Opexa Therapeutics Reports Favorable Two-Year Data in Phase I/II Retreatment Studies of Tovaxin® for Multiple Sclerosis

73% of patients remained relapse-free at two years

THE WOODLANDS, Texas--(BUSINESS WIRE)--Opexa Therapeutics, Inc. (NASDAQ:OPXA), a cell therapy development and commercialization company, today announced favorable safety and efficacy data for Tovaxin®, the Company’s investigational T-cell vaccination therapy for multiple sclerosis (MS), in the second year of open-label clinical retreatment studies in patients with MS.

The “intent to treat” population of 22 patients included 13 with relapsing remitting multiple sclerosis (RRMS) and nine with secondary progressive multiple sclerosis (SPMS). An analysis of disease progression of disability over a two year period, as measured by a 1.0 or greater change in Expanded Disability Scoring Scale (EDSS), showed that 27.3% of patients demonstrated sustained improvement, 59.1% had no disease progression and 13.6% experienced sustained worsening of disability. The improvement in the EDSS scores ranged from 1.0 to 4.5 (average 2.41). During the two-year study period 72.7% of patients remained relapse-free.

Brian Loftus, M.D., of Bellaire Neurology and the principal investigator of the studies, commented, “I’m pleased to see that subjects in the study experienced sustained positive clinical outcomes over the two-year period. It was especially encouraging to see a lack of disease progression in more than 86% of the patients after two years, given the later stage of disease of this subject population.”

The annualized relapse rate analysis of 17 patients (which excludes five patients with no prior relapses in their two-year pre-study baseline) showed Tovaxin therapy achieved an 82% reduction in annualized relapse rate (ARR) in patients over a two-year period (p<0.0001) to 0.21 relapses per year, compared with 1.38 relapses per year in the patients’ prior two-year baseline. For RRMS patients (n=12) the ARR over a two-year period was 0.26 relapses per year, compared with 1.63 relapses per year in the patients’ prior two-year baseline; for SPMS patients (n=5) the ARR over a two-year period was 0.10 relapses per year, compared with 0.80 relapses per year in the patients’ prior two-year baseline.

“Approximately three out of four patients re-treated in the second year exhibited a change in their myelin-reactive T-cell profile, which was the basis for producing their individualized T cell vaccine,” said David McWilliams, president and chief executive officer of Opexa. “We believe this new data supports the continuation of our development strategy of individually monitoring patients with our proprietary epitope analysis assay and re-treating them with a patient-specific therapeutic vaccine that associates with their clinical status.”

The combined analysis included patients participating in second-year extension protocols from the Phase I/II dose-escalation study and the Phase I/II re-treatment study, and 19 of 22 patients were re-treated with Tovaxin during the study period. Patients did not receive any other disease modifying therapies during the two-year study period.

Tovaxin was well-tolerated throughout the two-year study period. The safety profile revealed only mild-to-moderate injection site reactions and no serious adverse reactions related to T-cell vaccination.

About Multiple Sclerosis

In the U.S. approximately 400,000 people suffer from MS, a chronic progressive autoimmune disease of the central nervous system that is caused by myelin autoreactive T-cells progressively eroding the myelin that surrounds and insulates nerve fibers of the brain and spinal cord resulting in varying amounts of disability. Globally, there are approximately 2.5 million MS patients representing a drug therapy market believed to be approximately $5 billion in 2005. The US markets accounted for slightly more than half of global MS sales in 2005.

MS remains a challenging autoimmune disease to treat because the pathophysiologic mechanisms are diverse, and the chronic, unpredictable course of the disease makes it difficult to determine whether the favorable effects of short-term treatment will be sustained. Therapies that are easy to use and can safely prevent or stop the progression of disease represent the greatest unmet need in MS. The most common phase of MS at the time of diagnosis is relapsing-remitting, which affects approximately 70% of MS patients. This group experiences clearly defined flare-ups (relapses), followed by partial or complete remissions between attacks that are free of disease progression. Approximately 50% of the relapsing-remitting patients develop the secondary-progressive form of the disease within 10 years of diagnosis. This phase is characterized by an initial period of relapsing-remitting disease followed by steady worsening with or without flares or minor remissions.

About Tovaxin for Multiple Sclerosis

Tovaxin is an individualized T-cell therapeutic vaccine that consists of attenuated patient-specific myelin-reactive T-cells (MRTCs) against peptides of proteins from Myelin basic protein (MBP), Myelin oligodendrocyte glycoprotein (MOG) and Proteolipid protein (PLP) or combinations thereof. Patient-specific MRTCs are expanded in culture with specific peptides identified by assaying peripheral blood mononuclear cell reactivity against peptides derived from the three myelin proteins. Studies have shown that T-cell vaccination resulted in the in vivo induction of CD8+ cytotoxic T-cells and CD4+CD25+FoxP3 Tregs specific for T-cell vaccine. The induction of anti-idiotypic cytotoxic CD8+ effector T-cells and anti-ergotypic CD4+CD25+FoxP3 positive Tregs is believed to provide a therapeutically effective dual mechanism of protection to patients treated with Tovaxin. The observed regulatory immune responses have been shown to collectively relate with clinical improvement in treated patients. Tovaxin has been previously studied in two Phase I/II open-label trials. A 150-patient Phase IIb one-year double blind placebo controlled study to evaluate the efficacy, safety and tolerability of Tovaxin in subjects with clinically isolated syndrome (CIS) or relapse-remitting multiple sclerosis (RR-MS) is nearing completion.

About Opexa Therapeutics

Opexa Therapeutics develops and commercializes cell therapies to treat autoimmune diseases such as multiple sclerosis, rheumatoid arthritis and diabetes. The Company is focused on autologous cellular therapy applications of its proprietary T-cell and stem cell therapies. The Company's lead product is Tovaxin, a T-cell therapy for multiple sclerosis is in Phase IIb trials. The Company holds the exclusive worldwide license for adult multipotent stem cells derived from mononuclear cells of peripheral blood. The technology allows large quantities of monocyte-derived stem cells to be produced efficiently for use in autologous therapy, thus circumventing the threat of rejection. The Company is in preclinical development for diabetes mellitus. For more information visit the Opexa Therapeutics website at www.opexatherapeutics.com.

Cautionary Statement Relating to Forward-Looking Information for the Purpose of "Safe Harbor" Provisions of the Private Securities Litigation Reform Act of 1995

This press release contains "forward-looking statements," including statements about Opexa Therapeutics' growth and future operating results, discovery and development of products, strategic alliances and intellectual property, as well as other matters that are not historical facts or information. These forward-looking statements are based on management's current assumptions and expectations and involve risks, uncertainties and other important factors, specifically including those relating to Opexa Therapeutics' ability to obtain additional funding, develop its stem cell technologies, obtain FDA approval for its therapeutic products, achieve its operational objectives, and obtain patent protection for its discoveries, that may cause Opexa Therapeutics' actual results to be materially different from any future results expressed or implied by such forward-looking statements. Opexa Therapeutics undertakes no obligation to update or revise any such forward-looking statements, whether as a result of new information, future events or otherwise.

High-Dose Cyclophosphamide Reduces Disability in Aggressive Multiple Sclerosis

June 12, 2008 — High-dose cyclophosphamide (HiCy) reduces disease activity and disability in people with severe aggressive multiple sclerosis (MS) who have not undergone bone marrow transplantation.

In a 2-year open-label trial of 9 patients with aggressive relapsing remitting MS (RRMS), investigators at Johns Hopkins University in Baltimore, Maryland, found that administering a 1-time immunoablative regimen of 50 mg per kilogram of intravenous cyclophosphamide over 4 consecutive days resulted in a statistically significant reduction in disability that was durable at an average follow-up of 23 months, with no adjunctive immunomodulatory therapies.

"We did not expect this [reduction in disability]. We found that disability levels at the beginning of the study were much greater than at the end of the study. Patients had a return of function that, for some, translated into significant improvements, such as returning to work, dispensing with walkers or canes, and regaining bladder control," Douglas A. Kerr, MD, PhD, told Medscape Neurology & Neurosurgery.

Furthermore, the treatment appeared safe and well tolerated, with no deaths or unexpected serious adverse events.

The study was published online June 9 in the Archives of Neurology.

Starting From Scratch

Cyclophosphamide, a chemotherapeutic agent, has been used for about half a century, primarily to treat cancer. When it was used to treat MS in the 1980s, its efficacy as a single-pulse therapy was, at best, modest and did not justify its routine use, said Dr. Kerr.

Currently, cyclophosphamide is often used as a component of a chemotherapeutic cocktail given as adjunctive therapy preceding bone marrow transplantation for the treatment of RRMS.

The HiCy 1-time regimen used in the current study has been shown to be safe and effective in other autoimmune diseases, including lupus erythematosus, autoimmune aplastic anemia, and myasthenia gravis.

The regimen, which was developed about 15 years ago by Robert Brodsky, MD, and Richard Jones, MD, hematologists at Johns Hopkins, works by eliminating the "misbehaving" immune system while preserving hematopoietic stem cells, allowing the immune system to "recreate itself from scratch." Based on promising results and these other autoimmune conditions, the investigators decided to test it in MS.

