Dr. Paul B. Myrdal Memorial Fund for Pharmaceutical Education

Dr. Paul B. Myrdal Memorial Fund for Pharmaceutical Education



Dr. Paul Myrdal was born in Madison, Wisconsin on June 25th, 1967, the beloved child of Barbara and Gerald Myrdal. He grew up in Madison with his three siblings and graduated from Madison Memorial High school in 1985. Paul attended the University of Wisconsin at Madison, where he met his future wife, Kelly Jo Koch in freshman chemistry class. Paul moved to Arizona during college and graduated with a BS in Molecular and Cellular Biology from the University of Arizona in 1989. Paul and Kelly married in 1992 in Madison, Wisconsin at the site of their first date. Paul went on to earn his Ph.D. in Physical Pharmaceutical Chemistry from the University of Arizona in 1994, and completed a post-doctoral fellowship in 1995. Paul and Kelly welcomed their first child, Caitlyn, while living in Arizona. After completing his Ph.D., Paul and family moved to Minnesota where Paul worked as a pharmaceutical scientist for the Minnesota Mining and Manufacturing Company (3M) in the Drug Delivery Systems Division. He was awarded 3M’s Technical Circle of Excellence in 1998. During Paul and Kelly’s time in Minnesota they welcomed the birth of their son, Hunter. Paul and Kelly moved back to Tucson in 2000 after Paul joined the College of Pharmacy at the University of Arizona as an Associate Professor in Pharmacy Practice and Science. Dr. Myrdal contributed significantly to pharmaceutical science throughout his professional career and authored more than 80 peer reviewed publications and nine book chapters on a variety of aspects of analytical chemistry, solutions, solid state characterization, formulation development, and drug delivery. Paul was highly esteemed in his field and loved by his colleagues and students. He was dedicated to his pharmacy and graduate students and honored to contribute to their lives and education throughout the years. He was also very proud to be a member of a strong, brilliant, and supportive academic family and especially appreciative to his mentor, Dr. Samuel Yalkowsky. Paul will forever be remembered with great love and affection by his wife of 25 years, Kelly, and his two beautiful children, Hunter (20) and Caitlyn (23). Paul will also be remembered fondly by his parents, Barbara and Jerry; his sisters Kristi Reprogle and Michelle Chudy, his brother Gregory Myrdal, his brothers-in-law Mike Reprogle, Matt Chudy, and Chris Koch, his sister-in-law Kathyrn Koch, his nephews Joshua Reprogle, Jake Chudy, and Eben Koch, his nieces Lindsey Reprogle, Jessica and Annika Chudy, and his mother-in-law, Sharon Koch. Paul’s greatest legacy and joy were his wife, children, family, friends, work and the outdoors. He loved fishing and hunting, cultivating the plants in his gardens, hiking, working around his house, taking trips with his family, and enjoying the people around him. The motto that he left to his family was “be generous and be kind; always” and he lived by that expression every day. Paul was supported throughout his illness by his family and friends for whom we are forever grateful. He left us too soon and will be fiercely missed by those whose lives he touched.

To contribute to the Memorial Fund, please use this link or indicate on the donation form that your gift is in memory of Dr. Paul B. Myrdal. All donations to the Dr. Paul B. Myrdal Memorial Fund for Pharmaceutical Education will support AFPE’s Gateway Fellowship, which funds mentored research projects for B.S. and Pharm.D. students, and the Pre-Doctoral Fellowship, which supports mentored Ph.D. candidates’ research projects.


The 2023-2024 Dr. Paul B. Myrdal Pre-Doctoral Fellow is Kelsey Holdaway, University of Minnesota. Her research is titled “Development of Selective, Allosteric Inhibitors of Cyclin-Dependent Kinase 2 for the Therapeutic Treatment of Cancer”

Kelsey explains his project goals as:

“In diseases such as ovarian, breast, and colorectal cancers a particular enzyme termed CDK2 is overactivated, which leads to cancer cell growth. One approach toward the treatment of these types of cancers is to inhibit CDK2 and thus inhibit cancer cell growth. A main challenge in this approach is how to selectively target CDK2 over other similar enzymes, which if also inhibited will cause negative side effects. One such strategy to overcome this challenge is to design inhibitors that bind to a location on CDK2 that is unique and less conserved amongst other similar enzymes, which would result in improved selectivity and fewer or no undesirable side effects. Our lab has identified two such unique locations on CDK2 that are suitable for selective binding of an allosteric inhibitor. For the first site, our lab has already developed inhibitors capable of binding, however, they exhibit a problem with being outcompeted for binding by a small protein that activates CDK2. In order to improve the ability of our inhibitor to preferentially bind at this site, we propose to develop inhibitors capable of permanently binding. As the other protein binds in such a manner as it attaches and detaches cyclically, a permanently binding inhibitor could overcome the issue of being outcompeted. For the second site, computational analysis will be performed to help identify an inhibitor that would be compatible with binding at this location and inhibit the enzyme selectively. The outcome of this analysis is expected to identify an inhibitor that is compatible with binding to CDK2 at the specific location. With this knowledge, a variety of inhibitors can be synthesized and subsequently tested for their ability to selectively bind at this location and inhibit CDK2. Upon synthesis of inhibitors capable of selectively binding at either of these locations, the goal will be to test for inhibition activity against CDK2 and test the analogs for anticancer activity in several ovarian cancer cell lines. From this, it can be deduced how effective the inhibitors are at inhibiting CDK2 activity and thus inhibiting cancer cell growth. Ultimate goals are to test these inhibitors in animal models of cancer and then in clinical studies.”