Bay 60-7550 is an inhibitor of PDE2(Ki: 3.8 nM).

Bay 60-7550 in the presence of NMDA (30 μM) results in further increases in cGMP compared with NMDA alone. 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]. 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].

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 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]. 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.

439083-90-6

C27H32N4O4

476.57

BAY 607550

DMSO:33.3 mg/mL (69.87 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years