Secure access to strategy and planning files.
Cyclosporine and lifitegrast suppress activated T-cells. They do not directly engage the innate immune system.
No approved therapy directly engages innate immune resolution. Regadenoson is the first to target A2A-driven macrophage repolarization.
cAMP signaling hydrates mucin via CFTR/bicarbonate channels. Calms innate inflammation by shifting macrophages from M1 to M2 — the mechanism cyclosporine cannot access.
At ocular surface concentrations, regadenoson engages A1 receptors, driving calcium-dependent secretion from Krause and Wolfring glands.
Regadenoson binds A2A receptors on M1 macrophages in the conjunctival epithelium.
cAMP signaling brakes TNF-α, IL-1β, iNOS, and NLRP3 inflammasome activity.
Macrophages shift to Arg1, CD206, IL-10. Goblet cells secrete TGF-β.
Current therapies only address one side of the equation. We engage a dual-receptor mechanism that restores the ratio from both sides simultaneously.
Leveraging the existing Lexiscan NDA for systemic safety. Only route-specific ophthalmic data needs to be generated new.
Regadenoson (Lexiscan) has been used safely in hundreds of thousands of patients for cardiac imaging. We are repurposing it as a topical eye drop — leveraging existing safety data and the 505(b)(2) pathway to dramatically reduce development risk, cost, and time to clinic.
Unlike single-mechanism therapies that plateau, our approach engages both A2A (hydration, epithelial repair, innate immune resolution) and A1 (secretory recruitment from surface-accessory glands) — two parallel pathways that restore the tear film's functional ratio.
By targeting the corneal and conjunctival epithelium and surface-accessory glands of Krause and Wolfring — not the deep main lacrimal gland — we achieve therapeutic action where the drug is applied, with minimal systemic exposure and an excellent safety margin.