The CALLIPER trial reported a 30% relative risk reduction in 24-week confirmed disability worsening in PPMS patients. How does this compare to historical benchmarks, and what makes this result particularly meaningful in a field with so few treatment options?”

Vidofludimus calcium showed a 29% reduction in disability progression in patients without gadolinium-enhancing lesions—a subgroup often unresponsive to anti-inflammatory therapies. What does this suggest about the drug’s potential neuroprotective mechanism, particularly in non-inflammatory neurodegeneration?

The drug slowed thalamic brain volume loss by 20% versus placebo. Given the thalamus’s role in MS-related disability, how relevant is this MRI biomarker in evaluating future therapies targeting progression independent of relapse activity (PIRA)?

Vidofludimus calcium is the only MS drug in development known to activate Nurr1. What is the current understanding of Nurr1’s function in neuroprotection, and how might this translate into clinical benefit for PMS?

With only one approved drug for PPMS and limited options for naSPMS, where do you see vidofludimus calcium potentially fitting if confirmed in a phase 3 program—particularly in terms of disease stage or inflammatory status?

CALLIPER enrolled 467 patients, many with longstanding disease and low inflammatory activity. How important is this design in validating vidofludimus calcium’s effects beyond short-term inflammation control?

No new safety signals emerged in CALLIPER, and adverse event rates were balanced between drug and placebo arms. How does this influence long-term treatment planning, especially given the chronic nature of PMS?

Based on these results, what are the key data points regulators will likely scrutinize for a phase 3 trial? Do you expect vidofludimus calcium to pursue a broad PMS label, or will PPMS be the initial focus?