Amenamevir

Herpesvirus replication requires a helicase-primase complex to unwind and prime viral DNA, and amenamevir was designed to inhibit that complex. This places it outside the nucleoside-analogue class represented by acyclovir, which instead depends on viral thymidine kinase activation and chain termination. The mechanistic separation matters clinically, since it offers a route to activity against herpesvirus strains that have become resistant to nucleoside analogues. Approval in Japan covers herpes zoster, the reactivation syndrome caused by varicella-zoster virus. Structurally the agent is a small molecule with the formula C24H26N4O5S and a molecular weight of roughly 482.6 g/mol, and it has reached the final phase of clinical development.

SMILES

Cc1cccc(C)c1N(CC(=O)Nc1ccc(-c2ncon2)cc1)C(=O)C1CCS(=O)(=O)CC1

InChI

InChI=1S/C24H26N4O5S/c1-16-4-3-5-17(2)22(16)28(24(30)19-10-12-34(31,32)13-11-19)14-21(29)26-20-8-6-18(7-9-20)23-25-15-33-27-23/h3-9,15,19H,10-14H2,1-2H3,(H,26,29)