Based on rates of Raloxifene glucuronidation and known extrahepatic expression, UGT1A8 and 1A10 appear to be primary contributors to Raloxifene glucuronidation in human jejunum microsomes. For human liver microsomes, the variability of Raloxifene 4'-glucuronide formation is 4-fold. Treatment of expressed UGTs with alamethicin results in minor increases in enzyme activity, whereas in human intestinal microsomes, maximal increases of 9-fold for the Raloxifene 4'-glucuronide are observed. Intrinsic clearance values in intestinal microsomes are 95 μl/min/mg for the Raloxifene 4'-glucuronide[2].