Bay 60-7550 is a potent and selective PDE2 inhibitor with a Ki of 3.8 nM
CAS：439083-90-6
分子式：C??H??N?O?
分子量：476.57
纯度：98%
存储：Store at -20°C

Background:

Bay 60-7550 is a potent and selective PDE2 inhibitor with a Ki of 3.8 nM.

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].

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]

Reference:

[1]. Masood A, et al. Anxiolytic effects of phosphodiesterase-2 inhibitors associated with increased cGMP signaling. J Pharmacol Exp Ther. 2009 Nov;331(2):690-9.
[2]. Bubb KJ, et al. Inhibition of phosphodiesterase 2 augments cGMP and cAMP signaling to ameliorate pulmonary hypertension. Circulation. 2014 Aug 5;130(6):496-507.