Table 1.

Pharmacologic Treatments for AERD

Treatment	Mechanism
Corticosteroids: Inhaled/topical: eg, Fluticasone propionate Systemic: eg, Prednisone	Decreasing the transcription of inflammatory genes by inhibition of the gene transcriptional complex
Leukotriene Modifiers eg, Montelukast, Zileuton	Montelukast: Competitive antagonist of the Cys-LT1 receptor Zileuton: Direct inhibitor of 5-Lipoxygenase
Aspirin Desensitization	Exact mechanism currently unknown, but evidence of decrease in IL-4 and STAT 6 transcription, decrease in PGD2, LTE4, and IFN-γ production, as well as a decrease in density of Cys-LT receptors
Monoclonal antibodies: Dupilumab	Dupilumab: IL-4receptor-α antagonist monoclonal antibody – inhibits action of IL-4 and IL-13, decreasing Th2-cell mediated inflammation
Investigational Agents: Omalizumab (Positive results from Phase III trials POLYP1 and POLYP2) – currently undergoing FDA review Mepolizumab (currently undergoing phase III trials SYNAPSE) Benralizumab (currently undergoing phase III trials ORCHID) AMG-282 (phase I trial), PF-06817024 (phase I trial), Etokimab/ANB020 (phase II trial) GB001 (phase II trial), ACT-774312 (phase II trial), Fevipiprant (phase III trial) Ifetroban (phase II trial)	Omalizumab: anti-IgE monoclonal antibody – inhibits the binding of IgE to the high-affinity IgE receptor on surface of mast cells, basophils Mepolizumab: IL-5 antagonist monoclonal antibody – binds to IL-5 and inhibits IL-5 signaling, reducing the production and survival of eosinophils Benralizumab: monoclonal antibody against IL-5 receptor α on eosinophils, also attracts natural killer cells to induce apoptosis of eosinophils AMG-282, PF-06817024, Etokimab/ANB020: Anti-IL-33 monoclonal antibody GB001, ACT-774312, Fevipiprant: Prostaglandin D2 receptor 2 (CRTH2) antagonist Ifetroban – Thromboxane receptor (TP) antagonist

Note: Data from Li KL, Lee AY, and Abuzeid WM.⁵⁰