Worst of the Worst

Nine patients — 6 men and 3 women — with RRMS were selected for the study. The mean age of the participants was 29 years. Eight subjects had failed conventional therapy and 1 was treatment naive. All had ongoing active inflammatory disease and a high risk for continued progression and loss of function.

"These patients were the worst of the worst in terms of the severity of their disease," said Dr. Kerr.

The primary end point was safety and tolerability of the treatment. Secondary outcome measures included a change in gadolinium-enhancing lesions on magnetic resonance imaging and a change in disability measures on the Expanded Disability Status Scale (EDSS) and the Multiple Sclerosis Functional Composite (MSFC).

At a mean follow-up of 23 months, investigators found an average reduction of 39.4% in disability and an average improvement in MSFC scores of 87%. In addition, the average number of brain lesions decreased, from 6.5 at study outset to 1.2 at follow-up.

Of the 9 study subjects, 5 had no disease activity at follow-up. The other 4, said Dr. Kerr, "did well, but not perfectly, and had some evidence of disease activity, usually demonstrated by a brain lesion and not a clinical attack. Still, it wasn't perfect."

Nevertheless, he said, overall patients experienced a dramatic improvement with this 1-time high-dose therapy that appears to reverse MS-related disability and is unlike any previous MS treatment.

Currently, he said, MS drugs that are available, or even those that are on the horizon, are designed solely to hold the disease at bay and limit disease progression. However, once patients stop taking the medication, the disease continues to advance.

"This treatment is based on a completely different model — a 1-time therapy with a long-term benefit," said Dr. Kerr.

Less Toxicity, Lower Cost

HiCy also offers several advantages over bone marrow transplantation, which has been associated with a 5% to 7% mortality rate and toxicity to a number of organs, including the brain. To date, he said, there has been no mortality or organ toxicity associated with HiCy therapy in the more than 250 patients who have received the treatment for other types of autoimmune disease.

Furthermore, the cost of bone marrow transplantation runs about $300,000 in the first year alone; HiCy therapy costs approximately $25,000 to $30,000.

Although the mechanism is not entirely clear, Dr. Kerr said it was interesting to note that patients with a return of function tended to have a shorter disease duration (less than 10 years) and more active inflammatory disease.

This finding is important, he said, and suggests that inflammation itself plays a role in MS disability and that "once you get rid of that inflammatory cascade within the nervous system, patients start to improve."

Dr. Kerr said his team is currently working on improving the HiCy regimen, possibly by adding drugs that will help "reeducate" the immune system. In addition, he said, the investigators are also planning a multicenter phase 3 trial that will have broader inclusion criteria, enrolling patients with less severe, less aggressive disease.

The study was supported by General Clinical Research Center of the Johns Hopkins School of Medicine, the National Multiple Sclerosis Society, Mr. Alvin Myerberg, and the Johns Hopkins Project RESTORE.

Arch Neuro. Published online before print June 9, 2008.


Caroline Cassels is a Senior Journalist for Medscape Neurology & Neurosurgery. A medical and health journalist for 20 years, Caroline has written extensively for both physician and consumer audiences. She helped launch and was the editor of Health Digest, an award-winning Canadian consumer health publication. She was also national editor of the Heart & Stroke Foundation of Canada's Web site before joining Medscape Neurology & Neurosurgery in 2005. She is the recipient of the 2008 American Academy of Neurology Journalism Fellowship Award. She can be contacted at CCassels@medscape.net.

Medscape Medical News 2008. © 2008 Medscape


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New Data on Disease-modifying Therapies for Multiple Sclerosis

Mark J. Tullman, MD

Introduction

New data from key clinical trials of disease-modifying therapy were presented at the 60th Annual Meeting of the American Academy of Neurology. The results of some of these studies, along with the potential clinical implications of those results, are presented below.

Efficacy of Interferon Beta-1b and Glatiramer Acetate in Patients With Relapsing-Remitting Multiple Sclerosis: The BEYOND Trial

Results of the Betaferon/Betaseron Efficacy Yielding Outcomes of a New Dose (BEYOND) trial, which was funded by Bayer Healthcare Pharmaceuticals, were presented in a late-breaking session by Paul O'Connor, MD.[1] This trial was designed to compare the efficacy of 250 micrograms (mcg) and 500 mcg of interferon beta-1b given subcutaneously (SC) every other day in patients with relapsing-remitting multiple sclerosis (RRMS). The efficacy of these two doses of beta interferon-1b was also compared with glatiramer acetate (20 mg SC administered daily).

The trial randomized treatment-naive patients with RRMS with Expanded Disability Status Scale (EDSS) scores equal to or less than 5. Patients also had to have at least one relapse in the year prior to entry into the study. A total of 2244 patients were randomized in a 2:2:1 ratio to the 500-mcg dose of beta interferon-1b (n = 899), the 250-mcg dose of interferon beta-1b (n = 899) or to the 20-mg dose of glatiramer acetate (n = 448) for a period of 104 weeks or longer. Patients underwent clinical evaluations every 3 months and brain magnetic resonance imaging (MRI) scans annually.

The trial's primary endpoint was relapse risk. A per-protocol analysis and an intent-to-treat analysis were performed on the data. The clinical efficacy of each of the 3 treatment groups (beta interferon-1b 250 mcg, beta interferon-1b 500 mcg, and glatiramer acetate 20 mg) was similar in each of the analyses.

There were several supportive endpoints, including relapse rate, proportion of relapse-free patients, and time to first relapse. Secondary outcome variables were time to confirmed EDSS progression and T1 black hole development. Other endpoints of interest included the number and volume of T2 lesions. The annualized relapse rate fell by nearly 80% compared with the year prior to enrollment in the study, but there were no significant differences among the treatment groups.

There were some MRI endpoints that showed statistically significant differences between the treatment groups. The cumulative number of T2 lesions up to the last scan was significantly higher in the group receiving glatiramer acetate compared with the groups receiving 250 mcg (P = .17) or 500 mcg (P = .001) beta interferon-1b. Additionally, patients receiving 250 mcg or 500 mcg beta interferon-1b had a significantly lower increase in T2-lesion volume compared with the group receiving glatiramer acetate (P < .001 and P = .001, respectively). The authors note that it is unclear whether there is any long-term clinical significance to these findings.

All 3 treatments were generally well-tolerated. Dropout rates for 250 mcg interferon beta-1b, 500 mcg interferon beta-1b, and glatiramer acetate were 13%, 19%, and 17%, respectively. It is important to note that although this was a double-blind study for the interferon beta-1b groups (ie, they were unaware which dose they were receiving), this was not a double-blind trial for the patients who received glatiramer acetate. This may explain the higher dropout rate in the group receiving glatiramer acetate (17%) compared with the group receiving 250 mcg interferon beta-1b (13%) because the patients receiving interferon beta-1b were aware that there was a 50% chance that they could be receiving the higher, and potentially more effective, dose of interferon beta-1b.

The adverse events observed were similar to the known adverse event profiles of these compounds. Flulike symptoms were more common with interferon beta-1b and injection-site reactions (eg, pain, pruritis) were more common with glatiramer acetate.

The Results of the BEYOND trial[1] are similar to the recently presented results from the REGARD trial[2] that compared interferon beta-1a 44 mcg SC 3 times a week to glatiramer acetate. In these 2 studies, more than 2000 patients were randomized to either high-dose interferon or glatiramer acetate. Patients did very well and there were no major differences in terms of efficacy between the therapies. Unfortunately, the 500-mcg dose of interferon beta-1b was no more effective than the 250-mcg dose. In the absence of clear superior efficacy data between the high-dose interferons and glatiramer acetate, it seems to me that a high-dose interferon and glatiramer acetate are both reasonable initial treatment options for most patients with RRMS. Patients should be well informed and part of the treatment decision process. Some patients may prefer starting with a daily injection with fewer side effects and others would rather take a medication that has fewer injections but the potential to cause more side effects and requires periodic blood work.

Furthermore, for patients on a high dose interferon of glatiramer acetate who experience persistent side effects, switching from one agent to the other might improve tolerability and enhance quality of life without sacrificing efficacy.

Efficacy of Glatiramer Acetate in Delaying Conversion to Clinically Definite Multiple Sclerosis: The PreCISe Trial

Results from the Study to Evaluate the Effect of Early Glatiramer Acetate Treatment in Delaying the Conversion to CDMS of Subjects Presenting With a Clinically Isolated Syndrome (CIS) (PreCISe) trial, were presented in a late-breaking session by Giancarlo Comi.[3] The PreCISe trial was a randomized, double-blind, placebo-controlled, multicenter, 3-year study designed to evaluate the efficacy of early treatment with glatiramer acetate in delaying the progression to clinically definite MS (CDMS) in patients with clinically isolated syndromes (CIS), which are considered to be first events suggestive of MS.

The study randomized 481 patients who had a minimum of 2 T2-weighted brain lesions at least 6 mm in diameter shown on MRI and who had experienced a first clinical event to receive glatiramer acetate 20 mg/day SC (n = 243) or placebo (n = 238). Only patients with a unifocal disease manifestation were included. Key baseline characteristics were: age (31.1 ± 6.9 years), time from first event to randomization (74.0 ± 14.9 days), and corticosteroid use for first attack (64% of patients). There was no difference between the study arms in EDSS (1.0 ± 1.0), number (31.5 ± 30.7) and volume (6.0 ± 6.2ml) of T2 weighted lesions, and number (1.5±2.9) and volume (0.3 ± 0.6ml) of gadolinium enhanced lesions.

