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| Clinical data | |
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| Trade names | Cognex |
| AHFS/Drugs.com | Monograph |
| MedlinePlus | a693039 |
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| Routes of administration | Oral, rectal |
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| Pharmacokinetic data | |
| Bioavailability | 2.4–36% (oral) |
| Protein binding | 55% |
| Metabolism | Hepatic (CYP1A2) |
| Eliminationhalf-life | 2–4 hours |
| Excretion | Renal |
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| PDB ligand | |
| CompTox Dashboard(EPA) | |
| ECHA InfoCard | 100.005.721 |
| Chemical and physical data | |
| Formula | C13H14N2 |
| Molar mass | 198.269 g·mol−1 |
| 3D model (JSmol) | |
| Melting point | 183 °C (361 °F) |
| Boiling point | 358 °C (676 °F) |
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Tacrine is a centrally actingacetylcholinesterase inhibitor and indirectcholinergic agonist (parasympathomimetic). It was the first centrally acting cholinesterase inhibitor approved for the treatment ofAlzheimer's disease, and was marketed under the trade nameCognex. Tacrine was first synthesised byAdrien Albert at theUniversity of Sydney in 1949. It also acts as ahistamine N-methyltransferase inhibitor.[2]
Tacrine was the prototypicalcholinesterase inhibitor for the treatment ofAlzheimer's disease.William K. Summers received a patent for this use in 1989.[3][4][5] Studies found that it may have a small beneficial effect on cognition and other clinical measures, though study data was limited and the clinical relevance of these findings was unclear.[6][7]
Tacrine has been discontinued in theUS[8] in 2013, due to concerns over safety.[9]
Tacrine was also described as ananaleptic agent used to promote mental alertness.[10]
As stated above, overdosage of tacrine may give rise to severe side effects such as nausea, vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions.Atropine is a popular treatment for overdose.[12]
Major form of metabolism is in the liver via hydroxylation of benzylic carbon byCYP1A2. This forms the major metabolite1-hydroxy-tacrine (velnacrine) which is still active.[12]
