Previewing Potential ORIC Impact from Competitor PFE's Ph. 3 MEVPRO-1

Research evidence excerpt

Previewing Potential ORIC Impact from Competitor PFE's Ph. 3 MEVPRO-1

C O M PA N Y N O T E

J u n e 2 9 , 2 0 2 6

Key competitive read-through for ORIC's lead program, rinzimetostat, is coming in mid-

to 2H 2026 from PFE's Ph. 3 MEVPRO-1 of mevrometostat. ORIC is a clinical stage,

biopharmaceutical company advancing 2 lead programs: rinzimetostat in prostate cancer and

enozertinib in EGFRmut NSCLC. ORIC's lead program rinzimetostat is an allosteric PRC2

inhibitor with recent Ph. 1b clinical data presented in March (our recap here) in combination

with darolutamide in mCRPC patients, and a Ph. 3 HIMALAYAS-1 clinical trial set to initiate

imminently. First generation PRC2 inhibitors have been limited by their suboptimal drug

properties, specifically CYP autoinduction and short half lives, as well as poor in vivo and in

vitro potency. Next gen PRC2 inhibitors, including rinzimetostat and mevrometostat (PFE) have

demonstrated compelling clinical profiles that support the hypothesis that PRC2 inhibition may

allow prostate cancer cells to regain AR-dependence. Given the large market opportunity of

mCRPC (37,000 1L treated mCRPC US patients) and limited treatment options available, there

is clear investor interest in the PRC2 class. The next key catalyst for the space is the upcoming

Ph. 3 MEVPRO-1 data readout of mevrometostat + enzalutamide in post-abi mCRPC patients

coming later this year.

ORIC's rinzimetostat and PFE's mevrometostat inhibit the PRC2 complex by targeting 2

distinct subunits: EED and EZH2, respectively. The polycomb repressive complex 2 (PRC2)

is an epigenetic modifier that regulates gene expression by catalyzing the methylation of histone

H3K27, which facilitates chromatin compaction. PRC2 dysregulation can lead to tumorigenesis,