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| Other names | N-(3,3-diphenylpropyl)amphetamine |
| Routes of administration | Oral |
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| ECHA InfoCard | 100.006.246 |
| Chemical and physical data | |
| Formula | C24H27N |
| Molar mass | 329.487 g·mol−1 |
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Prenylamine (Segontin) is acalcium channel blocker of theamphetaminechemical class that was used as avasodilator in the treatment ofangina pectoris. It producesamphetamine as ametabolite.[1]
Prenylamine was introduced in the 1960s by German manufacturerAlbert-Roussel pharma gmbh,[2][3] which was acquired byHoechst AG in 1974 and which in turn became part ofSanofi Aventis in 2005.
It was withdrawn from market worldwide in 1988 because it causedQT interval prolongation andtorsades de pointes, greatly increasing the risk ofsudden death.[2][4] The cardiac side effects were not detected during clinical development, only becoming apparent after the drug was in wide use.[2]
Prenylamine has two primary molecular targets in humans:calmodulin andmyosin light-chain kinase 2, found in skeletal and cardiac muscle.[5] Pharmacologically, it decreasessympathetic stimulation on cardiac muscle, predominantly through partial depletion ofcatecholamines viacompetitive inhibition of reuptake by storage granules,[clarification needed] leading to further depletion due to spontaneous leakage as a result of disturbance of equilibrium.[clarification needed][6] This depletion mechanism is similar to that ofreserpine because both agents target the same site on the storage granule; however, prenylamine shows a high affinity for cardiac tissue, while reserpine is more selective toward brain tissue.[7]
Prenylamine slows cardiac metabolism via calcium transport delay by blockade of magnesium-dependent calcium transportATPase. It demonstratesbeta blocker–like activity that results in reduction of heart rate but shows an opposing effect on tracheal tissue response.[clarification needed][6]