Optivia Signs Agreement With U.S. FDA to Assess Role of Dietary Supplements in Drug-Induced Liver Injury

Research Will Evaluate Effect of Dietary Supplements on Key Drug Transporters

MENLO PARK, Calif.--()--Optivia Biotechnology Inc., a leading provider of in vitro transporter assay services, today announced that the company and the U.S. Food and Drug Administration (FDA) have signed a collaboration agreement to assess the effect of dietary supplements on key drug transporters. The goal of the collaboration is to identify potentially harmful drug-dietary supplement interactions, such as an interaction with acetaminophen and other drugs associated with liver toxicity.

The importance of drug transporters to drug safety is gaining increased attention, aided by a recent report from the International Transporter Consortium (“Membrane Transporters in Drug Development,Nature Reviews-Drug Discovery, March 2010), which identified the most clinically significant transporter-related drug-drug interactions.

The research collaboration will assess the ability of various dietary supplements, including black cohosh, green tea, ginko biloba, kava, usnic acid and potentially others, to affect various drug transporters. As a starting point, the seven transporters cited by the International Transporter Consortium and the FDA as the most clinically relevant to transporter-related drug-drug interactions will be examined using Optivia’s transporter technology platform. This novel platform features polarized mammalian cell assays that closely model human biology. Optivia and the FDA will then analyze and interpret the drug transporter data as preparation for publishing the results.

“This project further advances Optivia’s leadership position in the development of quantitative tools for optimizing the safety and efficacy of drugs,” stated Yong Huang, Ph.D., president and chief executive officer of Optivia Biotechnology. “We are excited about this opportunity to expand the use of our technology to examine the role of dietary supplements in causing drug-related liver injury.”

Drug-induced liver toxicity is estimated to be responsible for as many as five percent of all hospital admissions and 50 percent of all acute liver failures. It is well established that transporters greatly influence the disposition by the liver of a number of commonly used drugs (e.g. antibiotics, statins, and hypoglycemic agents) and others that were subsequently removed from the market (e.g. the antidepressant nefazodone).

About Optivia Biotechnology

Based in Menlo Park, CA, Optivia Biotechnology, Inc. is a leader in developing and providing comprehensive in vitro transporter assay services to help in the discovery and development of drugs with improved safety and efficacy. Optivia uses its proprietary Opti-ExpressionTM technology to create transporter assays that more closely model human biology, and is the only company to conduct all its assays in polarized mammalian cells as opposed to frog or insect-based models or non-polarized models. Optivia’s clients and collaborators include pharmaceutical and biotechnology companies, academic groups and research institutions. A pioneer in the field of transporter biology, Optivia is committed to leading the development of clinically relevant assays in support of the FDA’s goals to improve drug efficacy and safety. For more information about Optivia Biotechnology, its technologies and services, visit www.optiviabio.com.

Contacts

Optivia Biotechnology
Yong Huang, Ph.D., 650-324-3177, ext. 11
President and CEO
yhuang@optiviabio.com
or
For Optivia Biotechnology
Carole Melis, 650-342-5686
Media Relations
clmcomm1@gmail.com

Release Summary

The U.S. FDA and Optivia Biotechnology, leading providers of transporter assay services, entered into a research collaboration assessing the role of dietary supplements in drug-induced liver injury.

Contacts

Optivia Biotechnology
Yong Huang, Ph.D., 650-324-3177, ext. 11
President and CEO
yhuang@optiviabio.com
or
For Optivia Biotechnology
Carole Melis, 650-342-5686
Media Relations
clmcomm1@gmail.com