Atebimetinib Combinations with Anti-PD1 Cured 50% of Mice in a RAS-Mutant Colorectal Cancer Model and Nearly Doubled Survival in a RAS-Mutant Lung Cancer Model; New Data Presented at SITC 2026

On November 6, 2026 Immuneering Corporation (Nasdaq: IMRX), a late-stage clinical oncology company focused on keeping cancer patients alive and helping them thrive, reported compelling preclinical data demonstrating that atebimetinib, the Company’s novel Deep Cyclic Inhibitor of MEK, enhanced the activity of PD-1 checkpoint blockade in RAS-mutant colorectal and lung cancer models, including a 50% durable complete regression rate in a colorectal model and a 1.8-fold median survival improvement with a triple combination in a lung model. The data are being presented at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) 41st Annual Meeting, taking place November 4-8, 2026, in Phoenix, Arizona.

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!

"Curing 50% of mice in one tumor model and nearly doubling median overall survival in another are both incredibly exciting. These data add to the body of preclinical evidence that combining a pulsatile inhibitor of MEK with immunotherapy may lead to enhanced activity," said Ben Zeskind, Ph.D., Co-Founder and Chief Executive Officer of Immuneering. "The ultimate test of this hypothesis will be to show it in patients, and it starts very soon: we expect to dose the first patient by the end of the year in our Phase 2 clinical trial of atebimetinib in combination with anti-PD-1 and chemotherapy in first-line RAS-mutant NSCLC patients."

In the CT-26 syngeneic mouse model of colorectal cancer, both the 75 mg/kg and 125 mg/kg atebimetinib plus anti-PD-1 groups achieved complete tumor regression in 6 of 12 mice (50%) per group, with no regrowth even after treatment discontinuation. Vehicle-treated animals had median survival of 21 days, while anti-PD-1 alone resulted in median survival of 29 days and atebimetinib monotherapy extended median survival dose-dependently from 28 to 41.5 days. In contrast, median survival was not reached in the atebimetinib plus anti-PD-1 combination groups, which outperformed the single-agent arms (P<0.0001 versus vehicle for nearly all combinations).

In the LL2 syngeneic lung cancer model, a PD-1-cold model unresponsive to anti-PD-1 monotherapy, atebimetinib demonstrated enhanced antitumor activity in combination with anti-PD-1 and platinum-doublet chemotherapy. At 125 mg/kg BID, atebimetinib plus anti-PD-1, carboplatin and pemetrexed extended median survival to 25 days, compared with 14 days for anti-PD-1 plus chemotherapy alone, representing a 1.8-fold improvement. All 12 mice receiving the triple combination were alive at Day 18, compared with none of the 12 mice receiving anti-PD-1 plus chemotherapy alone. These data support further clinical investigation of this combination in first-line RAS-mutant non-small cell lung cancer (NSCLC).

Presentation Details:
Title: "Cyclic disruption of the mitogen-activated protein kinase (MAPK) pathway by the pulsatile MEK inhibitor, Atebimetinib, enhances PD-1 checkpoint blockade in RAS mutant tumors."
Abstract: #377
Presenting Author: Amy E. Axel, Immuneering Corporation
Presentation: Friday, November 6, 2026

Following presentation, the poster will be available on the publications section of Immuneering’s website at View Source

(Press release, Immuneering, NOV 6, 2026, https://www.globenewswire.com/news-release/2026/11/06/3397545/0/en/atebimetinib-combinations-with-anti-pd1-cured-50-of-mice-in-a-ras-mutant-colorectal-cancer-model-and-nearly-doubled-survival-in-a-ras-mutant-lung-cancer-model-new-data-presented-at.html [SID1234674425])