Dr. Stephen Hauser, chair of the neurology department at the University of California San Francisco, was instrumental in the early research and later clinical trials that ultimately led to Ocrevus (ocrelizumab), the first therapy approved by the U.S. Food and Drug Administration (FDA) for both relapsing MS (RMS) and primary progressive multiple sclerosis (PPMS) patients.
Indeed, his work is testament to how scientific inquiry and determination might turn observations made in the lab into medicines for those in need.
Ocrevus is an antibody that targets CD20-positive B-cells, a type of cells from the immune system that are believed to contribute to myelin degeneration and neuronal damage, the hallmarks of MS. As such, and because of the efficacy and overall safety demonstrated in those clinical studies, Ocrevus holds considerable promise as an MS treatment — and one that might help at least some people with progressive disease.
“The availability of a highly effective and well-tolerated treatment means that people at the dawn of their MS can be treated with a therapy that will essentially completely block the inflammation in myelin that causes relapses and remission,” Hauser said in a UCSF news story, reported by Nina Bai, on which this article is based. “And we are optimistic that by doing so, the outlook over many years will be even more favorable than it is today.”
Early steps and obstacles
The development of Ocrevus took several decades and encountered many obstacles along the waym Bai writes. For instance, when Hauser and his research team were trying to secure funding to study a drug that inhibited B-cells, the National Institutes of Health (NIH) told them their proposal lacked “biological plausibility.” Back then, T-cells (another type of immune system’s cells) were widely believed to be the major contributors to MS development.
But Hauser and his team felt they were on the right track when — while studying MS pathology using their own mouse model of the disease in the mid-1990s — they detected antibodies “tightly bound” to proteins in damaged myelin. These were the same antibodies found in samples of spinal fluid from patients, and which widely were used as biomarkers for MS although not considered to have a role in disease mechanisms.
The team also discovered that MS could be induced in healthy animals by transferring these antibodies and B-cells, as well as T-cells. This showed that these antibodies, which not many people seemed to care much about, were actually partners in crime — alongside T-cells — in causing MS.
“This was a paradigm change for the field,” said Hauser, though it would take another few years before he, too, would look beyond T-cells, Bai reported.
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