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Aileron Therapeutics Presents New Data on ALRN-6924 in Oral Presentations at 2017 American Society of Hematology MeetingPreclinical data show dual inhibition of MDM2 and MDMX restores p53 function Data demonstrate strong anti-cancer effects in models of T-cell lymphomas and acute myeloid leukemia ATLANTA, Dec. 11, 2017 (GLOBE NEWSWIRE) -- Aileron Therapeutics, the clinical-stage leader in the field of stapled peptides developing therapeutics for cancers and other diseases, today announced two oral presentations of preclinical data from collaborators on ALRN-6924 in T-cell lymphomas (TCL) and acute myeloid leukemia (AML). ALRN-6924, a stapled peptide therapeutic, is believed to be the first product candidate undergoing clinical evaluations that has been shown to disrupt both MDMX- and MDM2-mediated inhibition of the wild type p53 tumor suppressor gene. The data were reviewed in separate oral presentations by researchers from the Dana-Farber Cancer Institute and the Albert Einstein College of Medicine during the 2017 American Society of Hematology Annual Meeting. “We are encouraged by these positive preclinical data from our collaborators, which demonstrate that dual inhibition by ALRN-6924 induces strong p53 activity that leads to anti-cancer effects,” said Dr. Manuel C. Aivado, Chief Medical Officer. “These data support the clinical results we saw in our Phase 1 all-comers trial, and we look forward to continuing to evaluate ALRN-6924 in our ongoing PTCL and AML clinical trials.” TCL Study Highlights (Abstract #571) In an in vitro and in vivo preclinical study, MDMX and MDM2 were evaluated as potential targets for treating wild type p53 T-cell lymphomas by using ALRN-6924 to inhibit their expression. The data showed that ALRN-6924 induced apoptotic cell death in TCL lines, and significantly reduced tumor burden compared to the vehicle in animal models. Furthermore, ALRN-6924 had a favorable safety profile and demonstrated superior efficacy across multiple TCL subtypes compared to the current standard-of-care. Commented David Weinstock, M.D. of Dana-Farber Cancer Institute, “Given the need for new treatment approaches for T-cell lymphomas, we evaluated ALRN-6924 in animal models and found that the compound’s dual inhibition mechanism for restoring the function of p53 showed promising activity across multiple TCL subtypes, including PTCL. Animal models in our studies displayed key markers that demonstrated consistency with on-target p53 activation and apoptosis, supporting further clinical development of ALRN-6924 for PTCL.” i AML Study Highlights (Abstract #795) The preclinical data presented showed that dual inhibition of MDMX and MDM2 by ALRN-6924 led to activation of p53-dependent pathways in AML cells. The disruption of MDMX/p53 and MDM2/p53 interactions resulted in strong anti-leukemic effects, and induced cell cycle arrest and apoptosis in cell lines and wild type p53 AML patients’ cells. The compound exhibited strong on-target activity in AML cell lines and primary cells in vitro, as well as in a patient who received ALRN-6924. The data further demonstrated that ALRN-6924 showed superiority over MDM2-only inhibition, an led to improved survival in in vivo AML models. “These results support our understanding that in most patients with acute myeloid leukemia, a devastating disease with limited therapeutic options, p53 is circumvented by activation of its natural suppressor proteins, MDMX and MDM2,” said Ulrich Steidl, Ph.D., M.D. of the Albert Einstein College of Medicine. “The ability to reactivate the p53 pathway by inhibiting both MDMX and MDM2 using a novel therapeutic modality such as stapled peptides is an exciting new chapter in p53 research. The studies presented today strengthen the rationale for the use of ALRN-6924 in acute myeloid leukemia and other wild type p53 cancers.” ii About ALRN-6924 About Aileron Forward-looking Statements Actual results may differ materially from those indicated by such forward-looking statements as a result of various important factors, including whether Aileron’s cash resources will be sufficient to fund its continuing operations for the periods and/or trials anticipated; whether results obtained in preclinical studies and clinical trials will be indicative of results obtained in future clinical trials; whether Aileron’s product candidates will advance through the clinical trial process on a timely basis, or at all; whether the results of such trials will warrant submission for approval from the United States Food and Drug Administration or equivalent foreign regulatory agencies; whether Aileron's product candidates will receive approval from regulatory agencies on a timely basis or at all; whether, if product candidates obtain approval, they will be successfully distributed and marketed; and other factors discussed in the "Risk Factors" section of Aileron's quarterly report on Form 10-Q for the period ended September 30, 2017, filed on November 9, 2017, and risks described in other filings that Aileron may make with the Securities and Exchange Commission. Any forward-looking statements contained in this press release speak only as of the date hereof, and Aileron specifically disclaims any obligation to update any forward-looking statement, whether because of new information, future events or otherwise. Contacts Investors: Media: Source: Aileron Therapeutics i Dr. Weinstock’s research was financially supported by Aileron under a sponsored research agreement. |