Off-target toxicity in healthy tissues limits the therapeutic window of quinazoline-based compounds. Enhancing selective cytotoxicity reduces systemic side effects and improves patient outcomes.

HIV strains frequently develop mutations that render standard antiretroviral therapies ineffective. Increasing the genetic barrier to resistance prevents therapeutic failure and extends treatment durability.

Existing therapeutic interventions fail to sufficiently suppress the replication cycle of herpesviruses. Overcoming this limitation is essential for reducing viral load and preventing clinical disease progression.

The inability to prevent the insertion of viral DNA into the host genome leads to permanent infection. Inhibiting this specific step stops the replication cycle of HIV.