Stereochemistry | ACHIRAL |
Molecular Formula | C23H26N4O4S |
Molecular Weight | 454.542 |
Optical Activity | NONE |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CCN(CC1=CN=CC=C1)C(=O)CN(C2=CN=C(OC)C=C2)S(=O)(=O)C3=CC=CC=C3C
InChI
InChIKey=KJPHTXTWFHVJIG-UHFFFAOYSA-N
InChI=1S/C23H26N4O4S/c1-4-26(16-19-9-7-13-24-14-19)23(28)17-27(20-11-12-22(31-3)25-15-20)32(29,30)21-10-6-5-8-18(21)2/h5-15H,4,16-17H2,1-3H3
Molecular Formula | C23H26N4O4S |
Molecular Weight | 454.542 |
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 |
N-ethyl-2-[(6-methoxy-pyridin-3-yl)-(toluene-2-sulphonyl)-amino]-N-pyridin-3-ylmethyl-acetamide (EMPA) is a high-affinity, reversible and selective orexin type 2 (OX2) receptor antagonist. The in vivo activity of EMPA was assessed by reversal of orexin-B-induced hyperlocomotion during the resting phase in mice and the reduction of spontaneous locomotor activity (LMA) during the active phase in rats.
CNS Activity
Originator
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
1.1 nM [Ki] |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
---|---|---|---|---|
PubMed
Sample Use Guides
Male NMRI mice: Mice were injected i.p. with EMPA (1, 3, 10, 30, 100, 300 mg·kg−1, n= 8 mice per dose).
Male Wistar rats: one hour after the dark period onset, rats were injected i.p. with EMPA (3, 10, 30 mg·kg−1, n= 8 rats per dose) and immediately placed into the activity monitoring chambers.
Route of Administration:
Intraperitoneal
The distribution and abundance of in vitro binding sites of [3H]EMPA (1 nmol·L−1), measured by quantitative autoradiography and image analysis, was investigated in coronal rat brain sections. A high density of specific binding was observed in many brain regions including the limbic cortices, hippocampus, striatum and hypothalamic nuclei. Non-specific binding (NSB), determined in the presence of 10 µmol·L−1 Cp-5, a selective OX2 receptor antagonist.