Pomezia, Italy, December 7th, 2020 – Menarini Group announced today that it will present the results of two different preclinical studies on MEN1611, a potent and selective phosphatidylinositol 3-kinase inhibitor (PI3Ki) currently in clinical development for the treatment of breast cancer, at the upcoming 2020 San Antonio Breast Cancer Symposium, which will be held virtually on December 8-11.

“We are pleased to present at the San Antonio Breast Cancer Symposium and look forward to discussing in more detail the encouraging preliminary results achieved by our preclinical studies on MEN1611,” commented Andrea Pellacani, General Manager of Menarini Ricerche, R&D Division of the Menarini Group. “These data contribute to a greater understanding of the mechanism of action of MEN1611 and further support its clinical development for the treatment of breast cancer, reinforcing our strong commitment to advancing precision oncology to the benefit of patients living with difficult-to-treat cancer.”

MEN1611 is a potent and selective PI3Ki targeting the p110 α, β and γ isoforms, while sparing the δ subunit. B-PRECISE-01 is a multicenter, Phase Ib, dose escalation and expansion study, investigating MEN1611 in patients with HER2-positive, PIK3CA mutated, advanced or metastatic breast cancer.

The poster entitled “MEN1611 is a PI3K α/β selective and δ sparing inhibitor with long-lasting antitumor activity in different genetic backgrounds of PIK3CA mutant breast cancer models” presents the results of a preclinical study on the antitumor activity of MEN1611 in p110 α- and β-dependent tumors, providing evidence that in these animal models MEN1611 is active against HER2-positive, PIK3CA mutated and PTEN-null breast tumor.

A second poster, entitled “MEN1611 promotes immune activating myeloid cell polarization” presents the results of a study aimed at characterizing the effects of MEN1611 on the PI3Kγ isoform, highly expressed in tumor-associated macrophages, to investigate whether the anti-tumor activity of MEN1611 might also be mediated by MEN1611-mediated modulation of tumor inflammatory microenvironment. The results of this study show that MEN1611 inhibition of the PI3Kγ isoform leads to macrophage reprogramming, from an immune-suppressive to an immune-activating phenotype. Moreover, the tumor regression induced by MEN1611 was associated to changes of the inflammatory microenvironment, characterized by an increased recruitment of T cells, which may contribute to the anti-tumor activity of MEN1611 in this model.