| Stereochemistry | ACHIRAL |
| Molecular Formula | C21H25N3 |
| Molecular Weight | 319.4433 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CN1CCC2=C(C1)C3=C(C=CC(C)=C3)N2CCC4=CN=C(C)C=C4
InChI
InChIKey=JNODQFNWMXFMEV-UHFFFAOYSA-N
InChI=1S/C21H25N3/c1-15-4-7-20-18(12-15)19-14-23(3)10-9-21(19)24(20)11-8-17-6-5-16(2)22-13-17/h4-7,12-13H,8-11,14H2,1-3H3
| Molecular Formula | C21H25N3 |
| Molecular Weight | 319.4433 |
| 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 |
Dimebon (latrepirdine) is an orally available, small molecule, gamma carboline derivative that was developed and used in Russia as an over-the-counter oral antihistamine for allergy treatment since 1980s. In 1990s it was shown that Dimebon has promising potential in treating neurodegenerative diseases. In 2003, Medivation Inc acquired the rights to Dimebon. Medivation went public in December 2004, with Dimebon as the only drug in its pipeline. The product was being developed by Medivation and Pfizer as a treatment for early-stage Alzheimer's disease and Huntington's disease. However, development was discontinued by Medivation and Pfizer in early 2012. Dimebon inhibits alpha-Adrenergic receptors (alpha1A, alpha1B, alpha1D, and alpha2A), Histamine H1 and H2 receptors and Serotonin 5-HT2c, 5-HT5A, 5-HT6 receptors with high affinity. Dimebon may act by blocking NMDA receptors or voltage-gated Ca2+ channels and by preventing mitochondrial permeability pore transition.
CNS Activity
Originator
Approval Year
PubMed
Sample Use Guides
As anti-allergic medicine Dimebon was used in
doses 10–20 mg 2–3 times per day.
Oral dimebon, 20 mg three times a day was tested in Alzheimer's disease patients.
Route of Administration:
Oral
50 uM Dimebon stabilized glutamate-induced Ca2+ signals in primary striatal neuronal cultures (MSN) from YAC128 HD transgenic mice (YAC128 MSN) and protected cultured YAC128 MSN from glutamate-induced apoptosis. Lower concentrations of Dimebon (5 uM and 10 uM) did not stabilize glutamate-induced Ca2+ signals and did not exert neuroprotective effects in experiments with YAC128 MSN.
