...We Welcome You to the Zenith Epigenetics Hub withIn The AGORACOM COMMUNITY!

Zenith's BET Inhibitor ZEN-3694 is Currently Being Evaluated in Combo with Enzalutamide in Phase 2 Metastatic Prostate Cancer Clinical Trial and with Pfizer’s PARPi, talazoparib, in Phase 1b/2 Triple Negative Breast Cancer Trial

Free
AGORACOM NEWS FLASH

BREAKING: Mota Ventures Acquires Over 20,000 Customers in March, Launches New Immune Support Product Line

  • Immune Support product line received exceptionally well by consumers
  • Total number of customers acquired by First Class CBD in March 2020 is 20,959, including 6,419 immune customers
  • Initial average spend of Cdn$218.40 per customer

Mota large

Hub On AGORACOM / Read Release

Message: Found this thanks to Rndtbl's post on IV RVX bd

https://www.zenithepigenetics.com/programs/pipeline/oncology/solid-tumors

I missed this section of Zenith's site previously.  Wanted to hi-lite (or bold) that the ER+ market in the US is another large opportuntiy for a Pfizer's Palbociclib (I'm speculating here) & ZEN 3694 combo.

" reaching $13 Billion in 2020"

Zenith has a ER+ Breast Cancer trial listed as their 4th trial on slide 6 of the AGM deck.

 

ER+ Breast Cancer

About 70-80% of breast cancers are characterized by the expression of the estrogen receptor (ER).  The USA alone has about 250,000 new cases every year (2016), and ER+ breast cancer is part of a breast cancer market that is expected to grow ~6% per year, reaching over $13B by 2020. Constitutive ER signaling confers a proliferative advantage to cancer cells, hence the development of inhibitors that inhibit the synthesis of estrogen or the ER itself.  Despite potent clinical efficacy, resistance to these inhibitors occurs frequently and involves the recovery of ER signaling in 30% of cases, highlighting the need for other therapies that interfere with ER synthesis and signaling.  Recently, BET inhibitors have been shown to inhibit ER transcription, which in turn reduces ER protein and signaling while inhibiting cell proliferation and promoting cell death (apoptosis).

ZEN-3694 showed efficacy in various models of ER+ breast cancers, including in models that are resistant to ER inhibitors.  ZEN-3694 down-regulated ER signaling, as well as several pathways associated with resistance to ER-based therapies in the clinic.  These results suggest that ZEN-3694 could potentiate existing treatments for ER+ breast cancer patients by offering a novel approach to target ER signaling.

 

Share
New Message
Please login to post a reply