Compound Information | SONAR Target prediction |
Name: | Ticlopidine hydrochloride |
Unique Identifier: | Prest502 |
MolClass: | Checkout models in ver1.5 and ver1.0 |
Molecular Formula: | C14Cl2H15NS |
Molecular Weight: | 285.128 g/mol |
X log p: | 13.715 (online calculus) |
Lipinksi Failures | 1 |
TPSA | 28.54 |
Hydrogen Bond Donor Count: | 0 |
Hydrogen Bond Acceptors Count: | 1 |
Rotatable Bond Count: | 2 |
Canonical Smiles: | Cl.Clc1ccccc1CN1CCc2sccc2C1 |
Generic_name: | Ticlopidine |
Chemical_iupac_name: | 3-[(2-chlorophenyl)methyl]-7-thia-3-azabicyclo[4.3.0]nona-8,10-diene |
Drug_type: | Approved Drug |
Pharmgkb_id: | PA451686 |
Kegg_compound_id: | C07140 |
Drugbank_id: | APRD01257 |
H2o_solubility: | Freely soluble |
Logp: | 3.46 |
Cas_registry_number: | 55142-85-3 |
Drug_category: | Fibrinolytic Agents; Platelet Aggregation Inhibitors; ATC:B01AC05 |
Indication: | Used to reduce the risk of thrombotic stroke (fatal or nonfatal) in patients who have experienced stroke precursors, and in patients who have had a completed thrombotic stroke. |
Pharmacology: | Ticlopidine is a platelet aggregation inhibitor structurally and pharmacologically similar to clopidogrel. When taken orally, ticlopidine causes a time- and dose-dependent inhibition of both platelet aggregation and release of platelet granule constituents, as well as a prolongation of bleeding time. The intact drug has no significant in vitro activity at the concentrations attained in vivo; and, although analysis of urine and plasma indicates at least 20 metabolites, no metabolite which accounts for the activity of ticlopidine has been isolated. |
Mechanism_of_action: | The active metabolite of ticlopidine prevents binding of adenosine diphosphate (ADP) to its platelet receptor, impairing the ADP-mediated activation of the glycoprotein GPIIb/IIIa complex. It is proposed that the inhibition involves a defect in the mobilization from the storage sites of the platelet granules to the outer membrane. No direct interference occurs with the GPIIb/IIIa receptor. As the glycoprotein GPIIb/IIIa complex is the major receptor for fibrinogen, its impaired activation prevents fibrinogen binding to platelets and inhibits platelet aggregation. By blocking the amplification of platelet activation by released ADP, platelet aggregation induced by agonists other than ADP is also inhibited by the active metabolite of ticlopidine. |
Organisms_affected: | Humans and other mammals |