EPICS Therapeutics presents compelling in vivo efficacy in oncology with its proprietary METTL3 inhibitor at AACR 2023

Published: 11.04.2023

Gosselies, Belgium April 11th, 2023

– A proprietary, highly potent inhibitor of RNA methyltransferase 3 (METTL3) shows low nanomolar IC50 in proliferation assays with several AML and solid tumor cell lines.
– This METTL3 inhibitor significantly prolonged survival in an orthotopic (intratibial) models of CDX and patient-derived AML tumors with selective targeting of blood cancer cells (human CD45+) relative to general hematopoiesis

METTL3 is the RNA methyltransferase predominantly responsible for the addition of N-6-
methyladenosine (m6A), the most abundant modification to mRNA. The prevalence of m6A and the
activity and expression of METTL3 have been linked to the initiation and progression of acute myeloid
leukemia (AML) and several other tumor entities like non-small cell lung cancer, head and neck squamous cell carcinoma, etc. Epics has developed a series of highly potent and selective small molecule inhibitors which have been successfully tested in several different tumor entities.

Graeme Fraser CSO of EPICS Therapeutics said: ”Our research team has done well to optimize and deliver a METTL3 inhibitor candidate worthy of continued development. Also, our advanced candidate provides us with a unique means to continue to probe and validate the potential of METTL3 as a target relevant to various other cancers underserved by existing therapies.”

Franz Obermayr CEO of EPICS Therapeutics said: “We are excited to present for the first time data on our METTL3 program. The team has made a breakthrough in developing a series of highly potent and selective METTL3 inhibitors. The data presented at AACR and other unpublished data providing the rationale for future clinical development in AML and other solid tumors”.

Poster presented: #6282

EP102: Pharmacological Inhibition of METTL3 arrests tumor progression and prolongs survival in CDX and PDX models of AML

Time: 9-12h Wednesday, April 19th.