Immuneering Publishes New Findings In Cancer Research Characterizing The Differentiated Mechanism And Broad Preclinical Activity Of Atebimetinib; Atebimetinib Showed Broad Antitumor Activity Across KRAS-, NRAS-, And BRAF-mutant Models, Including Colorectal, Lung, And Melanoma, By Resisting The RAF-Mediated Bypass Signaling That Has Constrained Other MEK Inhibitors

- Atebimetinib showed broad antitumor activity across KRAS-, NRAS-, and BRAF-mutant models, including colorectal, lung, and melanoma, by resisting the RAF-mediated bypass signaling that has constrained other MEK inhibitors -

- In head-to-head in vivo studies, atebimetinib produced deeper, more durable tumor growth inhibition than the FDA-approved MEK inhibitor binimetinib -

- Atebimetinib was associated with favorable tolerability in preclinical models, consistent with Deep Cyclic Inhibitor technology’s design to decouple antitumor activity from the toxicity of continuous MAPK suppression -

- In a preclinical cancer cachexia model, atebimetinib-treated animals sustained body weight near baseline through approximately two weeks of dosing, while untreated controls lost a median of more than 20% of body weight -

NEW YORK, July 21, 2026 (GLOBE NEWSWIRE) -- Immuneering Corporation (NASDAQ:IMRX), a late-stage clinical oncology company focused on keeping cancer patients alive and helping them thrive, today announced the publication of new findings in Cancer Research, a leading peer-reviewed journal of the American Association for Cancer Research, characterizing the differentiated mechanism and broad preclinical activity of atebimetinib.

The article, "Dual-MEK Inhibitor Atebimetinib Displays Broad Activity in RAS- and RAF-Mutant Tumors via Deep Cyclic Inhibition and Resisting RAF-Bypass," (Kolitz et al., Cancer Research, doi.org/10.1158/0008-5472.CAN-25-4907) reports that atebimetinib demonstrated broad antitumor activity across RAS- and RAF-mutant models while resisting RAF-mediated bypass signaling, a key mechanism associated with resistance to other MEK inhibitors. Because the activity observed spanned a range of KRAS, NRAS, and BRAF alterations, the findings support the potential of atebimetinib to address RAS- and RAF-mutant cancers broadly — including the majority of RAS-mutant tumors that are not addressed by currently available mutation-selective inhibitors.