Bay 73-6691

Product NameBay 73-6691
CAS794568-92-6
MFC15H12ClF3N4O
MW356.73
EINECS
MOL File794568-92-6.mol

Chemical Properties

storage temp.	2-8°C
solubility	DMSO: >20mg/mL
form	powder
color	off-white
InChI	1S/C15H12ClF3N4O/c1-8(15(17,18)19)6-12-21-13-9(14(24)22-12)7-20-23(13)11-5-3-2-4-10(11)16/h2-5,7-8H,6H2,1H3,(H,21,22,24)/t8-/m1/s1
InChIKey	FFPXPXOAFQCNBS-MRVPVSSYSA-N
SMILES	C[C@H](CC1=Nc2c(cnn2-c3ccccc3Cl)C(=O)N1)C(F)(F)F

Safety Information

Hazard Codes	T,Xi
Risk Statements	25-36/37/38
Safety Statements	26-45
RIDADR	UN 2811 6.1 / PGIII
WGK Germany	3
Storage Class	6.1A - Combustible acute toxic Cat. 1 and 2 very toxic hazardous materials
Hazard Classifications	Acute Tox. 2 Oral Aquatic Chronic 4 Eye Irrit. 2 Skin Irrit. 2 STOT SE 3

Usage And Synthesis

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 neuroblastomaSH-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 Aβ_25-35-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 Aβ_25-35-induced decrease of the dwell time on the 10th day post Aβ_25-35 injection (day 10, F_(5,54)=27.360, P<0.001). Results reveal that the Aβ_25-35 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 Aβ_25-35-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

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