Rapid degradation or clearance of therapeutic components limits treatment efficacy. Extending biological half-life and improving targeting prevents premature loss of activity.

Unregulated signaling through KRAS, CCR6, and CB1 pathways leads to oncogenic growth and inflammatory tissue damage. Inhibiting these specific interactions prevents disease progression driven by aberrant protein activity.

Endothelial dysfunction and pulmonary hypertension are driven by insufficient nitric oxide production or high oxidative stress in the vasculature. Addressing this failure mode restores normal blood flow and prevents tissue ischemia.

Clinical outcomes in pancreatic and liver cancers are hindered by an inability to predict which patients will respond to specific anticancer therapies. Identifying these sensitivities allows for the mitigation of ineffective treatment cycles and disease progression.