HYPOPROTHROMBINEMIA RESULTING FROM THE ADMINISTRATION OF SULFAQUINOXALINE

¹ From the Merck Institute for Therapeutic Research, Rahway, N. J.

The mode of action of sulfaquinoxaline in inducing a prompt hypoprothrombinemia does not appear to be related to anatomic changes in the liver or to inhibition of intestinal bacteria. Although this compound does not destroy or inactivate prothrombin in vitro, the possibility of such an action in vivo has not been excluded.

The rapid prothrombinopenic effect of sulfaquinoxaline cannot be attributed alone to either the sulfanilamido or the quinoxaline portion of the molecule, but is due to the combination of both as present in this sulfonamide. Transposition of the sulfanilamido group from the 2 to the 6 position resulted in loss of this activity.

Vitamin K₁ (2-methyl-3-phytyl-l, 4-naphthoquinone) was found to be 100-250 times more effective, on a weight basis, than menadione (2-methyl-l,4-naphthoquinone) in preventing the hypoprothrombinemia which results from the administration of sulfaquinoxaline.