To report safety and efficacy at Week (W) 48 in the open-label extension (OLE) of the phase 2 trial (NCT04879628) of frexalimab in participants with relapsing multiple sclerosis (RMS).
Frexalimab is a second-generation anti-CD40L monoclonal antibody that blocks the costimulatory CD40/CD40L pathway, which is important for activation and function of adaptive and innate immunity. In the 12-week double-blind period (DBP), frexalimab demonstrated safety and efficacy with the high-dose treatment showing an 89% reduction (vs placebo) in new gadolinium-enhancing (Gd+) T1-lesions. Over 24 weeks in the OLE, frexalimab was well-tolerated, and the number of lesions further decreased.
In the DBP, participants were randomized to frexalimabhigh (N=52), frexalimablow (N=51), or matching placebo arms (placebohigh, N=12; placebolow, N=14). At W12, participants receiving placebos switched to respective frexalimab arms and entered the OLE. Key assessments during the OLE included safety and efficacy (number of Gd+ T1-lesions and new/enlarging T2-lesions).
125/129 (97%) participants completed the DBP and entered the OLE; 112 (87%) remained in the study at W48 cut-off. At W48, the number of Gd+ T1-lesions (mean [SD]) remained low in participants who continued receiving frexalimab and in those who switched from placebo to frexalimab at W12 (frexalimabhigh: 0.0 [0.2]; frexalimablow: 0.2 [0.5]; placebohigh/frexalimabhigh: 0.2 [0.6]; placebolow/frexalimablow: 0.1 [0.3]). Furthermore, 96% participants in frexalimabhigh, 87% in frexalimablow, 90% in placebohigh/frexalimabhigh, and 92% in placebolow/frexalimablow arms were free of Gd+ T1-lesions at W48. New/enlarging T2-lesion counts and T2-lesion volume change remained low with frexalimabhigh through W48, and lymphocyte counts were stable over 48 weeks. Overall, frexalimab treatment was well-tolerated through W48; the most common adverse events included nasopharyngitis, headache, and COVID-19.
Frexalimab continued to show favorable safety and efficacy in RMS participants through W48. These data support its further development as a potential high-efficacy, non-lymphocyte-depleting treatment option in MS.