Evaluation of Active Hexose Correlated Compound (Ahcc) on Phase Ii Drug Metabolism Pathways and the Implications for Supplement-Drug Interactions
|Larry W Coffer1, Lata Mathew1, Xue Zhang2, Norah A. Owiti3, Alan L Myers4, Jonathan Faro5 and Judith A Smith1,3*|
|1Department of Obstetrics, Gynecology and Reproductive Sciences, University of Texas Health Science Center Medical School at Houston, Houston, TX, 77030, USA|
|2The Division of Surgery, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA|
|3The University of Texas Graduate School of Biomedical Sciences, Houston, TX, 77030, USA|
|4Division of Pharmacy, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA|
|5Specialists in Obstetrics and Gynecology, Houston, TX, 77030, USA|
|Corresponding Author :||Judith A. Smith
Associate Professor, UT Health- University of Texas Medical School at Houston
Department of Obstetrics, Gynecology and Reproductive Sciences, Houston
Texas 77030, USA
Tel: 713- 500-6408
E-mail: Judith.Ann.Smith@ uth.tmc.edu
|Received: July 31, 2015; Accepted: August 13, 2015; Published: August 21, 2015|
|Citation: Coffer LW, Mathew L, Zhang X, Owiti NA, Myers AL, et al. (2015) Evaluation of Active Hexose Correlated Compound (Ahcc) on Phase Ii Drug Metabolism Pathways and the Implications for Supplement-Drug Interactions. J Integr Oncol 4:142.doi:10.4172/2329-6771.1000142|
|Copyright: © 2015 Coffer LW, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
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Background: The evaluation of active hexose correlated compound (AHCC) on hepatic metabolism mediateddrug interaction is critical in current clinical setting as there is little published information on the potential effect on drug efficacy and safety. The primary objective of this study was to evaluate the potential phase II hepatic metabolism pathways associated with the metabolism of AHCC and to determine potential drug/AHCC interactions.
Methods: Four primary hepatic metabolism phase II pathways were evaluated: glutathione S-transferase (GST), quinone oxidoreductase (QOR), catechol-O-methyltransferases (COMT) and uridine diphosphate (UDP)- glucuronosyltransferase (UGT). Pooled human liver microsomes and human liver S9 fractions were utilized to evaluate QOR and UGT metabolism inhibition assays. The pool human liver S9 fractions were used to assess GST activity. Cryopreserved inducible human liver hepatocytes were used to evaluate potential induction of UGT and COMT metabolism. All experiments were carried out in triplicate.
Results: Data demonstrated that AHCC is not an inhibitor of GST or UGT pathways, but may be a potential inhibitor of QOR pathway. Evaluation of induction of the phase II pathways demonstrated that AHCC showed potential induction of the UGT 1A3 and 1A6 pathways. There was no induction of the COMT pathway.
Conclusion: Historically, drug interaction studies have only focused on Phase I metabolism pathways, so currently there is very limited information regarding the phase II metabolism of most commonly used medications. In conclusion, additional studies are warranted to determine potential of any phase II hepatic interactions with AHCC when administered with other medications or supplement that are substrates of these pathways.