The primary endpoint of the study was time to CDMS based on a second clinical attack. The trial was stopped prematurely by the data and safety monitoring committee after a preplanned interim analysis. The group initially receiving placebo was then switched to active treatment on an open-label basis. At this point, about 80% of the planned drug exposure had been given, and CDMS had developed in about 43% of those patients in the placebo group compared with just 25% in the glatiramer acetate group. The odds ratio for progression to CDMS was 0.41 (P < .0001) and the hazard ratio for progression to CDMS was 0.55 (95% CI 0.40-0.77; P = .0005) in the group taking glatiramer acetate compared with the placebo group. This translates in to a 45% risk reduction for progression to CDMS in the group on active treatment compared with the group on placebo. Additionally, the 25th percentile time to CDMS was prolonged from 336 days in the placebo group to 722 days (115% increase in time to CDMS onset) in the group receiving glatiramer acetate.

The results of MRI scans also favored the group receiving glatiramer acetate compared with the group receiving placebo. The mean number of new T2-weighted lesions was reduced by 61% in the patients receiving glatiramer acetate compared with the patients receiving placebo (P < .0001). Similarly, patients receiving glatiramer had a 61% reduction in new T1 gadolinium-enhancing lesions compared with the group receiving placebo (P < .0001).

Glatiramer acetate was well tolerated, and side effects were similar to those previously reported in patients with CDMS, including local injection-site reactions and transient postinjection reactions including chest pain, flushing, dyspnea, palpitations, and anxiety.

The open-label extension phase of the study will continue to a 5-year follow-up to evaluate the potential for glatiramer acetate to prevent or delay clinical progression of the disease. Patients will receive glatiramer acetate and will be followed until the development of CDMS.

The PreCISe study results are really not surprising. However, we now have strong evidence that the interferons and glatiramer acetate are effective when initiated after a first MS attack in patients with at least minimally abnormal brain MRI. The 5-year PreCISe data may provide additional evidence that early treatment with MS immunomodulatory therapy prevents the development of disability.

This activity is supported by an independent educational grant from Teva Neuroscience.

Acorda Therapeutics Announces Positive Data from Second Phase 3 Study of Fampridine-SR on Walking Ability in People with Multiple Sclerosis

Company Plans to File New Drug Application (NDA) in First Quarter of 2009

Investor Conference Call and Webcast Today at 8:30 A.M. ET
HAWTHORNE, N.Y.--(BUSINESS WIRE)--June 2, 2008--Acorda Therapeutics, Inc. (NASDAQ: ACOR) today announced positive results from its second Phase 3 clinical trial of Fampridine-SR (MS-F204) on walking ability in people with multiple sclerosis (MS). A significantly greater proportion of people taking Fampridine-SR in the trial had a consistent improvement in walking speed compared to people taking placebo (42.9% vs. 9.3%), as measured by the Timed 25-Foot Walk (p less than 0.001). Consistent improvement in walking speed was the primary endpoint of the study as outlined in the Special Protocol Assessment (SPA) with the U.S. Food and Drug Administration (FDA).

"With the success of this trial, we have achieved a critical milestone for Fampridine-SR. We have now completed two successful Phase 3 trials demonstrating improved walking ability in people with MS," said Ron Cohen, M.D., President and CEO of Acorda Therapeutics. "We believe that, subject to FDA review, the results of our two Phase 3 trials are adequate to support an NDA. We expect to submit this application in the first quarter of 2009 and plan to request priority review."

The study's only prospectively defined secondary outcome measure, leg strength, showed a statistically significant increase in the Fampridine-SR Timed Walk responders compared to placebo (p = 0.028). There was a small improvement in leg strength for Fampridine-SR Timed Walk non-responders compared to placebo that was not statistically significant.

Additional measures in this study were consistent with the results of the first Phase 3 Fampridine-SR trial. The average increase in walking speed over eight weeks of treatment compared to baseline was 24.7 percent for the Fampridine-SR Timed Walk responders compared to 7.7 percent for the placebo group. The 12-Item Walking Scale (MSWS-12), a self-rated assessment of walking disability, was improved in Timed Walk responders compared to non-responders. Also, an increased response rate on the Timed 25-Foot Walk was seen across all four types of MS. The Company intends to present comprehensive data from this trial at an upcoming medical meeting.

"Difficulties with walking are among the most pervasive and debilitating problems faced by people with MS. Walking disability affects their ability to accomplish daily tasks and limits their independence," said Andrew Goodman, M.D., Director of the Multiple Sclerosis Center at the University of Rochester. "Because there are currently no therapies indicated to improve walking impairment in MS, clinicians are limited in their ability to address this aspect of the disease. The results of this study indicate that Fampridine-SR could represent an important new way to treat people with MS."

Study Design

The double-blind, placebo-controlled trial was designed to evaluate the safety and efficacy of Fampridine-SR in improving walking ability in people with MS. The primary endpoint of the study was response on the Timed 25-Foot Walk. A Fampridine-SR Timed Walk responder was defined as a study participant whose walking speed was faster at a majority of the four on-drug visits than any speed measured during the five off-drug visits. The trial, which enrolled 240 individuals at 39 MS centers in the United States and Canada, recruited patients between 18 and 70 years old with a definite diagnosis of MS and some degree of walking disability. Subjects were randomized to treatment with Fampridine-SR (n=120), at a dose of 10mg twice a day, or placebo (n=119), and the study was open to people with all four major types of MS: primary-progressive, secondary-progressive, relapsing-remitting and progressive-relapsing. Participants were permitted to remain on a stable regimen of their current medications, including immunomodulators.

Safety Statement

In this study, adverse events were generally mild to moderate and largely consistent with the safety profile observed in previous studies of Fampridine-SR in people with MS. The most common adverse events reported in the Fampridine-SR treatment group compared to the placebo group included: urinary tract infection (17.5% vs. 8.4%), falls (11.7% vs. 16.8%), insomnia (10.0% vs. 1.7%), headache (9.2% vs. 0.8%), asthenia (8.3% vs. 4.2%), dizziness (8.3% vs. 0.8%), nausea (8.3% vs. 0.8%), back pain (5.8% vs. 2.5%), balance disorder (5.8% vs. 1.7%), upper respiratory tract infection (5.8% vs. 6.7%), arthralgia (5.0% vs. 4.2%), nasopharyngitis (5.0% vs. 4.2%) and paraesthesia (5.0% vs. 1.7%).

There were three serious adverse events (SAEs) that led to discontinuation: two in the placebo group and one in the Fampridine-SR group. In the placebo group, one participant experienced a possible complex partial seizure and another experienced a combination of chest tightness and gastric reflux. Both of these events were judged by investigators, who were blinded at the time, to be possibly related to treatment. In the Fampridine-SR group, one participant had a patellar fracture, which was judged not to be treatment related. In addition, one participant treated with Fampridine-SR experienced an episode of syncope (fainting) one day after completing the treatment phase of the study. This was judged to be possibly related to treatment, but the participant was not discontinued from the trial. Follow-up assessment by the clinical investigators determined that these SAEs resolved completely with no residual effects. No deaths occurred during the study.

As of June 2, 2008, the total exposure in our MS studies to Fampridine-SR at 10mg twice a day, including both double-blind and open-label studies, is approximately 1,100 patient years. The incidence of seizures in these studies at the 10mg dose has been within the rates reported for placebo-treated groups in long-term controlled studies of immunomodulator drugs in MS patients. These rates have ranged up to two percent of patients in a two-year study, or one seizure per 100 patient years. The overall incidence of seizure appears to be dose-related.

About MS

Multiple sclerosis is a chronic, usually progressive disease in which the immune system attacks and degrades the function of nerve fibers in the brain and spinal cord. Over 400,000 Americans have MS, and someone is newly diagnosed with MS every hour in the United States. Most are between the ages of 20 and 50, and women are affected two to three times as much as men. Worldwide, MS may affect 2.5 million individuals.

According to the National Multiple Sclerosis Society (NMSS), the direct costs of medical care for MS patients in the United States exceed $6 billion annually. Additionally, a NMSS analysis estimated the total cost of MS, including medical and non-medical care, production losses, and informal care, at more than $47,000 per U.S. patient per year. Complications from MS may make it harder for people to work and may interfere with their ability to perform common daily activities.

For most people with MS, the disease slowly progresses with a series of unpredictable flare-ups, also called relapses. But for some, the progression of the disease is rapid. Each relapse tends to lead to increasing disabilities such as walking impairment, muscle weakness or speech or vision impairments. Approximately 85 percent of people with MS experience some form of walking impairment. Within 15 years of an MS diagnosis, 50 percent of patients often require assistance walking and, in later stages, up to a third of patients are unable to walk.

About Fampridine-SR

Fampridine-SR is a sustained-release tablet formulation of the investigational drug fampridine (4-aminopyridine or 4-AP). In laboratory studies, fampridine has been found to improve impulse conduction in nerve fibers in which the insulating layer, called myelin, has been damaged. Fampridine-SR is being developed by Acorda Therapeutics and manufactured by Elan Corporation plc.

