Single-pathway inhibition often fails to achieve complete remission in complex cardiopulmonary and inflammatory pathologies. Combining IRAK4 and BTK inhibitors addresses the limitation of redundant signaling pathways that cause treatment resistance.

Inadequate activation of immune pathways and poor drug exposure due to metabolic induction limit treatment efficacy. Overcoming these barriers enhances anti-tumor activity and clinical durability.

Standard inhibitors fail when target proteins undergo structural mutations that block binding. Overcoming these mutations restores therapeutic efficacy in resistant disease states.