The phase III trial datasets of Alemtuzumab have been published and show the drastic response of the immune system in patients with Multiple Sclerosis.
Alemtuzumab is a highly effective drug for multiple sclerosis, approved in more than 60 countries and used by more than 12,000 patients worldwide. However, it carries an almost 50 percent risk of secondary autoimmune diseases, such as platelet and kidney diseases. Although knowledge about these adverse effects was included in conference presentations and licensing submissions to European and US regulators, it was not published in journals. Journals, of course, are not required, and when it comes to biomedicine are far less likely to be rigorous than clinical trial results, where lawsuits will result if data are bad.
But a group of authors wanted to publish it ahead of the company schedule, and did so using a Freedom of Information request, which absolved the company from having to make the information presentable. The researchers note that the data showed, as evidenced in the regulatory declarations, a massive and rapid re-population of a subset of B cells in the absence of effective T cell regulation, which they say helps create an environment for secondary autoimmune disease. This also allows a marked anti-drug response that can become problematic in some people taking the drug. According to the researchers, controlling this B cell subset "overshoot" after Alemtuzumab administration until T cell regulation recovers, may limit the risk of secondary autoimmune disease and make it an even better medicine.
The data also noted a long term suppression of T cells believed by many to be the cause of the problem and loss of memory B cells, which they say offers a new explanation on why Alemtuzumab is effective in people with MS. It may provide insight of how all other drugs work in MS and ties aspects of the potential cause and treatments together.
Citation: Interpreting Lymphocyte Reconstitution Data From the Pivotal Phase 3 Trials of Alemtuzumab. David Baker, PhD; Samuel S. Herrod, BSc; Cesar Alvarez-Gonzalez, PhD; Gavin Giovannoni, PhD; Klaus Schmierer, PhD, FRCP. JAMA Neurol. doi:10.1001/jamaneurol.2017.0676