Copaxone also significantly reduced the number of relapses in RRMS patients by 33 percent over placebo (p=0.012) during the nine months of the study. Researchers noted a significant correlation between the cumulative number of enhancing lesions and the total number of relapses over the study period in both placebo-(p=0.0001) and Copaxone-treated patients (p=0.01).
"This result is consistent with findings in other clinical trials with Copaxone. Copaxone has repeatedly shown that it can reduce the relapse rate by at least one-third," said Jerry S. Wolinsky, M.D., director of the MS Research Center at the University of Texas Health Science Center. "This study is significant because these MRI trial results support the presumed mode of action of Copaxone and its ability to affect lesions and relapses in a timely and correlated manner."
The double-blind study determined the effect, onset and durability of any effect of Copaxone (glatiramer acetate for injection) on disease activity monitored with MRI. At 29 centers throughout Europe and Canada, 239 patients with RRMS were randomized to receive 20 mg of Copaxone (n=119) or placebo (n=120) by daily subcutaneous injection for nine months. This trial targeted patients with active disease because the eligibility criteria required patients to have one or more relapses in the two years preceding the study.
The primary outcome measure was the total number of enhancing lesions on T1-weighted images. Treatment with Copaxone showed a significant reduction in T1 lesions compared with placebo (the mean number of lesions were 36.8 for placebo and 25.96 for Copaxone, p=0.003). T1 enhancing lesions correlate to perivascular inflammation and blood brain barrier disruption. T2-weighted images examine the disease burden of lesions in the brain. This was one of the secondary outcome measures of this study.
The differences in accumulation of new T2 lesions over time in the placebo and treated groups paralleled those observations for enhancing lesions. By the end of the third month of the nine-month study, the rate of accumulation of new T2 lesions in the Copaxone-treated group began to move away from the placebo group. After the sixth month of treatment, the difference between the two groups became statistically significant.
The median percentage change in T2 lesion volume from baseline to the end of the trial was 20.6 percent in the placebo group and 12.3 percent for the Copaxone arm. This is a 40 percent reduction for the Copaxone group compared with placebo (p=0.011).
The most common side effects of Copaxone (glatiramer acetate for injection) are redness, pain, swelling, itching, or a lump at the site of injection, flushing, chest pain, weakness, infection, pain, nausea, joint pain, anxiety, and muscle stiffness. These reactions are usually mild and seldom require professional treatment. Patients should be sure to tell their doctor about any side effects.
Some patients report a short-term reaction right after injecting Copaxone. This reaction can involve flushing (feeling of warmth and/or redness), chest tightness or pain with heart palpitations, anxiety, and trouble breathing. These symptoms generally appear within minutes of an injection, last about 15 minutes, and go away by themselves without further problems.
Industries, Ltd. was granted approval by the U.S. Food and Drug Administration
(FDA) in December 1996, to market Copaxone. The drug was launched in April
1997. Copaxone is marketed in the United States by Teva Neuroscience, based
in Kansas City, Mo.