William L. Seibel, PhD
- Member, Division of Oncology
- Associate Professor, UC Department of Pediatrics
About
Biography
I collaborate with various scientific groups in my research lab, but I primarily focus on oncology and experimental hematology research. I am mainly interested in the application of medicinal chemistry, virtual screening and cheminformatics. I also participate in projects across other disciplines and focus areas.
I received my doctorate in chemistry from Harvard University and then spent 19 years in the discovery field of migraine and antimicrobial drugs. From my experience in the pharmaceutical industry, I moved toward utilizing and optimizing the technology and tools that streamline efforts in drug design. For example, I led technology groups in protein modeling, computational chemistry, structural biology and combinatorial chemistry. I later served as a project manager for the University of Cincinnati Drug Discovery Center and direct the College of Medicine’s Compound Library.
I began working at the Cincinnati Children’s Hospital Medical Center in 2013, after more than 25 years of experience in the field of drug discovery. My role at the Cincinnati Children’s Hospital Medical Center has been to employ these tools and expertise to assist others in their research studies. I’ve always been interested in working with numerous collaborators and investigators to 1) identify the most effective methods of discovering biologically active small molecules and 2) advance these findings toward the clinic. My research has been published in numerous respected journals, including Oncotarget, PLoS ONE, Methods in Molecular Biology, Cell Chemical Biology and Nature Communications.
Research Areas
Oncology, Cancer and Blood Diseases
Publications
Chemical genetic screens reveal defective lysosomal trafficking as synthetic lethal with NF1 loss. Journal of Cell Science. 2024; 137.
Small-molecule-induced epigenetic rejuvenation promotes SREBP condensation and overcomes barriers to CNS myelin regeneration. Cell. 2024; 187:2465-2484.e22.
Chaetocin-mediated SUV39H1 inhibition targets stemness and oncogenic networks of diffuse midline gliomas and synergizes with ONC201. Neuro-Oncology. 2024; 26:735-748.
Abstract 5912: Rational design of a small-molecule inhibitor targeting the allosteric site of sos1 in oncogenic k-ras pancreatic cancer. Cancer Research. 2024; 84:5912.
Rational polypharmacological targeting of FLT3, JAK2, ABL, and ERK1 suppresses the adaptive resistance to FLT3 inhibitors in AML. Blood Advances. 2023; 7:1460-1476.
Structure-Activity Relationship Analysis of Rhosin, a RhoA GTPase Inhibitor, Reveals a New Class of Antiplatelet Agents. International Journal of Molecular Sciences. 2023; 24.
Rational Polypharmacological Targeting of FLT3, JAK2, ABL and ERK1 By Pluripotin Suppresses the Adaptive Resistance to FLT3 Inhibitors in AML. Blood. 2022; 140:3101-3102.
High Throughput Pre-Clinical Models to Determine a Synergistic Molar Ratio of 5-Azacitidine to Venetoclax and Uncover Resistance Mechanisms to 5-Azacitidine and Venetoclax Combination Therapy in Acute Myeloid Leukemia. Blood. 2022; 140:10693-10694.
Brain pharmacokinetics and metabolism of the AMP-activated protein kinase selective inhibitor SBI-0206965, an investigational agent for the treatment of glioblastoma. Investigational New Drugs. 2022; 40:944-952.
Blocking UBE2N abrogates oncogenic immune signaling in acute myeloid leukemia. Science Translational Medicine. 2022; 14:eabb7695.
3333 Burnet Avenue, Cincinnati, Ohio 45229-3026
© 1999-2024 Cincinnati Children's Hospital Medical Center. All rights reserved.