Fampridine-SR and MS

A nerve cell has one extension, called an axon, which it uses to communicate via electrical signals to other nerve cells. All but the smallest axons have a special covering of a fatty substance called myelin that acts as insulation to preserve and speed these nerve signals, much like the insulating cover of an electrical cord helps preserve the transmission of electricity.

In MS, the myelin becomes damaged and the axon cannot effectively transmit electrical impulses. Specifically, the damaged myelin exposes channels in the membrane of the axon, which allow potassium ions to leak from the axon, dissipating the electrical current. In published studies, fampridine has been shown to block these exposed channels and help the electrical signals to pass through areas of damage.

Conference Call and Audio Webcast

Acorda will hold a conference call and audio webcast today at 8:30 a.m. ET to discuss the top-line results from the trial. To access the call, please dial 866-578-5801(domestic) or 617-213-8058 (international) and provide the access code 57594133. To access the audio webcast, please go to the Investor Relations "Calendar of Events" section of the Acorda website at www.acorda.com, or you may use the link: http://phx.corporate-ir.net/phoenix.zhtml?p=irol-eventDetails&c=194451&eventID=1866966 . (Due to its length, this URL may need to be copied/pasted into your Internet browser's address field. Remove the extra space if one exists.)

A replay of the call will be available from 10:30 a.m. ET on June 2, 2008 until 11:59 p.m. ET on July 2, 2008. To access the replay, please dial 888-286-8010 (domestic) or 617-801-6888 (international), and provide the access code 37448849. An archived version of the webcast will be available for 90 days on the Acorda website in the Investor Relations section.

Patient Information Line

Patients with questions regarding the results of this study or who want to join Acorda's mailing list to be kept informed of future company news may call 877-617-2494, toll-free, weekdays from 10:00 a.m. to 5:00 p.m. ET.

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, has completed two Phase 3 clinical trials to evaluate its safety and efficacy to improve 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 nervous system.

About Elan Drug Technologies

Elan's Drug Technologies group has developed Fampridine-SR tablets using one of its proprietary Oral Controlled Release Technologies, the MXDAS(TM) (MatriX Drug Absorption System) Technology. Elan Drug Technologies (EDT) is an established, profitable and growing specialty pharmaceutical business unit of Elan Corporation plc. For nearly 40 years, EDT has been applying its skills and knowledge to enhance the performance of dozens of drugs that have been marketed worldwide. EDT is focused on using its extensive experience, proprietary drug delivery technologies and licensing capabilities to develop innovative products that deliver clinically meaningful benefits to patients. More information about EDT's broad range of technologies including their Oral Controlled Release and NanoCrystal(R) Technology Platforms, their patent estate and range of services is available at www.elan.com/EDT.

Acorda Therapeutics, Inc. 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 delays in obtaining or failure to obtain FDA approval of Fampridine-SR, the risk of unfavorable results from future studies of Fampridine-SR, Acorda Therapeutics' ability to successfully market and sell Zanaflex Capsules(R), 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.

BIOMS MEDICAL’S RELAPSING-REMITTING MULTIPLE SCLEROSIS TRIAL RECEIVES POSITIVE REVIEW FROM DATA SAFETY MONITORING BOARD

Edmonton, Alberta, May 27, 2008 – BioMS Medical Corp. (TSX: MS), a leading developer in the treatment of multiple sclerosis (MS), today announced that the independent Data Safety Monitoring Board (DSMB) for the Company's phase II MINDSET-01 trial of MBP8298 (dirucotide) in patients with relapsing-remitting MS has completed a safety analysis and recommended that the trial continue as per the protocol.

This was the fourth of several regularly scheduled reviews by the DSMB that will occur over the duration of the trial. The purpose of the DSMB is to provide objective, independent safety monitoring of the trial.

MINDSET-01 Trial
The MINDSET-01 phase II, double-blind, placebo-controlled trial is designed to evaluate the safety and efficacy of MBP8298 (dirucotide) in patients with relapsing-remitting MS. The fifteen month trial is fully enrolled with 218 patients at 24 sites in 6 countries. The objectives of the study are to demonstrate safety and efficacy of MBP8298 (dirucotide) versus placebo as measured by relapse rate, MRI activity and disease progression.


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 (dirucotide), 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. In December 2007, BioMS entered into a licensing and development agreement granting Eli Lilly and Company exclusive worldwide rights to MBP8298 (dirucotide) in exchange for an $87 million upfront payment, milestone payments and escalating royalties on sales. 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

Extavia® approved in European Union for treatment of multiple sclerosis, first in planned portfolio of therapies from Novartis

Extavia is Novartis brand for interferon beta-1b - an established therapy with more than 700,000 patient-years' experience to date[1]

Launch of Extavia for early and relapsing forms of multiple sclerosis (MS) planned for US and Europe in first half of 2009
Novartis committed to MS through extensive research and development programs, including novel oral therapy FTY720 currently in Phase III trials

MS, a devastating disease causing progressive disability, affects an estimated 2.5 million people worldwide, including many young adults[2]

Basel, May 26, 2008 - The European Commission has approved Extavia® (interferon beta-1b) for the treatment of early and relapsing forms of multiple sclerosis (MS) - the first in a new portfolio of medicines from Novartis that is planned to include both established treatments and innovative therapies for patients with MS.

Extavia is the Novartis branded version of interferon beta-1b, a first-line disease-modifying therapy injected every other day for the treatment of MS. Interferon beta-1b has been available globally for more than 13 years and is supported by more than 700,000 patient-years of experience[1].

Formerly known as NVF233, Extavia is the same medicine as Betaferon®/Betaseron®, which is marketed by Bayer-Schering and was the first beta interferon treatment for MS. Novartis gained rights to its own branded version of this medicine in agreements with Bayer-Schering related to the acquisition of Chiron.

"Novartis is committed to MS and to providing effective treatments for patients with this disease," said Trevor Mundel, MD, Head of Global Development Functions at Novartis Pharma AG. "The approval of Extavia means we are able to offer the MS community a current standard of care while preparing for the introduction of innovative therapies such as FTY720."

Novartis also recently filed for approval of interferon beta-1b with the US Food and Drug Administration. Launches in the US and EU are planned for the first half of 2009, in line with an agreement with Bayer-Schering that established the opportunity for Novartis to introduce its own branded version of interferon beta-1b.

By the end of 2009, Novartis also plans to file for approval of the innovative oral therapy FTY720 (fingolimod). Results of an ongoing Phase II study extension presented in April show sustained benefits in patients with relapsing MS after three years of treatment with FTY720. Data showed that 68-73% of patients in the study remained free from relapses after three years' continuous treatment[3].

A number of other compounds for treating MS are also in early stage development by Novartis.

Multiple sclerosis is the most common disorder of the central nervous system in young adults2. It is a progressive and debilitating disorder caused by the destruction of myelin, which helps neurons carry electrical signals in the brain. MS causes problems with muscle control and strength, vision, balance, sensation and cognitive function2. MS typically presents in relapsing forms involving acute self-limiting attacks of neurological dysfunction (or "relapses") followed by complete or partial restoration of functions[4].

In the EU, Extavia is approved for patients with relapsing-remitting MS, the most common form of the disease involving relapses followed by complete or partial restoration of function, and for a steadily worsening form of the disease known as secondary progressive MS with relapses.

In addition, Extavia is approved to treat patients with early MS who:

Have experienced a single episode involving loss of myelin (or "demyelinating event")
Have an active inflammatory process that is severe enough to need treatment with intravenous corticosteroids, if alternative diagnoses have been excluded
Are at high risk of developing clinically definite MS.

Disclaimer
The foregoing release contains forward-looking statements that can be identified by terminology such as "plans", "will", "should" or similar expressions, or by express or implied discussions regarding potential new indications, labeling or regulatory filings or approvals for Extavia® or regarding potential future revenues from Extavia®. Such forward-looking statements reflect the current views of the management regarding future events, and involve known and unknown risks, uncertainties and other factors that may cause actual results with Extavia® to be materially different from any future results, performance or achievements expressed or implied by such statements. There can be no guarantee that Extavia® will be approved for any additional indications or labeling by the European Commission or that Extavia will be approved for any indications in any additional markets. There can also be no guarantee that Extavia® will achieve any particular levels of revenue in the future. In particular, management's expectations regarding Extavia® could be affected by, among other things, introduction of new MS therapies, unexpected regulatory actions or delays or government regulation generally or involving Extavia®, interferon beta-1b; unexpected clinical trial results, including unexpected new clinical data and unexpected additional analysis of existing clinical data; the company's ability to obtain or maintain patent or other proprietary intellectual property protection; competition in general; government, industry and general public pricing pressures, and other risks and factors referred to in Novartis AG's current Form 20-F on file with the US Securities and Exchange Commission. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those anticipated, believed, estimated or expected. Novartis is providing the information in this press release as of this date and does not undertake any obligation to update any forward-looking statements contained in this press release as a result of new information, future events or otherwise.

