IC50: By suppressing protein kinase Mξ (PKMξ), ZIP reverses late-phase LTP with an IC50 of 1 - 2.5 μM. Long-term potentiation (LTP), a persistent synaptic enhancement, is considered to be a substrate for memory. A typical LTP process includes two phases, induction and maintenance. PKMξ as an active form of protein kinase C (PKC) isozyme is necessary and potent for LTP maintenance. ZIP is applied as a novel and cell-permeable inhibitor for PKMξ and can therefore block LTP. In vitro: In order to determine the specific phase of LTP affected by PKMξ, ZIP was added at different concentrations to the bath before cells incubation. Experiments with ZIP were compared with experiments without the peptide. This study showed that ZIP could selectively inhibit PKMξ-induced synaptic potentiation in hippocampal slices in vitro. In vivo: ZIP was the first tool available to test the maintenance hypothesis in vitro. The effect of ZIP on late phase of LTP in vivo was also detected using the rat hippocampus. It was found that intra-hippocampal injection of ZIP with a dosage of 10 nmol in 1 ml saline rapidly reversed the late-phase LTP and led to persistent loss of 1-day-old spatial memory. Clinical trial: So far, no clinical trial has been conducted.