Aminaftone, a derivative of 4-aminobenzoic acid, inhibits endothelin-1 (ET-1) production and is used to study hypertension and systemic sclerosis.

In cell cultures, Aminaftone inhibits the production of Endothelin-1 (ET-1) by interfering with the transcription of the pre-pro-endothelin-1 (PPET-1) gene. Concentrations of ET-1 and PPET-1 relative gene expression increase upon incubation with IL-1beta. Aminaftone, when incubated in a concentration-dependent manner, significantly reduces the production of ET-1. A strong direct correlation is observed between ET-1 concentrations and PPET-1 relative gene expression. It is noteworthy that Aminaftone does not influence the activity of endothelin-converting enzyme (ECE)[2].

After 5 weeks, rats are randomly assigned to the following experimental groups: Control; Monocrotaline; Aminaftone 30 mg/kg/day; Aminaftone 150 mg/kg/day. In animals treated with Aminaftone at both doses, mortality is significantly lower compared to those treated with Monocrotaline alone. Aminaftone, especially at the highest dose, reduces the plasma concentration of ET-1 and appears to decrease right heart hypertrophy and the wall thickness of the pulmonary arteries. At the end of the experiment, no rats die in the control and Aminaftone 150 groups, while mortality is 38% in the Monocrotaline group and 13% in the Aminaftone 30 group. Overall, rats treated with Aminaftone show a significantly lower mortality compared to rats in the Monocrotaline group (P=0.044)[1].

DMSO: 60 mg/mL (193.97 mM), Sonication is recommended.