37th Annual Student Research Conference
Computational drug design for inhibition of the KIX protein to treat acute myeloid leukemia cell proliferation
Madisen A. Bromfman* and Emily C. Cobb
Dr. Bill R. Miller, Faculty Mentor
In normal cells, the interactions between c-Myb and the KIX domain of the cyclic-AMP response element binding protein (CBP protein) cause cells to grow and divide. Recent studies have shown that a theorized cause of acute myeloid leukemia (AML) are the interactions between the KIX domain and mutated c-Myb. Our research investigates small molecules that disrupt the interaction between c-Myb and KIX, a potential treatment for AML. Around 2.5 million drug candidates were screened from the ZINC12 database utilizing a computational molecular docking technique using the Qvina software. We are currently in the process of simulating the top 200 molecules using molecular dynamics (MD) from this screening process. These simulations allow us to calculate a free binding energy to determine the likelihood of the drug binding to the CBP domain. These drugs are promising treatment options for patients with AML that avoid the toxicity of chemotherapy.
Keywords: AML, c-Myb, KIX
Topic(s):Biochemistry and Molecular Biology
Presentation Type: Oral Presentation
Session: 306-2
Location: MG 2001
Time: 1:00