A total of 794 patients were randomized and treated with generic glatiramer acetate (n = 353), Copaxone (n = 357), or placebo (n = 84). Of these, 735 patients (92.5%) completed the nine-month double-blind treatment period. The estimated geometric mean numbers of gadolinium-enhancing lesions were 0.42 for generic glatiramer acetate and 0.39 for Copaxone, resulting in an estimated generic/brand lesion ratio of 1.097 with a 95% confidence interval of 0.884 to 1.362, which is within the predefined equivalence margin.
The estimated geometric mean number of gadolinium-enhancing lesions for both the generic and brand drug groups was lower than for the placebo group, confirming assay sensitivity. Annualized relapse rates were 0.31 for generic glatiramer acetate, 0.41 for Copaxone, and 0.39 for placebo. Comparable proportions of patients treated with the generic and branded drug were free from disease activity. EDSS was stable in all three groups. The incidence, spectrum, and severity of reported adverse events, including injection site reactions, were similar in the two treatment groups.
The generic version of glatiramer acetate is being developed by Synthon Biopharmaceuticals BV (Nijmegen, the Netherlands).
—Glenn S. Williams
Does Brain Reserve Protect Against Physical Disability in MS?
Patients with multiple sclerosis (MS) who have larger maximal lifetime brain growth may have less physical disability, according to researchers. Larger maximal lifetime brain growth may help preserve patients’ ambulation and fine motor function.
“Clinical consideration of maximal lifetime brain growth … may help identify patients with MS at highest risk for future physical disability,” said James F. Sumowski, PhD, Senior Research Scientist of Neuropsychology and Neuroscience Research at the Kessler Foundation Research Center in West Orange, New Jersey. “At-risk patients can be enrolled in early intervention treatments or research on such treatments.”
Dr. Sumowski and colleagues studied 352 patients with MS, including 255 people with relapsing-remitting MS and 97 people with secondary progressive MS. The researchers assessed participants’ disease burden using high-resolution, 3-D, T1 fast field echo. They used software to normalize patients’ total brain, gray matter, white matter, deep gray matter, and thalamus volumes. The researchers also used dual-echo turbo spin echo to quantify T2 lesion volume. Dr. Sumowski’s group estimated maximal lifetime brain growth with SIENAX v-scaling factor (adjusted for gender), a proxy for intracranial volume.
In addition, the investigators assessed 168 participants’ ambulation with the 25-Foot Walk. Participants who used assistive devices for walking were excluded. Fine motor function was assessed with the Nine-Hole Peg Test (in 323 patients) and Finger Tapping Test (in 330 patients). Cognitive status was assessed in 333 patients with the Paced Auditory Serial Addition Test-3 (PASAT-3).
Dr. Sumowski and colleagues found that maximal lifetime brain growth significantly predicted pyramidal and cerebellar function. Maximal lifetime brain growth accounted for the variance between patients in physical disability, as measured by the Finger Tapping Test. People with larger maximal lifetime brain growth performed better on that test. Disability was worse in people with smaller maximal lifetime brain growth, and the relationship did not change when the researchers controlled for demographics and deep gray matter atrophy.
The investigators found a similar relationship for cerebellar function. Participants with larger maximal lifetime brain growth had less disability and cerebellar dysfunction, even when the researchers controlled for demographics and disease burden. Patients with larger maximal lifetime brain growth completed the 25-Foot Walk more quickly, which indicated that they had less disability.
The researchers did not find a relationship between maximal lifetime brain growth and other functional systems, such as brainstem, visual, motor sensory, and bladder function.
—Erik Greb