ESSA Pharma Presents Therapeutic Potential of EPI-7386 at 32nd EORTC-NCI-AACR Symposium

On October 24, 2020 ESSA Pharma Inc. (Nasdaq: EPIX) (TSXV: EPI), a clinical-stage pharmaceutical company focused on developing novel therapies for the treatment of prostate cancer, reported new preclinical data on ESSA’s clinical candidate, EPI-7386, at the 32nd EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) Annual Symposium on Molecular Targets and Cancer Therapeutics ("ENA") (Press release, ESSA, OCT 24, 2020, View Source [SID1234568960]).

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In an oral poster presentation titled, "The pre-clinical characterization of the N-terminal domain androgen receptor inhibitor, EPI-7386, for the treatment of prostate cancer", was published on Saturday, October 24th.

The studies highlight new information about EPI-7386 including:

In an in vitro cellular thermal shift assay (CETSA), EPI-7386 was shown to physically interact with the both the full-length and the splice variant (AR-V7) form of the androgen receptor ("AR").
In an in vitro full-length AR-driven cellular model (LNCaP), RNAseq data was analyzed by pathway enrichment analysis. EPI-7386 demonstrates largely similar modulation of AR-regulated genes compared to enzalutamide, but with additional unique elements.
EPI-7386 exhibits superior activity to enzalutamide in the AR-V7-driven cellular models LNCaP95 and 22Rv1 by modulating AR-driven gene expression with or without the addition of an external androgen.
"Previously, we presented in vitro data demonstrating that EPI-7386 binds to the full-length androgen receptor and can inhibit the transcription of AR-regulated genes. These new data demonstrate that EPI-7386 can also physically interact with the splice variant form, AR-V7, of the androgen receptor and inhibit its activity. The importance of this interaction with AR-V7 is seen through the superior transcriptional inhibition of AR-regulated genes by EPI-7386 compared to enzalutamide in the AR-V7-driven cell models LNCaP95 and 22Rv1. Together, these data provide important new insights into mechanistic aspects related to the binding and utility of EPI-7386 against AR-V7 splice-variant driven prostate cancer models. The data further strengthen the rationale for studying EPI-7386 in men with prostate cancer resistant to current anti-androgens." said Dr. David R. Parkinson, President and Chief Executive Officer.