Nafazatrom [BAY G 6575] is a leukotriene synthesis inhibitor that was being developed by Bayer in Germany. It is a pyrazolinone derivative with potential antimetastatic activities. Nafazatrom, originally developed as an antithrombotic agent, inhibits the key prostaglandin catabolic enzyme, 15-hydroxyprostaglandin dehydrogenase, which prolongs the biological half-life of prostacyclin (prostaglandin I2; PGI2) and prevents intravascular coagulation. Nafazatrom, in the micromolar range, inhibits the metabolism of PGs (prostaglandins) by 15-OH PGDH in a dose-dependent manner. The IC50 for inhibition of 15-OH PGDH was estimated to be 18.5 uM when [3H]PGF2 alpha was used as substrate. This agent also serves as a reducing cofactor with the hydroperoxidase moiety of cyclooxygenase and accelerates the conversion of arachidonic acid into precursors of PGI2. An elevated level of PGI2 prevents aggregation of platelets; subsequently it decreases the formation of tumor cell-platelet aggregates as well as their sequestration in blood vessels, which is an important initiating step in the development of metastasis. Nafazatrom may have had potential as an antithrombotic, anti-ischaemic and antiasthmatic agent. However, the development of nafazatrom was discontinued.