Trapidil

205.26

205.26

239-434-2

EYG5Y6355E

DTXSID0045416

C - Cardiovascular system

2933990090

46.3

1.7

white to tan

1.20±0.1 g/cm3(Predicted)

100 °C

1.626

>30.8 [ug/mL]

room temp

LD50 in mice, rats (mg/kg): 115, 76 i.v.; 380, 235 orally; 155, 100 i.p.; 132, 100 s.c. (Fuller)

NONH for all modes of transport

3

36/37/38

26

Xi

P261-P305 + P351 + P338

H315-H319-H335

|Warning|H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]|P261, P264, P271, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 38 companies from 1 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Used in the treatment of chronic stable angina.

Trapidil exerts vasodilatory and antiplatelet effects. It also inhibits the activity of platelet derived growth factor (PDGF).

Drugs used to cause dilation of the blood vessels. (See all compounds classified as Vasodilator Agents.)|Compounds which inhibit or antagonize the biosynthesis or actions of phosphodiesterases. (See all compounds classified as Phosphodiesterase Inhibitors.)|Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system. (See all compounds classified as Platelet Aggregation Inhibitors.)

Trapidil has a Tmax of 1 h.|The apparent clearance is 179 mL/min for a single dose and 273 mL/min for steady state dosing.

The half life of elimination is 1.31 h for a single dose and 1.14 h for steady state dosing.

Trapidil is thought to inhibit cyclic adenosine monophosphate (cAMP) phosphodiesterase enzymes. The resultant increase in cAMP potentiates the inhibition of platelets by adenosine. The reduction in platelet activation is likely responsible for the decrease in thromboxane A2 generation seen with trapidil. The increase in cAMP is also likely responsible for the vasdilatory action of trapidil. The increase in protein kinase A activity due to increased cAMP activated L-type calcium channels in the heart leading to increased depolarization and a positive inotropic effect. Lastly, PKA inactivates Raf-1, an activator of mitogen activated protein kinase (MAPK), which leads to a reduction in MAPK activation. This reduction in MAPK prevents mitogenesis due to PDGF binding to PDGF receptors.

Rocornal