Benzinga | Oct 11, 2021 06:53AM EDT

Immuneering Reports Compelling Preclinical Data On IMM-1-104 At AACR-NCI-EORTC International Conference On Molecular Targets And Cancer Therapeutics

Immuneering Corporation (NASDAQ:IMRX), a biopharmaceutical company advancing a robust pipeline of oncology and neuroscience product candidates that are designed to uniquely disrupt cellular signaling dynamics, today announced that three key preclinical datasets highlighting the potential of its lead product candidate, IMM-1-104, were presented at the recent AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics that took place virtually from October 7-10, 2021.

IMM-1-104 is designed to be a highly selective dual-MEK inhibitor that further disrupts the kinase suppressor of RAS 1 and 2 (KSR1/2) for the treatment of advanced solid tumors in patients harboring RAS mutant tumors. The Company anticipates submission of an Investigational New Drug application (IND) for IMM-1-104 to the U.S. Food and Drug Administration (FDA) in the first quarter of 2022.

"We are delighted to share compelling data from multiple animal studies that underscore IMM-1-104's potential for activity against a wide range of RAS and RAF mutant tumors and further elucidate its novel mechanism of action for dual MEK inhibition," said Ben Zeskind, Ph.D., Co-Founder, President and Chief Executive Officer of Immuneering. "The totality of these data, along with the tolerability profile that we consistently observe across animal models, are particularly encouraging and further validate our plans to advance IMM-1-104 into human clinical trials in the first half of next year."

In a poster titled, "IMM-1-104: a novel, oral, selective dual-MEK inhibitor that displays broad antitumor activity and high tolerability across RAS and RAF mutant tumors in vivo," and presented by Brett Hall, Ph.D., Chief Scientific Officer at Immuneering, study authors concluded that, "IMM-1-104 was uniquely designed to normalize MAPK signaling dynamics while resisting pathway reactivation in RAS and RAF mutant tumors. Preclinical data showed broad activity in multiple animal models bearing tumors with diverse RAS and RAF mutations, including KRAS-G12C, KRAS-G12D, KRAS-G12S, NRAS-Q61R and BRAF-V600E. Further, IMM-1-104 demonstrated superior activity and tolerability versus other U.S. FDA registered MEK inhibitors in head-to-head animal studies."

Data presented by Peter King, Ph.D., Vice President, Head of Discovery at Immuneering, in a poster titled, "Benchmarking the novel dual-MEK inhibitor, IMM-1-104, head-to-head and in combination with sotorasib (AMG-510) in the MIA PaCa-2 (KRAS-G12C) pancreatic cancer xenograft model," demonstrated that "IMM-1-104 treatment resulted in tumor regressions similar to that observed for sotorasib in the recently benchmarked KRAS-G12C mutant pancreatic cancer xenograft model (MIA PaCa-2). IMM-1-104 in combination with sotorasib promoted deep, durable tumor regressions, when compared to either drug alone. Future drug-drug combinations with upstream inhibitors such as sotorasib may afford greater durability in combination for patients with KRAS-G12C and other select tumor types. Collectively, these data suggest the potential for broad, single agent activity of IMM-1-104 in tumors with inappropriately elevated MAPK signaling, including a large percentage of KRAS mutant pancreatic cancer."

Data highlighted in a third poster titled, "Transcriptional effects in C26 tumor highlight mechanistic aspects of a novel dual MEK inhibitor, IMM-1-104," was delivered by Sarah Kolitz, Ph.D., Vice President, Translational Medicine at Immuneering. She noted that "IMM-1-104 achieves deep cyclic inhibition of the pathway rather than constant blockade and prevents pathway reactivation, which has hampered U.S. FDA approved MEKi. These transcriptome level observations confirmed a pattern of deep cyclic inhibition by IMM-1-104, demonstrating strong MAPK pathway inhibition in tumors two hours after treatment and near complete release at 12 hours following treatment. This pattern was observed both after the initial dose as well as following chronic oral BID dosing for 18 days, indicating that deep cyclic inhibition was sustainable during chronic dosing."

Videos of each of the presentations can be viewed on the Company's website at www.immuneering.com/publications/