About Novartis

Novartis AG provides healthcare solutions that address the evolving needs of patients and societies. Focused solely on growth areas in healthcare, Novartis offers a diversified portfolio to best meet these needs: innovative medicines, cost-saving generic pharmaceuticals, preventive vaccines and diagnostic tools, and consumer health products. Novartis is the only company with leading positions in these areas. In 2007, the Group's continuing operations (excluding divestments in 2007) achieved net sales of USD 38.1 billion and net income of USD 6.5 billion. Approximately USD 6.4 billion was invested in R&D activities throughout the Group. Headquartered in Basel, Switzerland, Novartis Group companies employ approximately 98,000 full-time associates and operate in over 140 countries around the world. For more information, please visit http://www.novartis.com.

References
[1] Data on file. Wayne, NJ: Bayer HealthCare Pharmaceuticals Inc; 2007.
[2] Multiple Sclerosis International Federation at www.msif.org Accessed 15 May 2008.
[3] Comi G et al. Oral FTY720 (fingolimod) in patients with relapsing multiple sclerosis. 3-year extension shows sustained low relapse rate and MRI activity. Abstract presented at 60th annual meeting of American Academy of Neurology, Chicago, 12-19 April 2008.
[4] National Multiple Sclerosis Society at www.nationalmssociety.org, Accessed 15 May 2008.
# # #

Novartis Media Relations

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Novartis Global Media Relations
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Novartis Pharma Communications
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e-mail: media.relations@novartis.com
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Pediatric MS Affects Thinking, Memory

Researchers Say Multiple Sclerosis in Childhood Is Linked to Lower IQ Scores
By Kelli Miller Stacy

WebMD Medical News Reviewed by Louise Chang, MD

May 12, 2008 -- Multiple sclerosis (MS) that strikes during childhood may disrupt a key phase of brain development and appears to have a profound negative impact on a child's ability to think and pay attention.

Scientists reporting in the May 12 issue of Neurology say that the earlier MS develops, the more likely a child will have a lower IQ score.

MS is a central nervous system disease that attacks myelin, the material that covers and protects nerve fibers. The damage gets worse over time and leads to symptoms such as numbness, tingling, fatigue, loss of vision, and in severe cases, paralysis.

It most commonly develops in adults after age 20. However, pediatric MS affects about 8,000-10,000 people under age 18 in the U.S., according to the National Multiple Sclerosis Society.

Researchers theorize that pediatric MS strikes at a time when the part of the brain involved in cognition is maturing. Previous uncontrolled studies have shown a link between cognitive impairment and MS. However, information about the neuropsychological effects of MS in children and teenagers has been limited.

"It's possible that MS can show an even more dramatic effect on the thinking skills and intelligence in children than in adults, since the disease might affect the brain at a time when it is still developing," researcher Maria Pia Amato, MD, of the University of Florence in Italy, states in a news release.

Amato gave an array of intelligence tests to 63 children with MS and compared their scores to 57 healthy children of similar ages. The tests were designed to measure overall intelligence, memory, language ability, and other thinking skills.

The tests showed that the children with MS were more likely to have low intelligence scores and problems with memory, attention, and other thinking skills. Thirty-one percent of the children with MS met the criteria for significant cognitive impairment, meaning they failed at least three of the tests. Fifty-three percent of the children with MS failed at least two of the tests.

Amato's team noted language difficulties in about 30% of the children with MS. Language problems are uncommon in adults with the disease.

"Since the disease occurs during a critical phase for language development, children may be particularly vulnerable to language problems," Amato states. "Even subtle language difficulties are likely to have important functional consequences. Therefore ... assessment of language function in pediatric MS deserves particular attention in future studies," she writes in the journal article.

© 2008 WebMD, LLC. All rights reserved.

Gender influences MS’ effect on brain

By LOIS BAKER
Contributing Editor

A new multiple sclerosis study conducted by UB neurologists has shown that in addition to affecting women two-to-three times more than men, multiple sclerosis (MS) damages different regions of the brain in men and women.

The differences were defined by analyzing brain scans of 795 MS patients and 101 healthy controls using conventional magnetic resonance imaging (MRI) techniques, plus more advanced nonconventional MRI techniques, such as diffusion weighted imaging and magnetization transfer imaging.

Results of the study were presented recently at the annual meeting of the American Academy of Neurology.

The research showed that MS in women results in more atrophy of the brain’s white matter, the network of nerves that transport messages to the various brain regions, while the condition in men appears to cause more atrophy in the brain’s gray matter, the regions where messages are received and interpreted.

Ronald Antulov is first author on the study. He conducted the research while a neuroimaging fellow at the Buffalo Neuroimaging Analysis Center (BNAC), part of the Jacobs Neurological Institute, which is the Department of Neurology in the School of Medicine and Biomedical Sciences.

Antulov and colleagues examined consecutively 620 female and 175 male MS patients who were seen at the institute and compared scans with those of the healthy controls. All were assessed using conventional and nonconventional MRI measures.

“We found that atrophy of gray matter and central brain regions was more advanced in men, while atrophy of white matter was more advanced in women,” said Antulov. The phenomenon was not observed in healthy controls.

“We think these changes are influenced by a decrease in sex hormones,” Antulov said. “A recent study showing that male MS patients receiving testosterone treatment showed a lower rate of brain volume decline supports this concept. This finding also suggests that higher levels of estrogen may protect women against more severe MS-related brain damage.”

The BNAC is applying for grants to extend this research.

Contributing to the study, all from the BNAC-JNI, were Bianca Weinstock-Guttman, Jennifer Cox, Sara Hussein, Jackie Durfee, Michael Dwyer, Niels Bergsland, Nadir Abdelrahman, Milena Stosic, David Hojnacki, Frederick E. Munschauer and Robert Zivadinov.

The study was conducted in collaboration with the University of Rijeka, Croatia. Vladimir Miletic of that university also contributed to the research.

Fluoxetine (Prozac) Temporarily Slows MS Progression

By John Gever, Staff Writer, MedPage Today
Published: May 01, 2008

Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston.

GRONINGEN, The Netherlands, May 1 -- The antidepressant drug fluoxetine (Prozac) curbed progression of relapsing-remitting multiple sclerosis in a small placebo-controlled study, but the effect lasted only a few months, researchers here said.

After 16 weeks of double-blind treatment, patients taking 20 mg/day of fluoxetine showed significantly fewer new lesions in MRI scans compared with patients receiving placebo, reported Jop P. Mostert, M.D., of the University of Groningen, and colleagues, online in the Journal of Neurology, Neurosurgery, and Psychiatry.

Twelve of 19 fluoxetine-treated patients had no new gadolinium-enhancing lesions at the 16-week evaluation, compared with five of 19 in the placebo group (P=0.02), they said.

However, the treatment phase lasted 24 weeks, and most measures of disease activity showed no significant differences between the fluoxetine and placebo groups at the study's final evaluation.

Still, the researchers wrote, "the results of our exploratory trial are sufficiently encouraging to justify further studies with fluoxetine in patients with multiple sclerosis."

They recommended that future trials use a higher fluoxetine dose combined with immunomodulating drugs.

The study was prompted by in vitro research and animal experiments suggesting that fluoxetine can modulate the activity of astrocytes, a class of immune cells in the brain, working to elevate cAMP signaling in these cells.

Astrocytes are involved in antigen-presentation and are thought to play a role in multiple sclerosis. They also carry serotonin receptors and reuptake sites, suggesting that serotonin reuptake inhibitors such as fluoxetine could reduce their activity.

Dr. Mostert and colleagues recruited 40 patients with established relapsing-remitting or relapsing secondary progressive multiple sclerosis who did not have a depression diagnosis. The mean time from first MS symptoms was 11 years.

Patients had no contraindications for repeated MRI scans or recent history of corticosteroids or immunomodulating drug therapy.

Participants were evaluated clinically and with MRI scans at baseline and at treatment weeks 4, 8, 16, and 24. One patient in each group discontinued prematurely, leaving 19 in each group for efficacy analysis.

At week 16, the mean cumulative number of new gadolinium-enhancing lesions -- the study's primary endpoint -- was 1.21 among fluoxetine-treated patients and 3.16 in the placebo group (P=0.05).

In addition to the larger number of patients showing no new lesions at 16 weeks, fluoxetine treatment was also associated with a smaller number of total scans showing new lesions (24% versus 47%, P=0.03).

Impressive-seeming numerical differences between groups remained at week 24, but the statistical significance largely vanished.

For example, the mean number of new enhancing lesions at week 24 was 1.84 in the fluoxetine group and 5.16 in the placebo group (P=0.15).

In the fluoxetine group, 32% of patients showed no new enhancing lesions at week 24, versus 21% of the placebo group (P=0.71).

Mean cumulative volume of new lesions at week 24 was 124 mm3 in the fluoxetine patients and 398 mm3 in the placebo group (P=0.16).

The only significant difference at week 24 was in the number of scans showing new lesions (25% in the fluoxetine group, 41% of the placebo group, P=0.04).

The number of patients having exacerbations and the total number of exacerbations did not differ noticeably between the fluoxetine and placebo groups.

Significantly more patients in the fluoxetine group reported nausea (65% versus 30% in the placebo group, P=0.03).

