MEI Pharma Board of Directors Aligns on Strategy to Advance Voruciclib and ME-344 - Seite 3

With regards to ME-344, the plan is to develop a new formulation for further clinical development to better leverage the opportunity to advance a novel approach to inducing synthetic lethality in tumors in combination with VEGF inhibitors such as bevacizumab (Avastin). The Company has already initiated research and development activity of the new formulation with encouraging results, with the goal of increasing biological activity, improving convenience of administration and increasing commercial opportunity. Interrupting ME-344 clinical activity and developing a new formulation will immediately reduce ME-344 expenditures.

Voruciclib

The Company recently reported initiation of enrollment in an expansion cohort of the ongoing Phase 1 study evaluating voruciclib plus venetoclax (Venclexta), a B-cell lymphoma 2 (“BCL2”) inhibitor, in R/R AML. The decision to open the expansion cohort was based on encouraging initial data demonstrating anti-leukemic activity, including complete responses in heavily pretreated patients. Additionally, at doses of 100 mg or more, initial results from correlative biomarker assay analyses of available samples from patients treated with the combination demonstrated anticipated decreases of myeloid leukemia cell differentiation protein (“Mcl-1”), including a greater decrease in Mcl-1 at higher doses. Reductions in Mcl-1 are consistent with the known mechanism of action of CDK9. Further, there was no evidence of overlapping toxicity with venetoclax and no dose limiting toxicities were observed.

Increasingly, venetoclax is being used as a standard treatment in patients with AML, but salvage therapy after venetoclax failure is common and yields limited benefit; only about 10% of patients respond to salvage therapy after venetoclax failure, representing a significant need for patients with AML. While mutation specific therapies, such as FLT3, IDH, and menin inhibitors, may be used in patients with such mutations, the majority of patients with AML do not have therapeutically actionable mutations. Thus, inhibition of CDK9 is a mutation agnostic therapeutic opportunity across the majority of patients with R/R AML, representing an addressable patient population larger than that of any mutation specific therapy.