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Bay 60-7550

Potent PDE2 inhibitor CAS# 439083-90-6

Bay 60-7550

Catalog No. BCC1405----Order now to get a substantial discount!

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Chemical structure

Bay 60-7550

3D structure

Chemical Properties of Bay 60-7550

Cas No. 439083-90-6 SDF Download SDF
PubChem ID 25273570 Appearance Powder
Formula C27H32N4O4 M.Wt 476.57
Type of Compound N/A Storage Desiccate at -20°C
Synonyms BAY 607550
Solubility DMSO : ≥ 33.3 mg/mL (69.87 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name 2-[(3,4-dimethoxyphenyl)methyl]-7-[(2R,3R)-2-hydroxy-6-phenylhexan-3-yl]-5-methyl-1H-imidazo[5,1-f][1,2,4]triazin-4-one
SMILES CC1=C2C(=O)N=C(NN2C(=N1)C(CCCC3=CC=CC=C3)C(C)O)CC4=CC(=C(C=C4)OC)OC
Standard InChIKey MYTWFJKBZGMYCS-NQIIRXRSSA-N
Standard InChI InChI=1S/C27H32N4O4/c1-17-25-27(33)29-24(16-20-13-14-22(34-3)23(15-20)35-4)30-31(25)26(28-17)21(18(2)32)12-8-11-19-9-6-5-7-10-19/h5-7,9-10,13-15,18,21,32H,8,11-12,16H2,1-4H3,(H,29,30,33)/t18-,21+/m1/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Bay 60-7550

DescriptionBay 60-7550 is a potent PDE2 inhibitor with IC50 values of 2.0 nM (bovine) and 4.7 nM (human).
TargetsPDE2    
IC502.0 nM (bovine) 4.7 nM (human)     

Protocol

Kinase Assay [1]
COS-7 cells are maintained in complete DMEM (containing 10% fetal calf serum, 100 units/mL penicillin G, 100 mg/mL streptomycin, and 400 μM L-alanyl-L-glutamine) at 37°C in 5% CO2 atmosphere. A PDE2 expression plasmid is introduced into COS-7 cells using the FuGENE6 transfection reagent. Cells are lysed in solubilization buffer (275 mM NaCl, 1.5 mM MgCl2, 2 mM EGTA, 2% Triton X, 20% glycerol, and 40 mM Tris-HCl), and the cell lysates are used in the immunoprecipitation procedures. A protein A-agarose bead slurry (100 μL) is washed three times with ice-cold phosphate-buffered saline (100 mM NaCl, 2.7 mM KCl, 10.6 mM Na2HPO4, and 1.6 mM NaH2PO4) and mixed with the 5 μg of PDE2 antibody and 100 μL (2 μg/μL) of the lysate sample and rotated overnight at 4°C. The bead/sample mixture is then centrifuged at 1000g to separate the beads from the supernatant. The beads are resuspended in 100 μL of ice-cold lysis buffer (20 mM Tris, pH 7.4, 140 mM NaCl, 0.75 mM MgCl2, 1 mM EGTA, 1% Triton X-100, and 20% glycerol, containing protease and phosphatase inhibitors) to elute the PDE2 for use in the enzyme activity assays. The PDE2 activity assay is done. The recombinant PDE2 enzyme derived from COS-7 cell expression and diluted in KHEM buffer (50 mM KCl, 50 mM HEPES, 10 mM EGTA, and 1.9 mM MgCl2, pH 7.2) is mixed with different concentrations of PDE2 inhibitors (Bay 60-7550, ND7001, and EHNA) and [3H]cGMP/cGMP (5 μM) as the substrate. The mixture is then incubated for 30 min at 37°C (100 μL of reaction volume). To convert the [3H]GMP to [3H]guanosine, samples are incubated with snake venom from Crotalus atrox for 30 min at 37°C. The samples are then vortexed with a freshly prepared slurry of Dowex/water/ethanol [1:1:1, v/v] and then centrifuged for 10 min. [3H]Guanosine in the supernatant is then quantified by liquid scintillation counting. Bay 60-7550 is dissolved in dimethyl sulfoxide, EHNA is dissolved in distilled water, and ND7001 is dissolved in ethanol as 10 mM stocks and then diluted for use in assays with 20 mM Tris, pH 7.4; final concentrations of the respective solvents did not affect the assay. IC50 values at a single substrate concentration are determined by nonlinear regression analysis of the log concentration-response curves for each PDE2 inhibitor; Ki values are calculated[1].

Cell Assay [2]
Growth of human distal pulmonary artery smooth muscle cells isolated from patients with idiopathic pulmonary arterial hypertension (IPAH) or control cells from adults undergoing transplant or lung resection for suspected malignancy, are monitored following treatment with BAY 60-7550 (1 μM), ANP (1 μM), DETA-NONOate (10 μM), or Treprostinil (1 μM), alone or in combination[2].

Animal Administration [1]
Mice[1] Male ICR mice weighing 28 to 35 g are used. Bay 60-7550 (0.5, 1, and 3 mg/kg), ND7001 (0.5, 1.0, and 3 mg/kg), Detanonoate (0.5 mg/kg), L-NAME (50 mg/kg), or Diazepam (1 mg/kg) is administered after restraint stress and 30 min before behavioral testing. Mice also are treated with Bay 60-7550 (3 mg/kg), ND7001 (3 mg/kg), Detanonoate, (0.5 mg/kg), L-NAME (50 mg/kg), or diazepam (1 mg/kg) in the absence of restraint stress; drugs are administered 30 min before the behavioral tests. Bay 60-7550 shows 50-fold selectivity for PDE2 compared with PDE1, 100-fold compared with PDE5, and greater than 200-fold compared with the other PDE families. ND7001 exhibits at 1east 100-fold selectivity for inhibition of PDE2 relative to other PDE families. For antagonism tests to assess the role of cGMP signaling in the behavioral effects of the PDE2 inhibitors, ODQ, an inhibitor of soluble guanylyl cyclase (20 mg/kg), is administered 20 min before Bay 60-7550 or ND7001.

