Copaxone may protect against Neuronal injury in RRMS
"Copaxone (Glatiramer Acetate) Demonstrated Protection Against Neuronal Injury In Relapsing-Remitting Multiple Sclerosis"
KANSAS CITY, MO -- November 14, 2005 –
Clinical research data published in the December issue of Multiple Sclerosis provided evidence that Copaxone[® (glatiramer acetate injection) may offer protection from axonal injury and induced neuronal metabolic recovery in patients with relapsing-remitting multiple sclerosis (RRMS).
In a pilot study of 18 RRMS patients using brain imaging techniques, Copaxone was found to produce significant increases in n-acetylaspartate/creatine (NAA/Cr) ratio [an indicator of neuron and axon integrity] compared to four untreated control patients after one year of treatment. This increase was maintained at two years of follow-up.
Additionally, patients treated with Copaxone showed a significant, 50% reduction in relapses compared to baseline (p<0.001) while relapse rate in the untreated group remained unchanged.
"The increases in NAA/Cr ratios with Copaxone suggested sustained beneficial effects on cerebral axonal recovery. We believe this indicates a potential for improved electrical conduction pathways in the brain, supporting the emerging concept that, centrally, Copaxone may be acting as a neuro-protective agent," said Omar Khan, MD, associate professor of neurology and director of experimental therapeutics/clinical research, Multiple Sclerosis Center, Wayne State University. "This data is of critical significance because axonal transection is a well-known feature of active MS lesions and represents an irreversible stage of the disease process," said Dr. Khan.
Copaxone Demonstrated Protection/Page Two
Twenty-two treatment-naïve RRMS patients were included in the study. Baseline neurological assessments and magnetic resonance spectroscopy imaging (MRSI) scans were performed. Eighteen patients were treated with Copaxone (glatiramer acetate injection) and followed for 2 years with neurological assessments every six months and MRSI scans annually.
Due to needle phobia, four patients elected to remain untreated, and were followed using the same assessment and MRSI schedule. NAA/Cr ratio measurements were obtained in a selected volume of interest (VOI), within the brain and included normal-appearing white matter (NAWM) within the VOI.
In the Copaxone group, the NAA/Cr levels within the VOI were significantly increased by 9.1% at year one and by 10.7% at year two, compared to baseline (P =.03 for both assessments). Conversely, in the untreated group, a 5.5% decrease in NAA/Cr levels was observed in the VOI at year one (P =.04) and an 8.9% decrease at year two (P =.03).
Copaxone patients also demonstrated a 5.4% and 7.1% increase in NAA/Cr ratios within the NAWM at years one and two, respectively (P =.04 for both). Untreated patients had a two% (P = NS.) and 8.2% (P =.03) decrease in NAA/Cr ratios within the NAWM at year 1 and 2, respectively.
"We recognize our study contains limitations, such as the number of patients,
open-label design, and the MRS technique of evaluating NAA levels," stated Dr. Khan. "However, our recently presented three-year data showed sustained improvements in NAA/Cr ratios which clearly demonstrated a long-term clinical benefit and showed that Copaxone treatment may lead to neuronal recovery," said Dr. Khan.
About Copaxone
Current data suggest Copaxone (glatiramer acetate injection) is a selective MHC class II modulator. Copaxone is indicated for the reduction of the frequency of relapses in relapsing-remitting multiple sclerosis. The most common side effects of Copaxone are redness, pain, swelling, itching, or a lump at the site of injection, weakness, infection, pain, nausea, joint pain, anxiety, and muscle stiffness.
Copaxone is now approved in 44 countries worldwide, including Canada, the United States, Mexico, Australia, Israel, and all European countries. In Europe, Copaxone is marketed by Teva Pharmaceutical Industries Ltd. and sanofi-aventis. In North America, Copaxone is marketed by Teva Neuroscience.
SOURCE: Teva Neuroscience