Carbazochrome sodium sulfonate (AC-17) is an antihemorrhagic agent used for treating hemorrhoids.

Administering 10 mg/kg of Carbazochrome significantly inhibited the reduction of arterial oxygen levels. Additionally, at the same dosage, Carbazochrome reversed the iodocetate-induced increase in vascular permeability in rats in a dose-dependent manner.

Carbazochrome at concentrations of 0.1-1 M attenuates concentration-dependent synthesis of [(3)H]myo-inositol and [(3)H]-inositol induced by bradykinin and thrombin. It also counteracts the functional impairment caused by trypsin, thrombin, and bradykinin, with ionophores like ionomycin, A23187, or phorbol 12-myristate 13-acetate enhancing this effect without affecting endothelial permeability. In human umbilical vein endothelial cells, carbazochrome significantly reduces the ratio of t-PA antigen in the culture medium without notably affecting the PAI-1 antigen ratio. It reverses trypsin-induced actin stress fiber formation and disrupts VE-cadherin in monolayers of porcine aortic endothelial cells. Additionally, in cultured bovine vascular endothelial cells, carbazochrome distinctly inhibits hyperpermeability induced by trypsin, thrombin, and protease-activated receptor 2 agonist peptides.