Euclises has an open US IND. The Phase 1 study is on track to dose the first patient with our lead molecule, ECP-1014, in the third quarter 2021. Details can be found at (

Combination with Immuno-Oncology Agents

Numerous researchers have demonstrated the importance of the tumor immune microenvironment in determining an individual patient’s response to immunotherapy regimens. Euclises is studying the impact of ECP-1014 on disabling or reprogramming these immunosuppressive microenvironments that can drive non-responsiveness to immuno-oncology drugs.

Overproduction of prostaglandin E2 (PGE-2) by COX-2 promotes tumor proliferation, invasiveness, metastasis, and, most importantly for Euclises’ therapies, suppression of the immune system. PGE-2 mediated immune suppression in the TME has been suggested as the root of non-responsiveness to IO agents in certain tumors types and patients. These effects are especially pronounced in tumor types in which the COX-2 enzyme is known to be over-expressed or highly active.

In addition, animal tumor models show that ECP-1014 can quite effectively convert “cold” tumors (those that are typically non-responsive to checkpoint therapy) into “hot” tumors with dramatic immune responses. Combination with checkpoint inhibitors in these tumor lines has resulted in regression and even complete eradication of the tumor. These findings underscore the potential for Euclises’ drugs to work synergistically with IO agents and to transform patient outcomes particularly in the context of COX-2 dependent tumors that have historically shown poor response to IO therapy (e.g. murine models of colorectal and triple negative breast cancer).