Urokinase, or two-chain urokinase-type plasminogen activator (tcu-PA),
is an effective thrombolytic agent, Its single-chain precursor (scu-P
A), unlike tcu-PA, is able to selectively activate fibrin-bound plasmi
nogen. The induced clot lysis is amplified by plasmin-triggered conver
sion of scu-PA to tcu-PA. The aim of our study was to compare the hemo
static effects of recombinant unglycosylated scu-PA, INN saruplase, an
d urokinase, at doses considered optimal (80 mg saruplase and 3 millio
n units urokinase) in patients with acute myocardial infarction, withi
n 6 h of onset of pain. Complete sample sets from more than 230 patien
ts in each treatment group have been analyzed. The median hemostatic c
hanges caused by saruplase and urokinase were virtually identical indi
cating that saruplase is converted early in vivo to its active tcu-PA
derivative with the dose regimen used. Fibrinogen degradation products
were higher for saruplase with a maximum at 2 h. They rose markedly a
fter saruplase from 0.43 mg/l at 0 h to a maximum of 160 mg/l at 2 h,
whereas the increase after urokinase (from 0.45 mg/l to 89.0 mg/l) was
significantly smaller (P < 0.001).