Our lead product candidate ALRN-6924 reactivates p53-mediated tumor suppression by inhibiting the primary p53 suppressor proteins MDMX and MDM2, and is currently being evaluated in multiple clinical trials. About half of cancer patients at initial diagnosis have wild type p53 that is functionally suppressed through activation or overexpression of MDMX and MDM2, leaving cancer cell growth unchecked.
We believe ALRN-6924 is the first and only product candidate in clinical development that can inhibit both MDMX and MDM2, which we believe, based on published data and our preliminary clinical results, are equally important in restoring p53 function as the body’s first line of defense against cancer. As such, ALRN-6924 may have an effect in a broader range of tumors, an improved safety profile and be less prone to resistance than conventional approaches to modulating key intrinsic cellular proteins and their functions, such as small molecules.
Based on preclinical data and preliminary clinical evidence of anti-tumor activity across a broad spectrum of cancer patients, durable effect by trial responders and, to date, a favorable safety profile, we are pursuing a broad strategy of development with ALRN-6924 as a monotherapy or combination therapy across a wide range of solid and liquid tumors.
The Company presented data from its Phase 1 trial of ALRN-6924 in patients with advanced solid tumors and lymphomas at the 2017 American Society of Clinical Oncology (ASCO) Annual Meeting in early June.
We are currently conducting multiple clinical trials of ALRN-6924, including a Phase 1 All-comers trial in advanced solid tumors or lymphomas, a Phase 2a trial in peripheral T-cell lymphoma (PTCL), a Phase 1 trial in acute myeloid leukemia (AML) and advanced myelodysplastic syndrome (MDS) as a monotherapy, and a Phase 1b trial in AML/MDS in combination with cytosine arabinoside (Ara-C).