tcsc0279 Bay 60-7550

Bay 60-7550 is a selective inhibitor of PDE2 with K_i of 3.8±0.2 nM, also is a modulator of NO.

IC50 & Target: Ki: 3.8±0.2 nM (PDE2)^[1]

In Vitro: Bay 60-7550 (1 μM) increases cGMP in the neuronal cultures compared with control [F(6,14)=12.97, p<0.05 for Bay 60-7550]. Bay 60-7550 in the presence of NMDA (30 μM) results in further increases in cGMP compared with NMDA alone. The NMDA receptor antagonist MK-801 (10 μM) blocks both Bay 60-7550+NMDA-induced elevation in cGMP in neuronal cultures^[1]. Compared with untreated control cells, proliferation of PASMCs from IPAH patients is significantly reduced by BAY 60-7550 (1 μM)^[2].

In Vivo: The PDE2 inhibitors Bay 60-7550 (1 mg/kg) reverses restraint stress-induced alterations in behavior, resulting in increased percentages of open-arm entries and open-arm time compared with the vehicle + restraint stress condition. In nonstressed mice, Bay 60-7550 produces a dose-dependent increase in percentages of open-arm entries and open-arm time compared with the vehicle-treated group; significant increases are observed at a dose of 3 mg/kg. In nonstressed mice, Bay 60-7550 increases, in a dose-dependent manner, the number of head-dips and time spent head-dipping, compared with vehicle-treated mice; significant increases are observed at doses of 1 and 3 mg/kg^[1].