections were slightly more common in patients treated with TYSABRI. In MS trials, the incidence and rate of other serious and common adverse events, including the overall incidence and rate of infections, were balanced between treatment groups. Common adverse events reported in TYSABRI-treated patients include headache, fatigue, infusion reactions, urinary tract infections, joint and limb pain, and rash.

In addition to the United States and European Union, TYSABRI is also approved for MS in Switzerland, Canada, Australia, New Zealand and Israel. TYSABRI was discovered by Elan and is co-developed with Biogen Idec.

For more information about TYSABRI please visit www.tysabri.com, www.biogenidec.com or www.elan.com, or call 1-800-456-2255.

About Biogen Idec
Biogen Idec creates new standards of care in therapeutic areas with high unmet medical needs. Founded in 1978, Biogen Idec is a global leader in the discovery, development, manufacturing, and commercialization of innovative therapies. Patients in more than 90 countries benefit from Biogen Idec’s significant products that address diseases such as lymphoma, multiple sclerosis, and rheumatoid arthritis. For product labeling, press releases and additional information about the company, please visit www.biogenidec.com.

About Elan
Elan Corporation, plc is a neuroscience-based biotechnology company committed to making a difference in the lives of patients and their families by dedicating itself to bringing innovations in science to fill significant unmet medical needs that continue to exist around the world. Elan shares trade on the New York, London and Dublin Stock Exchanges. For additional information about the company, please visit www.elan.com.

Safe Harbor/Forward-Looking Statements
This press release contains forward-looking statements regarding TYSABRI. These statements are based on the companies’ current beliefs and expectations. The commercial potential of TYSABRI is subject to a number of risks and uncertainties. Factors which could cause actual results to differ materially from the companies’ current expectations include the risk that we may be unable to adequately address concerns or questions raised by the FDA or other regulatory authorities, that concerns may arise from additional data, that the incidence and/or risk of PML or other opportunistic infections in patients treated with TYSABRI may be higher than observed in clinical trials, that the companies may encounter other unexpected hurdles, or that new therapies for MS with better efficacy or safety profiles or more convenient methods of administration are introduced into the market. Drug development and commercialization involves a high degree of risk.

For more detailed information on the risks and uncertainties associated with the companies’ drug development and other activities, see the periodic and current reports that Biogen Idec and Elan have filed with the Securities and Exchange Commission. The companies assume no obligation to update any forward-looking statements, whether as a result of new information, future events or otherwise.


For more information contact:

Media Contacts:
Biogen Idec

Amy Reilly
Ph: 617 914 6524

Elan

Jonathan Birt
Ph: 212 850 5664

Elizabeth Headon
Ph: 353 1 498 0300

Investor Contacts:
Biogen Idec

Eric Hoffman
Ph: 617 679 2812

Elan

Chris Burns
Ph: 353 1 709 4444
800 252 3526