PERSANTIN INJECTION 10 mg2 ml

Country: Singapore

Language: English

Source: HSA (Health Sciences Authority)

Active ingredient:

DIPYRIDAMOLE

Available from:

ZUELLIG PHARMA PTE. LTD.

ATC code:

B01AC07

Dosage:

10 mg/2 ml

Pharmaceutical form:

INJECTION

Composition:

DIPYRIDAMOLE 10 mg/2 ml

Administration route:

INTRAVENOUS, INTRAMUSCULAR

Prescription type:

Prescription Only

Manufactured by:

Delpharm Dijon

Authorization status:

ACTIVE

Authorization date:

1988-03-28

Patient Information leaflet

 
0150-03 
20090424 
abcd 

PERSANTIN
®

COMPOSITION 
Yellow, clear solution.  
1 ampoule of 2 ml contains 

10 mg 
1 vial of 10 ml contains 

50 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  concentrations  of  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. 
Presumably  via  a  'steal  effect'  the  vasodilation  induced  by  PERSANTIN  administered  i.v.  in doses  used  for  cardiac  imaging  techniques  leads  to 
regional redistribution of coronary blood flow and may lead to abnormalities in thallium distribution and ventricular function in patients with coronary 
artery  disease.  The  normal  vessels  dilate  with  enhanced  flow,  leaving  relatively  reduced  pressure  and  flow  across  areas  of  haemodynamically 
important coronary stenoses. 
Dipyridamole  inhibits  phosphodiesterase  (PDE)  in  various  tissues.  Whilst  the  inhibition  of  cAMP-PDE  is  weak,  therapeutic  levels  inhibit  cGMP-

Summary of Product characteristics

Druckfarben
Datum/Signatur
KORREKTUR ERBETEN
DRUCKFREIGABE
Auftrags-Nr.
23/0315
erstellt
27.09.23
WO
Produktbezeichnung
PERSANTIN
AMPULLEN
SG
Maße in mm
148 X 210
PACKAGE INFORM.
N84
Artikel-Nr.
3502349801
706648
CODE 706648
Druckfarben
PANTONE BLACK C
kleinste Schriftgröße
9 PT / OFFICINA SANS
PERSANTIN®
COMPOSITION
Yellow, clear solution.
1 ampoule of 2 ml contains
10 mg
1 vial of 10 ml contains
50 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 concentrations of 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.
Presumably via a ’steal effect’ the vasodilation
induced by PERSANTIN administered i.v. in doses
used for cardiac imaging techniques leads to
regional redistribution of coronary blood flow
and may lead to abnormalities in thallium
distribution and ventricular function in patients
with coronary artery disease. The normal vessels
dilate with enhanced flow, leaving relatively
reduced pressure and flow across areas of
haemodynamically important coronary stenoses.
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 e