Trapidil
- 7 -diethylamino- 5-methyl- [1,2,4] triazolo [1,5- α ] pyrimidine (IUPAC)
- Trapymin (common name )
- Trapidilum (Latin )
C01DX11
White to off- white crystalline powder
Vasodilator
1.2 g · cm -3
98-99 ° C
2.79
Slightly soluble in water, soluble in dichloromethane and anhydrous ethanol
- 235 mg · kg -1 ( LD50, rat, oral)
- 155 mg · kg -1 ( LD50, mouse, ip)
Template: Infobox chemical / molecular formula search available
Trapidil is a drug which in the form of capsules and injections for the treatment of coronary heart disease ( CHD), is used for prophylaxis of cardiovascular complications after myocardial infarction and in the treatment of peripheral arterial occlusive disease. It acts primarily as a non-selective phosphodiesterase inhibitor with a widening of the coronary arteries and inhibits platelet aggregation beyond. Trapidil was developed in the 1960s by the hydrogenation plant in Rodleben and at the Institute of Pharmacology, Martin Luther University Halle- Wittenberg.
- 2.1 Mechanism of action ( pharmacodynamics )
- 2.2 intake and excretion ( pharmacokinetics )
- 3.1 Chemical Information
- 3.2 History
Clinical information
Areas of application (indications )
Trapidil is primarily used for the treatment of coronary heart disease (CHD ) by reducing the preload and afterload of the heart muscle, especially in patients with an intolerance to the standard used ingredients from the class of nitrates. In addition, it decreases after a myocardial infarction, the incidence of other cardiovascular complications. In patients with peripheral arterial occlusive disease Trapidil improves blood flow to the limbs and walking performance.
Route of Administration
The use of Trapidil made either orally in capsule form or by intravenous injection. The use in drug - eluting stents ( drug-eluting stents ) is in clinical trials.
Adverse effects (side effects)
Uncommon side effects of treatment with Trapidil are nausea and vomiting, loss of appetite, malaise and bloating in the abdominal area as well as headaches. The rarely occurring adverse effects include allergic reactions and orthostatic hypotension and a feeling of pressure in the chest area, both of which are possibly associated with a too rapid intravenous administration. Serious complications have not been described.
Pharmacological properties
Mechanism of action ( pharmacodynamics )
Trapidil acts primarily as a non-selective phosphodiesterase inhibitor on an extension of the coronary vessels ( vasodilation ). Moreover, it inhibits the platelet aggregation, and the synthesis of thromboxane A2, whereby the fluidity of the blood increases. It also regulates the concentration of calcium in vascular smooth muscle cells and cardiac myocytes.
Absorption and excretion ( pharmacokinetics )
Trapidil has a high bioavailability and a half-life of approximately 2.4 hours after oral uptake. Biotransformation takes place primarily in the liver, the main metabolite is Desethyltrapidil. Repeated application likely to result in induction of the appropriate metabolizing enzymes. Excretion is almost completely within 24 hours via the kidneys.
Other Information
Chemical information
From a chemical point of view, at Trapidil a triazolopyrimidine, the IUPAC name is N, N -diethyl -5-methyl - [ 1,2,4 ] triazolo [1,5 -a] pyrimidin-7 -amine.
History
Trapidil 1964 German VEB hydrogenizing in Rodleben in the former German Democratic Republic (GDR) was first synthesized, analyzed in subsequent years at the Institute of Pharmacology, Martin Luther University Halle- Wittenberg and 1971 allowed for the GDR market. Three years later, the licensing of sales in Japan, where it has been approved since 1979 and is the most commonly prescribed agents for the treatment of CHD. In addition, it is also on the Italian pharmaceutical market of relevance. It is thus one of the few preparations from drug research in the GDR, which have gained importance in Western countries. The approval in the Federal Republic of Germany took place in 1992 under the trade name Rocornal.