Rain Therapeutics Presents Data on Milademetan (RAIN-32) at the 2021 AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics

Presentations highlight potential of the oral MDM2 inhibitor, milademetan, in advanced cancers with MDM2 amplification, GATA3 mutant ER-positive breast cancer, and Merkel cell carcinoma

Excerpt from the Press Release:

NEWARK, Calif., Oct. 07, 2021 (GLOBE NEWSWIRE) — Rain Therapeutics Inc., (NasdaqGS: RAIN), (“Rain”), a late-stage company developing precision oncology therapeutics, today announced data on its oral mouse double minute 2 (MDM2) inhibitor, milademetan, presented at the 2021 AACR-NCI-EORTC Virtual International Conference on Molecular Targets and Cancer Therapeutics held virtually October 7-10, 2021.

Three poster presentations detailed: 1) in vivo and in vitro activity of milademetan using a rationally-derived MDM2 copy number threshold as a predictive biomarker for patient selection, 2) in vivo and in vitro activity of milademetan in Merkel cell carcinoma (MCC) models and 3) results demonstrating milademetan induces synthetic lethality of (ER)-positive breast tumors with GATA3 mutations.

Key findings from Rain’s presentations include:

• Milademetan demonstrated anti-tumor activity in patient-derived organoid models and xenograft models consisting of genetically selected tumors, representing many different histologies, using MDM2 gene amplification (amp) and wild-type (WT) p53 as selection criteria.
  • Robust induction of p53 target genes including MIC-1, p21 and PUMA was observed following milademetan treatment indicating re-activation of p53 by milademetan.
• Milademetan inhibited MCC cell lines in patient-derived xenograft models that lack TP53 mutations, representing the majority of MCC cases, for which no approved targeted therapies are available.
  • MCC has low rates of p53 mutation and MDM2 dependence in MCC is driven by polyoma virus-induced MDM2 expression in the majority of cases.
• Milademetan inhibited proliferation of GATA3 frameshift (fs) mutant ER+ breast cancers, demonstrating significant activity and the potential to treat ER+, GATA3 mutant breast cancers that have been unresponsive to the current standard of care.
  • GATA3 fs mutations are mutually exclusive of p53 mutations in ER+ breast cancer and are associated with higher expression of MDM2 and other genes in the MDM2/p53 axis associated with p53 inactivation.

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