Phalloidin, from Amanita phalloides, which accounts for the most frequent and severe intoxications due to wild mushrooms is selectively taken up by hepatocytes induces cholestasis, necrosis and hence hepatic insufficiency. In many cases liver transplant is the only possible therapy. As an alternative strategy it has been suggested to inhibit its hepatic uptake, promoting the urinary excretion. Several cholefilic compounds, aimed to inhibit phalloidin uptake have been synthesized. The biological characteristics of one of them, 3a-succinyl-7a,12a-dihidroxy-5b-colanoic acid (BALU-1) have been investigated. Using transporter expression in Xenopus laevis oocytes to carry out functional studies (Briz et al., 2002). BALU-1 was found to inhibit [3H]-taurocholic acid (TCA) uptake by human OATP1B1 (-95%), OATP1B3 (-15%) and rat Oatp1a1 (-50%), Oatp1a4 (-35%) and Oatp1b2 (-40%) but to have no effect on Ntcp, the major pathway for liver uptake of natural bile acids. Phalloidin (0.1 mg/100 g) was administred to anaesthetized rats receiving TCA or BALU-1 (i.v. 0.2 mmol/min/100 g for 2.5 h). BALU- a induced a marked increased in bile flow (70%), higher than that induced by TCA (20%). This enhanced choleretic ability probably was accounted for by the fact that critical micellar concentration of BALU-1 is 5-fold lower than that of TCA. Phalloidin administration decreased basal (-60%) and TCA-stimulated bile flow (-55%), without affecting total bile acid output. Cholestasis was accompained by signs of liver necrosis, nephrotoxicity and haematuria. In contrast, in BALU-1 was able to protect against phalloidin hepatotoxicity, probably due to delayed hepatic uptake and enhanced biliary secretion of the toxin.