Teva Derisks IL-15 Pathway In Vitiligo-Sets Bar/Path For Forte To Follow

Research evidence excerpt

Teva Derisks IL-15 Pathway In Vitiligo-Sets Bar/Path For Forte To Follow

TD Cowen Forte Biosciences

Global Research July 7, 2026

F-VASI and T-VASI Scoring System

Source: Teva Pharmaceuticals

CD122 Blockade May Offer A More Comprehensive Approach Than IL-15

Neutralization Alone

While TEV-408 directly neutralizes the IL-15 ligand, Forte's FB102 targets CD122 (IL-

2/IL-15 receptor), the shared signaling receptor through which IL-15 drives

activation, proliferation, and survival of pathogenic tissue-resident memory T cells

(TRM cells) believed to be central to vitiligo persistence and recurrence. IL-15 is highly

expressed within affected skin and functions through trans-presentation to maintain

autoreactive CD8+ TRM cells that continuously attack melanocytes, making the IL-

15/CD122 axis one of the most compelling biologic drivers of disease.

Importantly, CD122 sits downstream of the IL-15 ligand and serves as the critical

signaling node through which IL-15 exerts its biologic effects. As a result, receptor

blockade theoretically may provide more complete suppression of pathogenic IL-15

signaling regardless of local IL-15 concentrations or mechanisms of ligand

presentation.

From a mechanistic perspective, this raises the possibility that FB102 could more

effectively deplete or functionally silence disease-driving TRM cells, potentially

translating into greater durability of response after treatment discontinuation.

Durability Off Treatment Is The Key Differentiator As JAKs Lose Benefit Post-

Discontinuation

A key limitation of current JAK inhibitors is that many patients lose benefit following

treatment discontinuation and gradually drift back toward baseline, highlighting the

need for therapies capable of delivering durable disease control rather than