CD44 and infection: The two N-acylhydrazones showed a very different behavior: compound 13 lost activity 6 h after infection, in a time–window between AZT and EFV/NVP, in agreement with the hypothesis of targeting the retrotranscription step of the replicative viral cycle consistently with the inactivity against HIV-1 IN previously reported [30] and suggesting a mode of action different from nucleoside analogs and NNRTIs.