Laurence Hurley

laurence hurely

Laurence Hurley

Dr. Laurence H. Hurley was born in 1944 in Birmingham, England. He received his BPharm with honors in 1967 from Bath University and his PhD in medicinal chemistry in 1970 from Purdue. He has served on the faculties at the University of Maryland, the University of Kentucky and the University of Texas at Austin. In 2000, Hurley joined the University of Arizona as the Howard J. Schaeffer Chair in Pharmaceutical Sciences. He is the scientific founder of Cylene Pharmaceuticals, from 1998 to 2006, and of TetraGene, from 2012 to the present.

Hurley’s current research interests are in the areas of design and development of antitumor agents. In the past 20 years, work from his laboratory has led to elucidation of the structures of the drug-receptor complexes for seven different groups of compounds that are potentially useful in the treatment of cancer. In cooperation with the biopharmaceutical industry, several drugs developed from these studies have been evaluated in phase I and phase II clinical trials, and one is now approved for cancer treatment. Recently, his academic research program has centered on secondary DNA structures, particularly G-quadruplexes, as gene targets for drug design. A first-in-class G-quadruplex-interactive compound (Quarfloxin), developed from technology and a lead compound licensed from the University of Arizona and The University of Texas, was advanced into phase II clinical trials in 2006 while Hurley was the chief scientific officer at Cylene Pharmaceuticals.

Hurley has been a consultant to pharmaceutical companies and was a senior editor for the Journal of Medicinal Chemistry, 1992 to 2010. He was also a member and then chair of the National Cancer Institute Scientific Board of Councilors, 2008 to 2012. Hurley has received the 1988 George Hitchings Award in Innovative Methods in Drug Design, the 1989 Volwiler Research Achievement Award from the American Association of Colleges of Pharmacy, the 1992 American Pharmacists Association Research Achievement Award in Medicinal Chemistry and the 1994 American Chemical Society Medicinal Chemistry Award. In 1996, he was awarded a DSc degree from Bath University. In 2005, he received the George and Christine Sosnovsky Award in Cancer Therapy from the Royal Society of Chemistry. In 2007, he was inducted into the American Chemical Society Medicinal Chemistry Hall of Fame and named Innovator of the Year by the University of Arizona. In 2008, Hurley received the American Association of Colleges of Pharmacy’s Paul R. Dawson Biotechnology Award, and in 2011 he was the recipient of the Nucleic Acids Award by the Royal Society for Chemistry. He is the recipient of a number of lectureships, including the 2001 Frank Rose Memorial Lecture at the British Association for Cancer Research; the 2007 Mary E. Kapp Lecturer in Chemistry, Virginia Commonwealth University; and the 2012 Hecht Lecturer at the University of Virginia.

His first lecture will be presented on Thursday March 30th 2016 at 3:00 PM

A Century of the Evolution of DNA as a Target for Drugs:  From Mustard Gas to Real Molecular-Targeted Drug

A method for the large-scale production of mustard gas was developed in 1916 and used extensively in the First World War, and this compound was subsequently found to alkylate DNA. Alkylating agents such as cyclophosphamide are still used extensively in the treatment of cancer, but I would like to propose that 100 years later we are close to developing clinically approved drugs that target DNA that can truly be thought of as molecular-targeted therapy. Most molecular-targeted drugs work by targeting proteins and RNA transcripts. If specific targets in DNA could be identified, then the stoichiometry for drug targeting would be very different than for those other targets where many copies of the protein or RNA target are present, and this could lead to greater selectivity. We have shown that secondary DNA structures called G-quadruplexes and i-motifs are globular elements in promoters that bind to transcription factors to turn off and on gene expression. Transcriptionally induced torsional stress is required to activate this system. Using conventional drug-screening methods, we have identified small drug-like molecules that bind to these secondary DNA structures to mimic the effect of the transcription factors to turn gene expression on and off. In this presentation I will provide examples of these transcriptional control systems in which we have characterized the naturally occurring on/off switches and identified molecules that can modulate these systems in predictable ways. The translational opportunities from this work are being applied to targeting glioblastoma multiforme, multiple myeloma, diffuse large B-cell lymphoma, acute myeloid leukemia, melanoma, and pancreatic cancer.

His second lecture will be presented on April 1st 2016 at 2:00 pm

Drug Discovery and Development in Academia:  Fighting the Odds and Sometimes Winning

In this presentation I will describe my own efforts, starting in 1997, to commercialize research discoveries we have made in the drug discovery area in my academic labs. Through this effort three drugs have progressed into phase 1 and 2 clinical trails, but none have gone beyond these stages. This effort, which is still ongoing, has covered almost two decades and has been both a personally and professionally satisfying experience, but not without its frustrations and disappointments. It is this journey I will describe, from when my father died of pancreatic cancer many years ago right up to last week, when we met with a new group of potential investors to fund our latest company, Tetragene. It is my hope that the lessons I learned during this process will be informative to other academics interested in pursuing this type of parallel career and perhaps reduce some of the “learning experiences” that I “enjoyed” during my last two decades. My marriage has survived this experience (so far).