Other adverse effects did not differ significantly between groups, although 55% of fluoxetine patients reported drowsiness compared with 30% of those taking placebo.

The researchers noted that their small sample size limited the study's ability to detect significant treatment effects.

Nevertheless, they concluded, the results support their hypothesis about the role of cAMP signaling in astrocytes and its effect on inflammatory activity in multiple sclerosis.

The researchers added that fluoxetine may have other beneficial effects relevant to multiple sclerosis. For example, other studies have suggested it may help ward off axonal loss by stimulating release of neurotrophic factors.

The study was supported by Multiple Sclerosis anders [sic]. The researchers declared no potential conflicts of interest.

Primary source: Journal of Neurology, Neurosurgery and Psychiatry

Source reference:
Mostert J, et al "Effects of fluoxetine on disease activity in relapsing multiple sclerosis: A double-blind, placebo-controlled, exploratory study" Journal of Neurology, Neurosurgery, and Psychiatry 2008; DOI: 10.1136/jnnp.2007.139345

Merck Serono Announces Initiation of Phase II Clinical Trial of Atacicept in Relapsing Multiple Sclerosis

Geneva, Switzerland, April 30, 2008 – Merck Serono, a division of Merck KGaA, Darmstadt, Germany, and its partner ZymoGenetics, Inc. (NASDAQ: ZGEN) today announced the initiation of a Phase II clinical trial to evaluate the safety and efficacy of atacicept in patients with relapsing multiple sclerosis (RMS).

“This trial with atacicept underlines Merck Serono’s long-term commitment to patients with multiple sclerosis,” said Dr. Anton Hoos, Head of Global Development at Merck Serono. “Atacicept has the potential to complement existing MS drugs by offering a novel mode of action and convenient administration.”

“Patients with multiple sclerosis need more treatment options,” said Nicole Onetto, M.D., Senior Vice President and Chief Medical Officer of ZymoGenetics. “Our preclinical models have shown biological activity of atacicept in multiple sclerosis and, because of the growing body of supporting data in the literature indicating the importance of B cells and antibodies in the pathology of multiple sclerosis, we believe there is strong rationale for the clinical testing of atacicept in patients with RMS.”
The four-arm randomized, double-blind, placebo-controlled, multicenter study will evaluate the safety and efficacy of atacicept in patients with RMS over 36 weeks of treatment. The primary objective of the study is to evaluate the efficacy of atacicept in reducing central nervous system inflammation in subjects with RMS as assessed by frequent MRI measures.

Approximately 300 RMS patients meeting the eligibility criteria will be randomly assigned to receive one of three subcutaneous doses of atacicept or placebo for 36 weeks. Patients will be followed up until week 48.

About atacicept

Merck Serono and ZymoGenetics are developing atacicept (formerly referred to as TACI-Ig) as a potential treatment of autoimmune diseases, such as systemic lupus erythematosus (SLE), lupus nephritis (LN), rheumatoid arthritis and multiple sclerosis, as well as B-cell malignancies.

Atacicept contains the soluble TACI receptor that binds to the cytokines BLyS and APRIL. These cytokines are members of the tumor necrosis factor family that promote B-cell survival and autoantibody production associated with certain autoimmune diseases such as systemic lupus erythematosus. Current data indicates that levels of BLyS and APRIL are elevated in patients with rheumatoid arthritis, lupus erythematosus, B-cell malignancies and multiple sclerosis. Atacicept has been shown to affect several stages of B-cell development and may inhibit the survival of cells responsible for making antibodies.

About Merck Serono and multiple sclerosis

Merck Serono is a leader in multiple sclerosis (MS) with Rebif® (interferon beta-1a), a disease-modifying drug used to treat relapsing forms of MS, which is registered in more than 80 countries worldwide. In addition to Rebif®, the Company also offers a second therapy within its US portfolio of MS therapies: Novantrone® (mitoxantrone for injection concentrate) for worsening forms of MS. Full prescribing information for these products can be obtained by contacting the Company or visiting its website. Additional therapeutic options are currently under development at Merck Serono, including oral cladribine, currently in Phase III and potentially the first oral therapy for MS, as well as several products in early stage development. Merck Serono also is taking a leading role in developing an understanding of the role of genetics in MS.

About multiple sclerosis

Multiple sclerosis (MS) is a chronic, inflammatory condition of the nervous system and is the most common, non-traumatic, neurological disease in young adults. The World Health Organization estimates that up to 2.5 million people suffer from MS worldwide. While symptoms can vary, the most common symptoms of MS include blurred vision, numbness or tingling in the limbs and problems with strength and coordination. The relapsing forms of MS are the most common.

About Merck Serono
Merck Serono is the division for innovative prescription pharmaceuticals of Merck, a global pharmaceutical and chemical group. Headquartered in Geneva, Switzerland, Merck Serono discovers, develops, manufactures and markets innovative small molecules and biopharmaceuticals to help patients with unmet medical needs. Its North American business operates in the United States and Canada as EMD Serono.

Merck Serono has leading brands serving patients with cancer (Erbitux®), multiple sclerosis (Rebif®), infertility (Gonal-f®), endocrine and cardiometabolic disorders (Glucophage®, Concor®, Saizen®, Serostim®), as well as psoriasis (Raptiva®).
With an annual R&D investment of around € 1bn, Merck Serono is committed to growing its business in specialist-focused therapeutic areas including neurodegenerative diseases, oncology, fertility and endocrinology, as well as new areas potentially arising out of research and development in autoimmune and inflammatory diseases.

About Merck

Merck is a global pharmaceutical and chemical company with total revenues of EUR 7.1 billion in 2007, a history that began in 1668, and a future shaped by 31,681 employees in 60 countries. Its success is characterized by innovations from entrepreneurial employees. Merck's operating activities come under the umbrella of Merck KGaA, in which the Merck family holds an approximately 70% interest and free shareholders own the remaining approximately 30%. In 1917 the U.S. subsidiary Merck & Co. was expropriated and has been an independent company ever since.

For more information, please visit www.merckserono.net or www.merck.de

SLU Researchers to Test New Oral Medication for Multiple Sclerosis

Apr 29, 2008 - 4:38:53 PM


(HealthNewsDigest.com) - ST. LOUIS – Researchers at Saint Louis University are preparing to test an investigational pill to treat relapsing-remitting multiple sclerosis, the most common form of the potentially disabling neurological disease.

There are currently no oral medications approved to treat MS, which affects some 400,000 people in the United States (with approximately 10,000 new cases diagnosed each year). There are various medications to slow or modify the progression of the disease, but all must be injected into the skin, muscle or veins, making the search for an oral medication a top priority.

SLU will be one of several dozen sites around the world where researchers will study how patients with relapsing-remitting MS respond to the experimental drug laquinimod, which is taken in tablet form once a day. About 1,000 patients will be enrolled worldwide.

MS is a disease in which the body’s immune system attacks the protective coating – called myelin – surrounding the nerves within the central nervous system, as well as the nerve fibers themselves. Symptoms can vary widely from person to person, but they generally include fatigue, muscle weakness, numbness, impaired mobility, balance and cognition and vision disturbances.

About 85 percent of people newly diagnosed with the disease have relapsing-remitting MS. This form of the disease is characterized by periodic attacks or flare-ups (relapses), followed by months or even years of little to no signs of the disease (remission).

“Laquinimod seems to modulate how the immune system works,” said Florian P. Thomas, M.D., Ph.D., professor of neurology at the Saint Louis University School of Medicine and the study’s principal investigator. “In smaller, earlier trials, the drug reduced the likelihood of relapses in patients, as well as the number of MS lesions seen on MRI tests.”

In the randomized, double-blind study – the largest such investigation of the drug to date – half the volunteers will receive laquinimod while the remainder will be given a placebo.

They’ll remain in the trial for up to 30 months, during which time researchers will periodically assess how their disease develops. At various visits throughout the trial, patients will be given complete physical and neurological examinations, as well as an MRI scan to determine the extent of scarring on the brain – a defining characteristic of multiple sclerosis.

For the study, SLU researchers are looking for patients with relapsing-remitting MS between the ages of 18 and 55. Among other criteria, patients must not have taken any immuno-suppressive drugs within the last six months. Women must not be pregnant or breast feeding, and those of child-bearing age must be on at least two forms of birth control.

People wanting more information or to find out whether they qualify to participate in the study should call 314-977-4900.

Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first medical degree west of the Mississippi River. The school educates physicians and biomedical scientists, conducts medical research, and provides health care on a local, national and international level. Research at the school seeks new cures and treatments in five key areas: cancer, liver disease, heart/lung disease, aging and brain disease, and infectious disease.

www.HealthNewsDigest.com

© Copyright by HealthNewsDigest.com

MorphoSys Announces Completion of First Dosing in Phase 1 Trial for MOR103 Program

04/28/2008 at 07:30 AM

MorphoSys AG (FSE: MOR; Prime Standard Segment, TecDAX) today announced the completion of a first dosing regimen in a phase 1 clinical study on healthy volunteers of the HuCAL-derived antibody MOR103 with no adverse events reported. Six healthy volunteers in the first dosing group have been enrolled and received MOR103 injections, while three volunteers received placebo. The safety review of the medical data from the lowest dosing group yielded a determination that it was safe to proceed with the second dosing group. The randomized, double-blind, placebo-controlled, single-ascending dose trial will be conducted in approx. 50 healthy volunteers and is being conducted in a Clinical Pharmacology Unit (CPU) in Utrecht, the Netherlands. The trial is scheduled to be finalized in 2008 and final reporting is expected in Q1 2009.

