| Stereochemistry | ACHIRAL |
| Molecular Formula | C20H14ClN3 |
| Molecular Weight | 331.798 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
ClC1=CC(NC2=NN=C(C3=CC=CC=C3)C4=CC=CC=C24)=CC=C1
InChI
InChIKey=CEHQLKSLMFIHBF-UHFFFAOYSA-N
InChI=1S/C20H14ClN3/c21-15-9-6-10-16(13-15)22-20-18-12-5-4-11-17(18)19(23-24-20)14-7-2-1-3-8-14/h1-13H,(H,22,24)
| Molecular Formula | C20H14ClN3 |
| Molecular Weight | 331.798 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
MY-5445 is specific inhibitor of cyclic GMP phosphodiesterase with potent platelet anti-aggregation activity. MY-5445 significantly elevated cyclic GMP content in human plateıts but had no effect on cyclic AMP content, suggesting that the drug affects principally the cyclic GMP metabolism in the platelet. MY-5445 significantly increases contractility, measured in the perfused heart and isolated cardiomyocytes, in hypertrophied right ventricle (RVH) but not normal right ventricle (RV).
Originator
Approval Year
Targets
| Primary Target | Pharmacology | Condition | Potency |
|---|---|---|---|
| 500.0 nM [IC50] | |||
| 16000.0 nM [Ki] | |||
| 9500.0 nM [Ki] |
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
PubMed
Patents
Sample Use Guides
Male Wistar rats were treated with MY-5445 (50 mkg/paw) as a single dose.
Route of Administration:
Other
Human citrated PRP containing 5 x 10^6 platelets/mkl was prepared from blood obtained from healthy volunteers. The effect of MY-5445 on platelet aggregation was studied by the turbidimetric method, with an aggregation meter (RAM41; Rikadenki Kogyo Co., Ltd., Japan). MY-5445 (5 mkl) was added to 0.25 ml of PRP and incubated at 37’C with stirring for 2 mm before the addition of aggregating agents (25 zl of collagen, ADP or arachidonic acid). Final concentrations ofeach aggregating agents were 3 mkM ADP, 3 mkg/ml collagen and 100 mkg/ml arachidonic acid. The extent of aggregation was expressed by the maximum change of light transmission for PRP and platelet-poor plasma as a value of 100%. The percent inhibition of aggregation by the test compounds was calculated by dividing the percent aggreıtion in the presence of the test compound by that observed in the control run, and multiplying by 100.
