| Stereochemistry | ABSOLUTE |
| Molecular Formula | C15H17N3O2 |
| Molecular Weight | 271.3144 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 1 / 1 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
O=C(N[C@H]1CN2CCC1CC2)C3=CC4=C(OC=C4)C=N3
InChI
InChIKey=IPKZCLGGYKRDES-ZDUSSCGKSA-N
InChI=1S/C15H17N3O2/c19-15(12-7-11-3-6-20-14(11)8-16-12)17-13-9-18-4-1-10(13)2-5-18/h3,6-8,10,13H,1-2,4-5,9H2,(H,17,19)/t13-/m0/s1
| Molecular Formula | C15H17N3O2 |
| Molecular Weight | 271.3144 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ABSOLUTE |
| Additional Stereochemistry | No |
| Defined Stereocenters | 1 / 1 |
| E/Z Centers | 0 |
| Optical Activity | UNSPECIFIED |
PHA-543613 was discovered by Pfizer and has been under development primarily as a potential treatment of schizophrenia. PHA-543613 acts as an agonist to the Neuronal acetylcholine receptor protein alpha-7 subunit. A single human trial was conducted in healthy human volunteers, but the compound has been studied extensively in rat models for schizophrenia as well as Parkinson's disease and Alzheimer's disease.
CNS Activity
Originator
Approval Year
Doses
AEs
Overview
| CYP3A4 | CYP2C9 | CYP2D6 | hERG |
|---|---|---|---|
OverviewOther
| Other Inhibitor | Other Substrate | Other Inducer |
|---|---|---|
Drug as perpetrator
Drug as victim
Tox targets
Sourcing
PubMed
Patents
Sample Use Guides
Absorption, metabolism, and excretion of PHA-543613 were studied in an open-label human trial. Each participant was given PHA-543613 orally dissolved in 10 mL of Pedialyte followed by 100 mL of water. Subjects were required to fast 10 h before and 4 h after dosing.
Route of Administration:
Oral
Coronal Slices (250 micrometer thickness) were obtained from Sprag-Dawley Rats and equilibrated in buffer containing 50 nM PHA-543613 hydrochloride for 1 hour. Voltammetric recordings were taken in striatal tissue in the dorsal lateral striatum from slices cut posterior 1.5–2 mm from bregma. The combination of PHA-543613 with 500 nM nicotine reduced evoked dopamine to 47 ± 10% (n = 4, p < 0.05) of pre-drug evoked dopamine.
