Teva Pharmaceutical Industries (NYSE and TASE: TEVA) reported Phase Ib data for TEV-'408 (TEV-53408), its internally discovered anti-IL-15 monoclonal antibody, and announced plans to advance the molecule into a Phase IIb study in vitiligo in Q4 2026. The decision positions Teva as one of the few large pharma companies pursuing a systemic biologic specifically engineered for vitiligo — a disease where the only approved pharmacological treatment remains a topical therapy restricted to limited body surface area.
The Phase Ib study is an ongoing, open-label trial enrolling adults with active or stable non-segmental vitiligo. At week 24, 42% of evaluable participants achieved F-VASI50 — a 50% reduction in facial vitiligo area and severity — and 21% achieved F-VASI75. Nearly 75% of patients reported improvement in facial vitiligo, with half describing themselves as "much" or "very much" improved on a patient-reported measure. Total body response was more modest: 55% reported improvement, while only 7% achieved T-VASI50. TEV-'408 was administered as two subcutaneous injections on day 0 and at week 12, consistent with a planned quarterly (Q12W) dosing schedule. No safety signals were observed. The study enrolled a notably severe population — 66% of participants had vitiligo affecting more than 10% of body surface area.
These are early-stage, open-label data from a small evaluable cohort, and the absence of a control arm limits interpretation. Cross-trial comparisons are limited, but the F-VASI50 rate of 42% at week 24 from just two doses is broadly in the range reported in early trials of Incyte's Opzelura (ruxolitinib) cream, which achieved F-VASI75 of approximately 30% at week 24 in its pivotal TRuE-V trials. The key distinction is that ruxolitinib is a topical JAK inhibitor approved for up to 10% body surface area, leaving patients with more extensive disease — precisely the population enrolled here — without an approved systemic option.
Mechanism and competitive positioning
TEV-'408 blocks IL-15, a cytokine that drives the autoimmune destruction of melanocytes in vitiligo by activating cytotoxic CD8+ T cells. This upstream mechanism differs from the JAK inhibitor approach of ruxolitinib, which suppresses downstream IFN-γ signaling. The closest systemic competitor is Forte Biosciences' anti-CD122 antibody FB102, which also targets IL-15 biology through the shared IL-2/IL-15 receptor. Both programs remain in early clinical development.