ECTRIMS 2025 is in coming to an end and whilst we wait for the late-breaking session rather than look at the science, I note the demise of MS pharma. As the gravy train for some ends it is evident that generic and biosimilar prodicing drugs are appearing…….There is a notable absense to me and that is the Biogen stand has gone. They leave because their interest in MS has all but gone. There is Sandoz the maker of tyruko but there is no Biogen maker of tecfidera, tysabri, vumerity, avonex, plegridy. I wonder who of the old guard will be next. We will find out at ACTRIMS Toronto 2026 with a joint gamboree. The pipelines for MS of some are thin to non existant. It is part of the churn but a 40 year era seens to be all but gone. In the pipeline there is a peripheral BTK inhibitor….if this is the answer what is the question…The data of a CNS penetrant is looking OK.
Abstract Number: 711/O112 Abstract Number: Fenebrutinib maintains early and sustained low disease activity in patients with relapsing multiple sclerosis: Jiwon Oh et al.
Introduction: Bruton’s tyrosine kinase inhibitors (BTKi) have potential to impact relapsing and progressive MS disease biology, but the durability of the effect on acute inflammation is unclear. Fenebrutinib (FEN) is a potent, highly selective, noncovalent, reversible BTKi. In the double‑blind treatment (Tx) period (DBTP) of the Phase II FENopta study (NCT05119569), FEN rapidly reduced acute inflammatory disease activity and showed central nervous system penetrance in people with relapsing MS (pwRMS). PwRMS could then receive FEN in an openlabel extension (OLE). Objectives/Aims: Objectives/Aims: To evaluate the efficacy and safety of FEN Tx over 2 y (96 wk) in the FENopta OLE. :
Methods: PwRMS received FEN 200 mg or placebo orally twice daily during the 12-wk DBTP. All received FEN during the OLE. Disease activity was evaluated through protocol-defined relapses and brain MRI. No evidence of disease activity-3 (NEDA-3), exploratory biomarkers (B‑cell count, immunoglobulin [Ig] and neurofilament light chain [NfL]) and safety were also assessed.
Results: All eligible pwRMS were enrolled in the OLE (n=99); 93 (94%) remain on study. At OLE Y2, NEDA-3 was achieved by 78.7% of pwRMS. The annualised relapse rate was 0.06, 92% of pwRMS were relapse free and median change from study baseline in Expanded Disability Status Scale was 0. Per OLE Y2 MRI, the mean number of new T1 gadolinium-enhancing (Gd+) lesions/scan was 0 (n=89); therefore, 100% of pwRMS were free of new Gd+ lesions. Suppression of the annualised rate of new/enlarging T2 lesions (NET2L) observed during Y1 of FEN Tx was sustained at OLE Y2, with a NET2L rate of 0.22 in pwRMS who received FEN during DBTP and OLE (FEN-FEN). At OLE Y2, in FEN-FEN pwRMS, the mean change from baseline in B-cell count was −46% (95%CI: −42 to −51), −27% for IgM and −9% for IgG. Mean serum NfL levels decreased to within the normal range for healthy volunteers in Y1 of Tx and remained in that range in Y2. Most common adverse events (>5% of pwRMS) were urinary tract infection (10%), COVID-19 (10%),pharyngitis (6%) and respiratory tract infection (5%). No new liver enzyme elevations were recorded in OLE Y2, and no new safety signals were identified.
Conclusion: PwRMS treated with FEN for 2 y had near complete suppression of acute inflammatory disease activity, and a high percentage met NEDA-3. Reductions in B-cell, Ig and NfL levels were observed. These results are consistent with the proposed dual mechanism of action, acting on the underlying pathophysiology of both relapses and nonrelapsing progression
Source: multiple-sclerosis-research.org