ReviewDrugs2026
Bruton's Tyrosine Kinase Inhibitors in Multiple Sclerosis.
Review in Drugs, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a chronic, inflammatory disorder of the central nervous system (CNS) characterized by overlapping relapsing and progressive pathologies. Although they exist along a continuum, pathology in relapsing MS (RMS) is primarily driven by the peripheral adaptive immune system, while progressive MS (PMS) pathology is underpinned by innate immune activity and other pathologic processes compartmentalized within the CNS. While currently approved therapies are highly effective in targeting aspects underpinning relapsing pathology, they have limited efficacy in PMS due to either inability to cross the blood brain barrier (BBB) or inability to modulate pathologies driving PMS. Bruton's tyrosine kinase (BTK) inhibitors are an emerging class of oral agents that represent a novel approach to MS treatment. These agents target BTK, an enzyme which plays a pivotal role in both adaptive and innate immune signaling. As small molecules, some BTK inhibitors can cross the BBB at biologically relevant concentrations. Therefore, BTK inhibitors may potentially modulate both relapsing and progressive MS pathology. Data from Phase 2 and Phase 3 trials have been promising in this regard. The unique pharmacological profile of each BTK inhibitor may underpin observed differences in efficacy and safety outcomes to date. In particular, tolebrutinib has demonstrated efficacy against disability progression in non-relapsing secondary progressive MS, while fenebrutinib has recently shown promise in both relapsing and primary progressive MS. However, adverse events include elevated liver enzymes, which can reach life-threatening levels. This review highlights the role of BTK in immune signaling and the rationale for BTK inhibition in MS, discusses the evolution of BTK inhibitors for MS and other indications, summarizes findings from Phase 2 and Phase 3 trials in RMS and PMS, and explores practical questions around the potential use of BTK inhibitors in real-world practice.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.