| Identification | Back Directory | [Name]
BAY 73-6691 | [CAS]
794568-92-6 | [Synonyms]
(R)-BAY 73-6691
BAY 736691,BAY 73 6691
BAY 73-6691 >=98% (HPLC), powder
1-(2-Chlorophenyl)-6-[(2R)-3,3,3-trifluoro-2-methylpropyl]-1,5-dihydro-4H-pyrazolo[3,4-d]pyrimidine-4-one
4H-Pyrazolo[3,4-d]pyrimidin-4-one, 1-(2-chlorophenyl)-1,5-dihydro-6-[(2R)-3,3,3-trifluoro-2-methylpropyl]- | [Molecular Formula]
C15H12ClF3N4O | [MDL Number]
MFCD08705319 | [MOL File]
794568-92-6.mol | [Molecular Weight]
356.73 |
| Hazard Information | Back Directory | [Uses]
BAY 73-6691 has been used as a phosphodiesterase 9 inhibitor in ischemic heart samples and in structural studies. It may be used as a PDE 9 inhibitor in neuroblastoma?SH-SY5Y cells. | [Biochem/physiol Actions]
BAY 73-6691 was characterized in vitro as the first potent and selective inhibitor of phosphodiesterase 9 (PDE9), which is currently under preclinical development for the treatment of Alzheimer′s disease. This compound selectively inhibits human (IC50 = 55 nM) and murine (IC50 = 100 nM) PDE9 activity in vitro and shows only moderate activity against other cyclic nucleotide-specific phosphodiesterases. BAY 73-6691 alone did not significantly increase basal cGMP levels. The PDE9 inhibitor significantly potentiated the cGMP signals generated by sGC activating compounds such as BAY 58-2667 or 5-cyclopropyl-2-[1-(2-fluorobenzyl)-1H-pyrazolo[3,4-b]pyridin-3-yl]pyrimidin-4-ylamine (BAY 41-2272) and induced leftward shifts of the corresponding concentration-response curves. The newly generated PDE9 reporter cell line show that BAY 73-6691 is able to efficiently penetrate cells and to inhibit intracellular PDE9 activity. | [in vivo]
BAY 73-6691 dose-dependently improves the acquisition performance in the Aβ25-35-injected mice on days 7 to 10 (day 7, F(5,54)=65.153; day 8, F(5,54)=62.340; day 9, F(5,54)=37.529; day 10, F(5,54)=38.624; P<0.001). BAY 73-6691 at 3 mg/kg can almost completely abolish the prolongation of escape-latency on days 9 to 10. BAY 73-6691 dose-dependently elevates the Aβ25-35-induced decrease of the dwell time on the 10th day post Aβ25-35 injection (day 10, F(5,54)=27.360, P<0.001). Results reveal that the Aβ25-35 injection and BAY 73-6691 treatment cause no influence on the swimming speed. Treatment with BAY 73-6691 does not cause detectable alteration of spatial memory in sham mice. BAY 73-6691 alleviates Aβ25-35-induced abnormalities of the above indices. The BAY 73-6691 causes no influence on the four indices mentioned above in sham mice. The BAY 73-6691 has no significant effect on the apoptosis of hippocampal neurons in sham mice[1]. | [IC 50]
PDE9 | [storage]
Store at -20°C |
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| Company Name: |
BOC Sciences
|
| Tel: |
1-631-485-4226; 16314854226 |
| Website: |
https://www.bocsci.com |
| Company Name: |
Sigma-Aldrich
|
| Tel: |
021-61415566 800-8193336 |
| Website: |
https://www.sigmaaldrich.cn |
| Company Name: |
Twochem Co.Ltd.
|
| Tel: |
021-58111628 15800915896 |
| Website: |
cn.twochem.com |
| Company Name: |
Energy Chemical
|
| Tel: |
021-58432009 400-005-6266 |
| Website: |
http://www.energy-chemical.com |
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