The Company's lead development program, MOR103, is a fully human HuCAL antibody directed against GM-CSF (granulocyte macrophage-colony stimulating factor), being developed in the area of inflammatory diseases, such as rheumatoid arthritis, where current treatment options are inadequate. Due to its diverse functions in the immune system, GM-CSF can be considered a target for a broad spectrum of anti-inflammatory therapies. MorphoSys had submitted the clinical trial application in December 2007 and received the approval by the Dutch authorities six weeks later. The study will evaluate the safety and tolerability as well as pharmacokinetics of escalating doses of MOR103.

"We are very pleased to see our first proprietary drug candidate progress according to plan," commented Dr. Marlies Sproll, Chief Scientific Officer of MorphoSys AG. "Antibodies that neutralize GM-CSF could represent a new generation of medicines that reduce inflammation with greater beneficial effects."

For further information please contact: Dr. Claudia Gutjahr-Löser, Head of Corporate Communications & Investor Relations, Tel: +49 (0) 89 / 899 27-122, gutjahr-loeser@morphosys.com or Mario Brkulj, Manager Corporate Communications & Investor Relations, Tel: +49 (0) 89 / 899 27-454, brkulj@morphosys.com

About MorphoSys:
MorphoSys is a publicly traded biotechnology company focused on the generation of fully human antibodies as a means to discover and develop innovative antibody-based drugs against life-threatening diseases. MorphoSys's goal is to establish HuCAL as the technology of choice for antibody generation in research, diagnostics and therapeutic applications. The Company currently has therapeutic and research alliances with the majority of the world largest pharmaceutical companies including Boehringer Ingelheim, Centocor/Johnson & Johnson, Novartis, Pfizer and Roche. Within these partnerships, more than 50 therapeutic antibody programs are ongoing in which MorphoSys participates through exclusive license and milestones payments as well as royalties on any end products. Additionally, MorphoSys is active in the antibody research market through its AbD Serotec business unit. The business unit has operations in Germany (Munich), the U.S. (Raleigh, NC) and U.K. (Oxford). For further information please visit http://www.morphosys.com/


About MOR103 to treat RA:
Rheumatoid arthritis (RA) is traditionally considered a chronic, inflammatory autoimmune disorder that causes the immune system to attack the joints and affects in particular a membrane, called synovium, which lines each movable joint. It is a disabling and painful inflammatory condition, which can lead to substantial loss of mobility due to pain and joint destruction. As a systemic disease, RA often affects extra-articular tissues throughout the body including the skin, blood vessels, heart, lungs, and muscles. The disease affects approximately 4-6 million people worldwide. In patients suffering from RA, white blood cells move from the bloodstream into the synovium. Here, these blood cells appear to play an important role in causing the synovial membrane to become inflamed. The HuCAL-based antibody MOR103 targets GM-CSF as a means to treat inflammatory diseases such as psoriasis, multiple sclerosis (MS), chronic obstructive pulmonary disease (COPD), asthma, and especially RA. The granulocyte macrophage colony-stimulating factor (GM-CSF) stimulates stem cells to produce granulocytes and macrophages, and subsequently activates these differentiated immune cells. GM-CSF is part of the natural immune and inflammatory cascade but has also been identified as an inflammatory mediator in autoimmune disorders like RA leading to an increased production of pro-inflammatory cytokines, chemokines and proteases and thereby ultimately to articular destruction. By neutralizing GM-CSF the HuCAL-based antibody MOR103 reduces undesired proliferation and activation of inflammatory granulocytes and macrophages and intervenes in several pathophysiological pathways. More information and picture material is available at: http://www.morphosys.com/en/mor103


HuCAL® and HuCAL GOLD® are registered trademarks of MorphoSys AG


This communication contains certain forward-looking statements concerning the MorphoSys group of companies. The forward-looking statements contained herein represent the judgment of MorphoSys as of the date of this release and involve risks and uncertainties. Should actual conditions differ from the Company's assumptions, actual results and actions may differ from those anticipated. MorphoSys does not intend to update any of these forward-looking statements as far as the wording of the relevant press release is concerned.

Minor injuries unlikely to trigger disease: judge

No strong evidence traumas like whiplash cause multiple sclerosis, B.C. Supreme Court rules

Ian Mulgrew
Vancouver Sun

Saturday, April 26, 2008

A decade-long, $3-million lawsuit about whether a minor injury can trigger or exacerbate the onset of multiple sclerosis has collapsed after the B.C. Supreme Court ruled the underlying theory is likely bogus.

After hearing from the world's foremost neurological authorities, Justice Austin Cullen concluded in a recent pretrial ruling that medical consensus no longer considers trauma to be a potential catalyst of the disease linked to the body's auto-immune system.

The lengthy and complicated decision abruptly ended this specific suit, involving the Insurance Corporation of B.C., but it also may halt lots of other outstanding litigation launched across the continent on similar grounds -- the now-debunked hypothesis put forward by renowned researcher Dr. Charles M. Poser.

From the Harvard Medical School and a senior neurologist with the Beth Israel Deaconess Medical Centre, Poser has been a leading figure in multiple sclerosis research for decades. He is broadly published and highly respected.

Yet in the legal community, many blame him for creating a "courtroom problem driven by medical hogwash."

Justice Cullen came down on their side. He pummeled the octogenarian doctor for giving at times contradictory evidence, misinterpreting medical studies and slanting his testimony.

"Dr. Poser, who was the primary witness for the plaintiff, testified as an advocate for a theory that once had currency but has since been eroded by the advance of scientific studies and knowledge," the justice wrote.

"I found in his evidence a tendency to overstate the implications of studies that he relied on, and to be unduly dismissive of those that undermined his theory. While he has clearly achieved the status of a foremost expert in his field of neurology, I find that his commitment to his own theory of causation has to some extent impaired his objectivity and reliability as an expert witness."

Kirsten Mehl, lawyer for the winning side, was ecstatic: "I don't think he'll come back to our jurisdiction -- we got him!"

She blamed Poser's pet hypothesis for having set off a brush fire of litigation around the globe. At one point, U.S. court activity spurred the American Academy of Neurology to appoint a panel of specialists in an attempt to douse the conflagration and the National MS Society in 2003 was forced to weigh in, too.

"This theory only had a life in the courtroom," Mehl insisted. "He created the theory and gave evidence all over the world. That's why a lot of claims were brought and settlements were made."

It was cheaper for insurance companies to settle than go to court and risk that a judge would consider the medical evidence but still back an injured individual also suffering the debilitating effects of MS. That will change.

Besides listening to international authorities, Cullen reviewed more than 100 reports, studies and medical articles. His conclusion should put an end to litigation based on the belief minor trauma can exacerbate MS.

Lawyers in this case say dispelling Poser's opinion and aura was difficult and expensive.

That is in part because he was doing exactly what scientists are supposed to do -- posit a theory and examine the evidence. And, as you might expect, he enthusiastically and passionately defended his ideas.

But what is useful in one profession can disrupt another.

Poser's curiosity and conjecture were fine in the lab; in the courtroom, his research and analysis muddied the waters of liability by raising the rare possibility of causation. Cullen clarified the issue.

"This is the first case in Canada to really go into this situation in depth," said Robert Hartshorne, a lawyer for the defence. "It is the first North American case which analyses what has occurred here medically and it should put an end to these suits. You couldn't afford to do this every time this allegation came up. We brought in experts from the U.S., England, around the globe."

Opposing counsel Ronald Nairne agreed: "ICBC drew a line in the sand and threw everything at this. And they did very, very well. There were a number of cases like this out there and they won't proceed now."

This case has its roots in a minor fender-bender at the entrance to the SkyTrain parking lot on 10th Avenue on May 22, 1998. Both cars were only slightly damaged and were driven from the scene.

Later, driver Harris Taylor reported that as a result of the bump, she had strained the muscles in her right arm, suffered a twinge in her lower mid-back, and experienced a bit of agitation in her right shoulder. She had a history of lower-back problems.

On Sept. 8, 1998, she was diagnosed with MS at Vancouver General Hospital. The advanced stage of the disease supported the conclusion that it had been latent for some years before the accident. Nevertheless, at that time, there was a noisy debate over the controversial theory first proposed by Poser in the 1980s -- that minor trauma, whiplash or seemingly insignificant head injuries could bring on or exacerbate MS.

Back then, there was contemporaneous litigation under way in Australia, the U.S. and the U.K.

Nairne said a B.C. colleague had successfully handled a similar case here in 1995 that was settled out of court. It was thought Taylor had a similar claim that could be successfully pursued. She sued the owners of the other car -- Linda and Timothy Liong -- for more than $3 million in damages, most of which was associated with the MS claim.

At issue was whether, on a balance of probabilities, trauma could alter the natural course of the multiple sclerosis, and the lawsuit was fought as a "test case."

