On March 8, 2022 MEI Pharma, Inc. (NASDAQ: MEIP), a late-stage pharmaceutical company focused on advancing new therapies for cancer, reported that two abstracts highlighting data from two oncology drug candidates in its pipeline will be presented at the upcoming American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2022 to be held April 8 – 13, 2022 (Press release, MEI Pharma, MAR 8, 2022, View Source [SID1234609706]).

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Details of the poster presentations:

Title: Efficacy and immune profiling of the PI3K delta inhibitor zandelisib (ME-401) in a preclinical model of chronic lymphocytic leukemia (CLL)
Authors: Dr. Maharaj, et. al.
Date: Friday, April 8, 2022, 8:30 AM ET
Abstract ID: 5496

Summary of results: data from preclinical studies with zandelisib ex vivo in normal human T cells and in vivo in a murine CLL model suggest that zandelisib has immunomodulatory properties on human T cells including decreased activation and expression of suppressive markers such as PD-1 and CTLA-4 on inducible regulatory (Tregs) and CD4+ T cells. In the murine CLL model, a reduction in Treg numbers, markers of terminal memory differentiation and T-cell exhaustion on CD4+ and CD8+ T cells, as well as improvement in overall survival was observed.

Title: ME-344, a novel isoflavone mitochondrial inhibitor, in combination with venetoclax constitutes a new metabolism-targeted approach to overcome resistance to Bcl-2 inhibition and standard of care treatment in AML
Authors: Katie Hurrish, et. al.
Date: Wednesday, April 13, 2022, 10:00 AM – 1:30 PM ET
Abstract ID: 3785

Summary of results: data from in vitro and in vivo preclinical studies evaluating the combination of ME-344 with venetoclax in standard-of-care-resistant acute myeloid leukemia (AML) cell lines and relapsed or refractory (R/R) AML patient samples suggest that ME-344, both alone and in combination with venetoclax, inhibits purine biosynthesis, suppresses oxidative phosphorylation, induces apoptosis and decreases Mcl-1, which together target metabolic vulnerabilities of AML cells.