Dormant HSV-1 is Activated by External Triggers and Amplifies its Own Replication via Cyclooxygenase (COX-1 and COX-2) Enzyme
Cyclooxygenase upregulation is critical for efficient HSV-1 viral replication
COX-2 and COX-1 exhibit a 14.5-fold and a 1.8-fold increase, respectively,
during active HSV-1 infection
IMC-1’s Novel, Synergistic Antiviral Mechanism Suppresses Viral Replication, Demonstrates FM Treatment Effect
Our most advanced medicine, oral IMC-1, combines 2 specific mechanisms of action purposely designed to inhibit HSV-1 activation and replication, thereby keeping HSV-1 in a latent (dormant) state or down-regulating HSV-1 from a lytic (active) state back to latency. The famciclovir component of IMC-1 inhibits viral DNA replication and thus inhibits upregulation of the HSV-1 virus. The celecoxib component of IMC-1 inhibits cyclooxegenase-2 (COX-2) and to a lesser degree COX-1, enzymes used by HSV-1 to amplify or accelerate its own replication.
Antivirals, NSAIDs and COX-2 Inhibitors have individually failed as FM monotherapy
The synergistic response in the IMC-1 P2a data served as the basis for both FDA fast-track designation and a synergy patent on the composition of the combined drugs