To answer the question, Justice Cullen embarked on a lengthy voir dire -- a trial within a trial --to determine the admissibility of expert evidence about the possible causal connection between trauma, including mild head trauma or whiplash injury, and the onset of symptomatic MS. He chose to hear specialists from both sides.

Surprisingly, Cullen was guided in his reasoning by a legal decision made in Scotland about the time this well-aged action was launched.

In that 1998 ruling on a similar suit, judge Lord Rodger concluded: "I do not find it proved, on a balance of probabilities, that trauma in general, or whiplash injury in particular, can trigger the onset of symptomatic MS . . . . I am not satisfied that whiplash injury can ever cause the onset of symptomatic MS."

Though it didn't bind him, Cullen found the reckoning behind the ruling "compelling by its lucid, careful and thorough analysis and conclusion. The fact that since that decision was pronounced (but not because of it) the relevant scientific community can be seen as coalescing around the scientific proposition that no causal relationship exists between trauma and MS symptoms in light of additional studies and discoveries, can only lend weight to the guidance implicit in Lord Rodger's extensive judgment."

Referring to study after study, Cullen averred: "All represent an erosion of support for the theory of a causal link between trauma and MS symptom onset within the medical world."

The idea that trauma could trigger the onset or exacerbation of MS symptoms is not a novel theory in the sense of being new. Researchers since at least the 1930s had suggested a link between an injury and the disease. Poser, however, had become its primary advocate -- the last man standing, if you will.

In 1999, the therapeutics and technology assessment sub-committee of the American Academy of Neurology published a "special article" written by a blue-ribbon panel that included Dr. William Sibley of the University of Arizona, Dr. George Ebers of the University of Western Ontario and Dr. Douglas Goodin, director of the MS Center at the University of California, San Francisco Medical Center. All of them testified before Justice Cullen.

Dr. Goodin said that the subcommittee was formed to conduct an assessment of the association between trauma and MS onset or exacerbation in response to a person who "felt that this [issue] was being misused in the courtroom."

Subsequently, in 2003, the National MS Society published its position referencing the AAN article and two separate epidemiological studies:

"Both studies showed that there are more traumatic events among people with MS than in the healthy control group. Many traumas were caused by MS symptoms such as incoordination, impaired balance, or abnormalities with gait or vision. These events, however, were not precipitating factors in the onset or exacerbation of the disease."

Recent medical texts also reflect that view: a complete reading of the literature provides no direct evidence in support of the hypothesis that trauma influences the expression or natural history of multiple sclerosis. Justice Cullen found the consensus compelling:

"I find that the likelihood of a causal connection between trauma and MS exacerbation is significantly less than that of a coincidental connection, in light of all the evidence adduced, and the opinion of a substantial majority of the scientific community. I thus conclude that even on a robust and pragmatic view of the evidence, it does not support proof of a causal connection between mild trauma, including whiplash, and MS exacerbation, on a balance of probabilities."

Which might put an end to the controversy in the courtroom, but it should do nothing to deaden the curiosity and enthusiasm of medical researchers -- no matter how esoteric or eccentric.

imulgrew@png.canwest.com




WHAT IS MULTIPLE SCLEROSIS?

B.C. Supreme Court Justice Austin Cullin provided the following sketch in his judgment of multiple sclerosis and its effects:

Multiple sclerosis is believed to be an autoimmune disease and that in North America, about one out of 1,000 people will be diagnosed with the affliction.

Another one in 1,000 will go undiagnosed despite having the condition.

Women were historically at double the risk of men.

Surprisingly and somewhat alarmingly, that ratio has changed dramatically (by an increase in incidence among women, rather than a decrease among men) in the past 50 years.

This strongly suggests environmental factors at play.

MS is characterized by the appearance of patches of inflammation associated with demyelination (loss of fatty insulation of nerve fibres) in the white matter of the brain, brain stem, optic nerve and spinal cord.

These patches, also called plaques or simply lesions, often occur in crops and they cause the common symptoms -- visual loss, double vision, numbness and/or weakness of the limbs.

The advent of magnetic resonance imaging (MRI) in about 1985 greatly aided researchers.

There is believed to be a strong genetic influence on the development of MS as studies have shown a relatively high correlation among family members.

Though environmental factors are also believed to be involved, they are as yet largely unidentified.

As to the triggers of the disease, epidemiological studies implicate viral infections as potential triggers in roughly 25 per cent of the cases.

There is no general acceptance of what other triggers may be responsible for the remaining 75 per cent of MS onset or exacerbation.

© The Vancouver Sun 2008

Accelerated Cure Project for Multiple Sclerosis is One Thousand Steps Closer to a Cure for MS

Nonprofit has collected 1,000 blood and data samples from MS sufferers and controls across the U.S.; Samples will be used in dozens of individual research studies this year


WALTHAM, Mass., April 23 /PRNewswire-USNewswire/ -- Accelerated Cure Project for Multiple Sclerosis, a national nonprofit organization, today announced that they have completed their initial drive to collect one thousand blood and data samples to build the largest openly accessible, multi-disciplinary repository ever assembled for use in Multiple Sclerosis (MS) research.

"This is a major milestone for the Accelerated Cure Project", says Art Mellor, founder of the Accelerated Cure Project. "Limited sample size is one of the most frequently cited reasons for inconclusive results in MS research. Our repository provides researchers with immediate access to a far greater number of samples than most scientists could collect themselves."

In addition, the repository will provide a common population of samples useful for a wide variety of different studies, which will enable results from different research perspectives to be easily combined and correlated. The repository contains various types of samples and data that can support scientists working in many fields - genetics, nutrition, virology, and more. Researchers gaining access to the repository must return their results to the database to be shared with other researchers; this will allow cross-correlation of their results with all other studies performed using the same samples.

Subjects enrolled in the repository will be followed over time to allow new samples to be taken and to record important changes in clinical status. Studying the same sample population over time, and pooling knowledge in a central database, is a major step toward understanding what causes MS, thereby accelerating a cure.

Additionally, samples and data are collected from a number of other similar diseases including Transverse Myelitis, Neuromyelitis Optica, ADEM, and Optic Neuritis to enable studies in these rare neurological disorders and to provide controls for MS studies.

Collection Sites

Contributing to the success of the project is an impressive list of research centers across the country that have joined Accelerated Cure Project as collection sites for the repository. These include Johns Hopkins Medical Center (Baltimore, MD), University of Massachusetts Memorial Medical Center (Worcester, MA), University of Texas Southwestern (Dallas, TX), Multiple Sclerosis Research Center of New York (New York, NY), Barrow Neurological Institute (Phoenix, AZ) and the Shepherd Center (Atlanta, GA).

The Accelerated Cure Project intends to continue collecting samples from as many as 10,000 subjects for its MS Repository. If you have MS (or another demyelinating disease) or are related to someone with MS and would like to participate in the project, please call 781/487-0008, visit acceleratedcure.org/repository, or send an email to info-web1207@acceleratedcure.org.

About Accelerated Cure Project

Accelerated Cure Project for Multiple Sclerosis, http://www.acceleratedcure.org, is a national nonprofit organization dedicated to curing Multiple Sclerosis (MS) by determining its causes. Accelerated Cure Project believes this effort can be accelerated by organizing the research process and encouraging collaboration between research organizations and clinicians. A "Cure Map" is currently being developed by the Accelerated Cure Project to establish what is known and what is not known about the causes of MS. From the Cure Map, Accelerated Cure Project will facilitate research most likely to reveal the causes of MS in the shortest time through a large-scale, multidisciplinary, MS Repository. For more information about the Accelerated Cure Project or to make a corporate or individual donation, call 781/487-0008, visit acceleratedcure.org, or send an email to info-web1207@acceleratedcure.org.

About Multiple Sclerosis

Multiple Sclerosis is a chronic demyelinating disorder of the central nervous system that often results in severe disability including the inability to walk, blindness, cognitive dysfunction, extreme fatigue and other serious symptoms. MS affects over 400,000 people in the US and 2 million individuals worldwide. The disorder occurs twice as often in women as in men. The cause is not known and there is no known cure.



SOURCE Accelerated Cure Project for Multiple Sclerosis

Stem-cell treatment could reverse multiple sclerosis effects ‘within 15 years’

The effects of multiple sclerosis could be reversed with stem-cell treatment within 15 years, a leading expert on the disease said today.

Professor Charles ffrench-Constant, the director of a groundbreaking MS research centre in Edinburgh, said the treatment could be used to help patients suffering from the condition that weakens their body's central nervous system.

He said stem cells could be used to help repair nerve damage caused by MS. Currently, only medicines can help reduce the inflammation that causes MS.

Prof ffrench-Constant said he wants to find a way to make the body rebuild myelin – the sheath that protects nerve fibres – using stem cells, which have the ability to turn into different types of tissue.

He told The Herald newspaper: "My vision for a patient coming into a clinic in 10 or maybe 15 years' time is they will be given a mixture of drugs to prevent the inflammation and to promote repair.

"That way, MS would no longer be a chronic, disabling disease."

The MS research centre is part of the Scottish Centre for Regenerative Medicine at the University of Edinburgh.

It was launched thanks to a major donation from Harry Potter author JK Rowling, whose mother died from the condition.

MS affects an estimated 85,000 people in the UK