| Stereochemistry | ACHIRAL |
| Molecular Formula | C24H22F3N |
| Molecular Weight | 381.4334 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
FC(F)(F)C1=CC=CC(=C1)C2=CCN(CCC3=CC=C4C=CC=CC4=C3)CC2
InChI
InChIKey=WJJYZXPHLSLMGE-UHFFFAOYSA-N
InChI=1S/C24H22F3N/c25-24(26,27)23-7-3-6-22(17-23)20-11-14-28(15-12-20)13-10-18-8-9-19-4-1-2-5-21(19)16-18/h1-9,11,16-17H,10,12-15H2
| Molecular Formula | C24H22F3N |
| Molecular Weight | 381.4334 |
| 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 |
Xaliproden is an orally active 5HT1-A receptor antagonist that was being developed by Sanofi. It has been evaluated for the treatment of Alzheimer's disease and amyotrophic lateral sclerosis (ALS), and protection against peripheral neurotoxicity associated with certain cancer chemotherapies. Two large, 18-month, clinical trials of xaliproden (monotherapy or
adjunctive therapy, respectively) in patients with mild to moderate AD (MMSE, 16–26,
inclusive) were completed in 2007. Failure to demonstrate sufficient efficacy in both trials
resulted in cancelation of the xaliproden development program for AD in September 2007.
CNS Activity
Originator
Approval Year
PubMed
Patents
Sample Use Guides
Patients with clinically probable or definite ALS of more than 6 months and less than 5 years duration were randomly assigned to placebo, 1 mg or 2 mg xaliproden orally once daily as monotherapy in Study 1
Route of Administration:
Oral
Xaliproden (1 uM) increases the phenotypic survival of embryonic purified mouse motoneurons in vitro to the same extent as brain-derived neurotrophic factor (100 ng/ml), and increases the outgrowth and number of their neurites. It acts in a dose-dependent manner up to 1 uM which is the optimal concentration. Above this concentration, its neurotrophic effect decreases.
