Th2 Inflammation

Type 2 inflammation is the immune program behind some of the most common chronic diseases in the world. It is coordinated by a small set of cytokines — IL-4, IL-13, IL-5, and the epithelial alarmins TSLP, IL-25, and IL-33 — that together drive IgE production, eosinophil recruitment, mucus hypersecretion, and barrier dysfunction.

Where it shows up

The same underlying biology produces very different clinical pictures depending on the tissue it acts in:

• Atopic dermatitis — itchy, inflamed skin with impaired barrier function, affecting up to 20% of children and 10% of adults in high-income countries.
• Asthma — roughly half of all asthma is type 2 driven, characterized by eosinophilia and responsiveness to anti-IL-4/IL-13 therapy.
• Eosinophilic esophagitis — a food-triggered, Th2-mediated disease that can cause strictures and dysphagia.
• Chronic rhinosinusitis with nasal polyps — persistent type 2 inflammation of the sinus mucosa, often refractory to corticosteroids.

The unmet need

Several biologics now target type 2 cytokines, and they work — for some patients. But response rates in atopic dermatitis hover around 40–50% for clear or almost-clear skin, and many patients lose response over time. Oral options remain limited and carry broad immunosuppression. There is a clear opening for therapies that act earlier in the cascade or that resolve inflammation more durably.

Our approach

Our lead Th2 program targets the alarmin axis upstream of IL-4 and IL-13, with the goal of interrupting the loop at its initiation rather than at its output. A second program pairs type 2 blockade with a resolution-pathway agonist, aiming for deeper and more durable responses than cytokine neutralization alone.