Zenith Epigenetics Announces a Publication Highlighting the Role of ZEN-3694

Zenith Capital Corp. announces the publication of an important study which has uncovered the role of ZEN-3694.

CALGARY, Alberta, June 24, 2021 (GLOBE NEWSWIRE) -- Zenith Capital Corp. (“Zenith” or the “Company”), a clinical stage pharmaceutical company focused on the development of novel epigenetic combination therapies for the treatment of cancers, announces the publication of an important study which has uncovered the role of ZEN-3694, a BET bromodomain inhibitor (BETi), in overcoming the resistance of metastatic castration resistant prostate cancer (mCRPC) to androgen receptor signaling inhibitors (ARSi). The study, led by a team of renowned prostate cancer researchers, has been published in Clinical Cancer Research, a high impact journal.

The study demonstrated that mCRPC, when treated with ARSi, can switch its lineage from adenocarcinoma to a more aggressive neuroendocrine type which is less dependent on androgen receptor signaling. This treatment induced neuroendocrine prostate cancer is becoming more prevalent with increasing use of ARSis and is associated with very poor patient clinical outcomes. ZEN-3694 inhibits BRD4 and E2F1 which epigenetically regulate this lineage switch. Blocking BET bromodomain proteins in cell models stopped the activation of this program that drives the development of neuroendocrine prostate tumors, the research team found. Furthermore, this was supported by clinical data from ZEN-3694 Phase 1b/2a mCRPC study which showed that ZEN-3694 was most effective in patients whose tumors were less dependent on androgen receptor signaling and did not respond to prior ARSi. High expression of BRD4 and E2F1 were also observed in the tumors of two patients with treatment emergent neuroendocrine prostate cancer, and both patients had a response to ZEN-3694 + enzalutamide, consistent with the role of ZEN-3694 in overcoming resistance to ARSi in this aggressive form of prostate cancer.

“This was an important study which highlights the role of ZEN-3694 in the treatment of mCRPC,” said Donald McCaffrey, President and Chief Executive Officer of Zenith. “ARSis are the cornerstone therapy for advanced prostate cancer but almost all patients ultimately become resistant. There is a particularly significant unmet need in mCRPC patients who do not respond to an ARSi and their current treatment options only include cytotoxic therapy with considerable side effects. Our upcoming Phase 2b mCRPC study will be evaluating the efficacy of ZEN-3694+ enzalutamide in this group of patients. The aforementioned publication provides additional rationale for this well-designed study.”

About prostate cancer

Prostate cancer is the second most commonly diagnosed cancer among men and the fifth most common cause of male cancer death worldwide. Adenocarcinoma of the prostate is dependent on androgen for tumor progression and depleting or blocking androgen action has been a mainstay for over six decades. Although tumors are often initially sensitive to medical or surgical therapies that decrease levels of testosterone, the treatment of prostate cancer patients has evolved rapidly over the past ten years with second generation ARSis. Despite these advances, many patients with mCRPC fail or develop resistance to existing treatments, leading to low survival rates.

About Zenith

Zenith Capital Corp. is a biotechnology investment company originally spun out of Resverlogix Corp. (TSX: RVX) in 2013. Zenith Epigenetics Ltd., a wholly-owned subsidiary of Zenith Capital Corp., is a clinical stage biotechnology company focused on the discovery and development of novel therapeutics for the treatment of cancer and other disorders with significant unmet medical need. Zenith Epigenetics is developing various novel combinations of BET inhibitors with other targeted agents. The lead compound, ZEN-3694, is in clinical development for:

  1. mCRPC in combination with androgen receptor inhibitor, XTANDI, with Astellas and Newsoara as collaborators
  2. Triple Negative Breast Cancer in combination with the PARP inhibitor TALZENNA with Pfizer as a collaborator
  3. Androgen receptor independent mCRPC in combination with immune checkpoint inhibitor KEYTRUDA and XTANDI with University of California, San Francisco as a collaborator

For further information, please contact:

Investor Relations & Communications

Zenith Epigenetics
Phone: 587-390-7865
Email: info@zenithepigenetics.com
Website: www.zenithepigenetics.com

This news release may contain certain forward-looking information as defined under applicable Canadian securities legislation, that are not based on historical fact, including without limitation statements containing the words “believes”, “anticipates”, “plans”, “intends”, “will”, “should”, “expects”, “continue”, “estimate”, “forecasts” and other similar expressions. In particular, this news release includes forward looking information relating to the Company’s upcoming Phase 2b study to evaluate the efficacy of the combination of ZEN-3694 and enzalutamide relative to single agent enzalutamide in mCRPC patients who have progressed on a prior ARSi, the Company’s development of ZEN-3694 and its potential role in the treatment of cancer and other disorders. Our actual results, events or developments could be materially different from those expressed or implied by these forward-looking statements. We can give no assurance that any of the events or expectations will occur or be realized. By their nature, forward-looking statements are subject to numerous assumptions and risk factors including those discussed in our most recent MD&A which are incorporated herein by reference and are available through SEDAR at www.sedar.com. The forward-looking statements contained in this news release are expressly qualified by this cautionary statement and are made as of the date hereof. Zenith disclaims any intention and has no obligation or responsibility, except as required by law, to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise.


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