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  • Title: SIN-1, the main metabolite of molsidomine, inhibits prostaglandin endoperoxide analogue- and arachidonic acid-induced platelet aggregation as well as platelet thromboxane A2 formation.
    Author: Block HU, Förster W, Heinroth I.
    Journal: Arzneimittelforschung; 1982; 32(3):189-94. PubMed ID: 6896278.
    Abstract:
    N-Carboxy-3-morpholinosydnone imine ethyl ester (molsidomine) and its main metabolite 3-morpholinosydnone imine (SIN-1) were investigated in rabbit platelet-rich plasma (PRP) for antiaggregatory activity and inhibition of thromboxane A2 (TXA2) generation (arachidonic acid (AA)-induced) as well as in human PRP regarding prostaglandin endoperoxide analogue (U-46 619)- and AA-induced aggregation and TXB2 formation. The results were compared with the effects of nictindole. In rabbit PRP the inhibitory effects of molsidomine on aggregation and TXA2 generation were 20fold lower than that of SIN-1. The IC50-values of SIN-1, which is the pharmacologically active biotransformation product of molsidomine, were about 1 mumol/l in the experimental models used. The inhibitory effects of nictindole were about 50 times higher than those of SIN-1. In human PRP the inhibitory potency of SIN-1 decreased in the following sequence: U-46 619-induced aggregation (IC50 = 0.9 mumol/l) greater than AA-induced aggregation (IC50 = 1.4 mumol/l) greater than TXB2 formation (IC50 = 2.9 mumol/l). Molsidomine was nearly without effect in human PRP. Our own preliminary results and findings obtained by other authors seem to exclude a direct effect of SIN-1 on cyclooxygenase and thromboxane synthetase. The possible clinical significance of our findings in different types of angina pectoris and for myocardial infarction is discussed.
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