CONy 2024 | BTK inhibitors for MS treatment: what do the recent trial readouts mean for the field?
Giancarlo Comi, MD, Vita-Salute San Raffaele University, Milan, Italy, discusses the recent readouts of two Phase III trials, which compared the experimental BTK inhibitor (BTKi) evobrutinib to the disease-modifying drug teriflunomide in patients with multiple sclerosis (MS). The results of these studies were negative, causing disappointment within the community. However, although the BTKi was not found to be superior to teriflunomide in reducing acute inflammation, its effect was comparable. Therefore, Prof. Comi highlights the need to remain open to the potential of the BTKi drug class to have an effect on the mechanisms of neurodegeneration in MS and not simply rule it out as a treatment option due to the lack of a superior anti-inflammatory effect. This interview took place at the 18th Annual Congress on Controversies in Neurology (CONy 2024) in London, UK.
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Transcript
All those who are in the business of MS, and particularly patients, have been disappointed by this negative result, there was a lot of expectation. However, the trial was performed in relapsing-remitting MS, and the expectation was that because of the mechanism of action of this class of drugs, we had to observe not only an effect on acute inflammation, which was there by the way, but also on the top of that, an effect of protection from mechanism of neurodegeneration...
All those who are in the business of MS, and particularly patients, have been disappointed by this negative result, there was a lot of expectation. However, the trial was performed in relapsing-remitting MS, and the expectation was that because of the mechanism of action of this class of drugs, we had to observe not only an effect on acute inflammation, which was there by the way, but also on the top of that, an effect of protection from mechanism of neurodegeneration. The trial was against a drug that is active on inflammation, teriflunomide. So, the fact that there was no difference doesn’t mean that the BTK were not active in inflammation. It means that they were not superior to teriflunomide from this point of view.
We have many different other members of this class of drug, and they have different profile in terms of penetration of the CNS and concentration in the CNS, and also in the way they act. So, I think we should be still remain open to the possibility that these drugs may target some of the mechanism of neurodegeneration, not only having an anti-inflammatory activity. And I think that we still need to maintain some open possibility to succeed with this class of drug.
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