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BAY-60-7550

Cat. No. M1734

All AbMole products are for research use only, cannot be used for human consumption.

BAY-60-7550 Structure
Synonym:

BAY 607550

Size Price Availability
5mg USD 180  USD180 Out of stock
10mg USD 300  USD300 Out of stock
50mg USD 880  USD880 Out of stock
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Quality Control & Documentation
Biological Activity

BAY-60-7550 is a potent Type 2 cyclic nucleotide phosphodiesterases (PDE2) inhibitor with IC50 values of 2.0 nM (bovine) and 4.7 nM (human). BAY-60-7550 is an analog of EHNA, which is more than 100-fold more potent and is highly selective for PDE2A.

Customer Product Validations & Biological Datas
Source Neurobiol Aging (2015). Figure 1. BAY-60-7550
Method i.v.
Cell Lines mice
Concentrations 3 mg/kg
Incubation Time 24 h
Results Bay 60-7550-treated mice (3 mg/kg) took significantly less time to reach the platform position, and made more crossings over the platform, than stressed mice
Protocol (for reference only)
Cell Experiment
Cell lines human distal pulmonary artery smooth muscle cells
Preparation method Cell proliferation.
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, were monitored as we have described previously 29 following treatment with BAY 60-7550 (1μmol/L), ANP (1μmol/L), DETA-NONOate (10μmol/L), or treprostinil (1μmol/L), alone or in combination.
Concentrations 1μmol/L
Incubation time unknow
Animal Experiment
Animal models Oxidative Stress on Behavior in mice
Formulation dissolved in 50% dimethyl sulfoxide (Fisher Scientific Co., Pittsburgh, PA)
Dosages 3 mg/kg; given 30 min before each BSO treatment
Administration i.p.
Chemical Information
Molecular Weight 476.57
Formula C27H32N4O4
CAS Number 439083-90-6
Solubility (25°C) DMSO 5 mg/mL
Storage Powder          -20°C   3 years ;  4°C   2 years
In solvent       -80°C   6 months ;  -20°C   1 month
References

[1] Bubb KJ, et al. Circulation. Inhibition of phosphodiesterase 2 augments cGMP and cAMP signaling to ameliorate pulmonary hypertension.

[2] Xu et al. Int J Neuropsychopharmacol. Phosphodiesterase-2 inhibitor reverses corticosterone-induced neurotoxicity and related behavioural changes via cGMP/PKG dependent pathway.

[3] Ren et al. Hypertension. Mechanisms of carbon monoxide attenuation of tubuloglomerular feedback.

[4] Rodefer et al. Neuropharmacology. Selective phosphodiesterase inhibitors improve performance on the ED/ID cognitive task in rats

[5] Lee et al. Basic Res Cardiol. PDE5A suppression of acute beta-adrenergic activation requires modulation of myocyte beta-3 signaling coupled to PKG-mediated troponin I phosphorylation.

[6] Masood A, et al. J Pharmacol Exp Ther. Reversal of oxidative stress-induced anxiety by inhibition of phosphodiesterase-2 in mice.

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  Catalog
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Keywords: BAY-60-7550, BAY 607550 supplier, PDE, inhibitors, activators

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