On July 19, 2023 Tempest Therapeutics, Inc. (Nasdaq: TPST), a clinical-stage oncology company developing first-in-classi therapeutics that combine both targeted and immune-mediated mechanisms, reported that in vivo and in vitro data on the unique mechanism of TPST-1495, the company’s novel dual receptor inhibitor of prostaglandin E2 (PGE2) signaling, were published in Cancer Research Communications, a journal of the American Association for Cancer Research (AACR) (Free AACR Whitepaper) (Press release, Tempest Therapeutics, JUL 19, 2023, View Source [SID1234633320]).
Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:
Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing
Schedule Your 30 min Free Demo!
"While the biology of PGE2 in promoting tumor growth and immune suppression is well established, there are still no approved drugs for cancer that effectively block the prostaglandin pathway," said Tom Dubensky, Ph.D., president of Tempest. "Our innovation with TPST-1495 shows for the first time the effect of blocking PGE2 signaling through the EP2 and EP4 pro-tumor receptors while maintaining the important anti-tumor signaling of PGE2 through the EP1 and EP3 receptors, which could be an important advance to inhibiting PGE2. Additionally, these results further support what we believe is an innovative and robust pipeline at Tempest that includes TPST-1120, a novel PPAR⍺ antagonist, which has shown early positive data from an ongoing global randomized study in first-line HCC patients."
About TPST-1495
Described in the Cancer Research Communications publication, TPST-1495 is an orally-available and potent small molecule designed to block the receptors EP2 and EP4 in the prostaglandin pathway. PGE2 both promotes tumor cell growth and has strong immune-suppressive signaling through these receptors. Several malignancies are thought to be prostaglandin driven through expression of high levels of COX-2, the cellular enzyme that produces PGE2, including endometrial, bladder, breast, colorectal, and cervical cancers. Tempest has conducted multiple studies with peripheral blood mononuclear cells (PBMCs) from healthy adult donors and in several mouse tumor models that demonstrate a significant increase in immune activation and anti-tumor potency by inhibiting both EP2 and EP4, when compared to EP4-only targeted molecules and non-steroidal anti-inflammatory drugs (NSAIDS), such as celecoxib.