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. Author manuscript; available in PMC: 2019 Jul 15.
Published in final edited form as: J Enzyme Inhib Med Chem. 2016 Jul 17;31(SUP2):148–161. doi: 10.1080/14756366.2016.1193734

Figure 7.

Figure 7.

Computational docking of clotrimazole (A, CYP26A1; B, CYP26B1), zafirlukast (C, CYP26A1) and candesartan cilexetil (D, CYP26B1) into the active sites of CYP26. The docking orientation of clotrimazole in the active sites of CYP26A1 and CYP26B1 suggests the potential for the imidazole moiety to inhibit the enzyme through type II binding interactions. Active site residues involved in the binding of zafirlukast in the active site of CYP26A1 (R90, W112, F222, and F299) and candesartan cilexetil in the active site of CYP26B1 (W117, F295, F299 and Y372) are similar to the active site residues known to be involved in retinoic acid binding for each isoform. Portions of the protein structure are not displayed for added clarity.