References:
[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.

Bay 60-7550 Dilution Calculator

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Preparing Stock Solutions of Bay 60-7550

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.0983 mL 10.4916 mL 20.9833 mL 41.9666 mL 52.4582 mL
5 mM 0.4197 mL 2.0983 mL 4.1967 mL 8.3933 mL 10.4916 mL
10 mM 0.2098 mL 1.0492 mL 2.0983 mL 4.1967 mL 5.2458 mL
50 mM 0.042 mL 0.2098 mL 0.4197 mL 0.8393 mL 1.0492 mL
100 mM 0.021 mL 0.1049 mL 0.2098 mL 0.4197 mL 0.5246 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Bay 60-7550

Bay 60-7550 is a potent and selective inhibitor of 3’,5’-cyclic nucleotide phosphodiesterase type 2 (PDE2) with IC50 value of 4.7 nM for human recombinant PDE2 [1].
In the signal transduction process, the redundant second messenger cGMP is degraded by the cyclic nucleotide phosphodiesterases. Among the 11 families of PDEs, PDE2 can hydrolyse both cAMP and cGMP and control the levels of both them in the areas which are important for memory formation and storage. Therefore, the inhibition of PDE2 activity is thought to be good to improve memory functions via enhancing neuronal plasticity. Bay 60-7550 is a highly potent and selective inhibitor of PDE2. It increased the levels of cGMP in both hippocampal slices and cultured neurons. In animal models, Bay 60-7550 was found to have positive effects on there cognition performance [1].
As a potent PDE2 inhibitor, Bay 60-7550 suppressed activity of the purified enzyme obtained from bovine heart with an IC50 value of 2 nM. It showed no significant effects on other PDEs including PDE1, 3B, 4B, 5, 7B, 8A, 9A, 10A and 11A. For other similar receptors or enzymes, the IC50 values of Bay 60-7550were all more than 10 μM. Besides that, Bay 60-7550 had no effects on adenosine deaminase even though the concentration was up to 10 μM. In cultured rat cortical neurons and hippocampal neurons, the combination therapy of Bay 60-7550 and Bay 41-8543 resulted in notably increase of cGMP levels. In rat hippocampal slices, treatment of Bay 60-7550 caused a significant higher potentiation of the field excitatory postsynaptic potential slope [1].
In rodent models, oral administration of Bay 60-7550 at doses of 1 and 3 mg/kg resulted in improvement of memory performance. In addition, Bay 60-7550 was found to mediate decrease of oxidative stress in mice models. It significantly reversed the decrease of both percentage of open arm entries and percentage of open arm time induced by oxidative stress at dose of 3 mg/kg in the elevated plus-maze test [1 and 2].
References:
[1] Boess FG, Hendrix M, van der Staay FJ, Erb C, Schreiber R, van Staveren W, de Vente J, Prickaerts J, Blokland A, Koenig G. Inhibition of phosphodiesterase 2 increases neuronal cGMP, synaptic plasticity and memory performance. Neuropharmacology. 2004 Dec;47(7):1081-92.
[2] Masood A, Nadeem A, Mustafa SJ, O'Donnell JM. Reversal of oxidative stress-induced anxiety by inhibition of phosphodiesterase-2 in mice. J Pharmacol Exp Ther. 2008 Aug;326(2):369-79.

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References on Bay 60-7550

The phosphodiesterase type 2 inhibitor BAY 60-7550 reverses functional impairments induced by brain ischemia by decreasing hippocampal neurodegeneration and enhancing hippocampal neuronal plasticity.[Pubmed:27813297]

Eur J Neurosci. 2017 Feb;45(4):510-520.

Cognitive and affective impairments are the most characterized consequences following cerebral ischemia. Bay 60-7550, a selective phosphodiesterase type 2 inhibitor (PDE2-I), presents memory-enhancing and anxiolytic-like properties. The behavioral effects of Bay 60-7550 have been associated with its ability to prevent hydrolysis of both cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) thereby interfering with neuronal plasticity. Here, we hypothesize that PDE2-I treatment could promote functional recovery after brain ischemia. Mice C57Bl/6 were submitted to bilateral common carotid artery occlusion (BCCAO), an experimental model of transient brain ischemia, for 20 min. During 21 days after reperfusion, the animals were tested in a battery of behavioral tests including the elevated zero maze (EZM), object location task (OLT) and forced swim test (FST). The effects of Bay 60-7550 were evaluated on neuronal nuclei (NeuN), caspase-9, cAMP response element-binding protein (CREB), phosphorylated CREB (pCREB) and brain-derived neurotrophic factor (BDNF) expression in the hippocampus. BCCAO increased anxiety levels, impaired hippocampus-dependent cognitive function and induced despair-like behavior in mice. Hippocampal neurodegeneration was evidenced by a decrease in NeuN and increase incaspase-9 protein levels in BCCAO mice. Ischemic mice also showed low BDNF protein levels in the hippocampus. Repeated treatment with Bay 60-7550 attenuated the behavioral impairments induced by BCCAO in mice. Concomitantly, Bay 60-7550 enhanced expression of pCREB and BDNF protein levels in the hippocampus of ischemic mice. The present findings suggest that chronic inhibition of PDE2 provides functional recovery in BCCAO mice possibly by augmenting hippocampal neuronal plasticity.

Description

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

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