PERSANTIN TABLET 75 mg

البلد: سنغافورة

اللغة: الإنجليزية

المصدر: HSA (Health Sciences Authority)

اشتر الآن

العنصر النشط:

DIPYRIDAMOLE

متاح من:

BOEHRINGER INGELHEIM SINGAPORE PTE. LTD.

ATC رمز:

B01AC07

جرعة:

75 mg

الشكل الصيدلاني:

TABLET, SUGAR COATED

طريقة التعاطي:

ORAL

نوع الوصفة الطبية :

Prescription Only

المصنعة من قبل:

Delpharm Reims

تاريخ الترخيص:

1988-06-08

نشرة المعلومات

                                PROPOSED PI FOR MY/SG-DELPHARM-FINAL TEXT 
PERSANTIN 
 
 
 
abcd 
 
 
COMPOSITION 
1 sugar coated tablet contains 25 mg or75 mg  
2,6-bis(diethanolamino)-4,8-dipiperidino-pyrimido(5,4-d)-pyrimidine
 (= dipyridamole) 
 
PROPERTIES  
Dipyridamole inhibits the uptake of adenosine into
erythrocytes, platelets and endothelial cells in vitro and in
vivo; the inhibition amounts to 80% at its maximum and occurs
dose-
dependently at therapeutic concentrations (0.5 – 2
mcg/ml). Consequently,there is an increased concentration
of adenosine locally
to act on the platelet A2-receptor, stimulating 
platelet adenylate cyclase, thereby increasing platelet cAMP
levels. Thus, platelet aggregation in response to various stimuli
such as PAF, collagen and ADP is inhibited. 
Reduced platelet aggregation reduces platelet consumption towards
normal levels. In addition, adenosine has a vasodilator effect and
this is one of the mechanisms by which 
dipyridamole produces vasodilation. 
Dipyridamole inhibits phosphodiesterase (PDE) in various
tissues. Whilst the inhibition of cAMP-PDE is weak, therapeutic
levels inhibit cGMP-PDE, thereby augmenting the 
increase in cGMP produced by EDRF (endothelium-derived relaxing
factor, identified as NO). 
Dipyridamole also stimulates the biosynthesis and release
of prostacyclin by the endothelium . 
Dipyridamole reduces the thrombogenicity of subendothelial
structures by increasing the concentration of the protective
mediator 13-HODE (13-hydroxyoctadecadienic acid). 
 
PHARMACOKINETICS 
(Most pharmacokinetic data refer to healthy volunteers.) 
Dipyridamole shows dose linearity for all doses used in therapy . 
After dosing with the sugar-coated tablets there is a lag
time of 10 - 15 min associated with disintegration of the
tablet and gastric emptying. Thereafter the drug is rapidly 
absorbed and peak plasma concentrations are attained after 1
hour. Geometric mean (range) peak plasma concentrations
at ste
                                
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