More than half of all tumors rely on inappropriate activation of the RAS/RAF/MEK pathway, yet existing drugs targeting this pathway are limited by toxicity or are narrowly focused on subpopulations with specific mutations. Immuneering’s novel drug candidates spare healthy normal cells by modulating cell signaling dynamics to selectively impact tumor cells.
Oncology – Select Therapies
Immuneering is developing its lead candidate IMM-1-104 as a dual inhibitor of MEK and a related target, to inhibit this important pathway driving the growth of many tumors while avoiding the feedback loop that causes many patients to develop resistance to traditional MEK inhibitors. By targeting MEK in a novel way, our preclinical models have demonstrated greater durability with reduced overall toxicity.
Our Clinical Candidate, IMM-1-104, is in IND-enabling studies.
Immuneering is developing a differentiated inhibitor of the MAPK signaling pathway. The MAPK pathway is a central signaling cascade involved in cell proliferation, cell growth, malignant transformation and drug resistance. Increased expression of this pathway is associated with a poor prognosis in cancers.5
The Covalent MEK program is currently in the discovery stage of drug development.
Immuneering is developing molecules for KRAS-driven cancers including pancreatic, colorectal and lung cancers. KRAS is the most commonly mutated of the RAS isoforms and represents an attractive target for treatment given its ubiquity, central role as a driver mutation and association with poor prognosis. KRAS mutations occur in approximately 25 percent of all human cancers, including more than 90 percent of pancreatic cancers, 35 to 45 percent of colorectal cancers and approximately 25 percent of lung cancers.6 Activating mutations of KRAS lead to cell transformation and increased resistance to chemotherapy. Currently, no effective treatments exist that target mutant variants of KRAS.
The KRAS4B program is currently in the discovery stage of drug development.
1 DOI: 10.1038/oncsis.2016.3
2 DOI: 10.1038/sj.onc.1210422
3 DOI: 10.1158/1078-0432.CCR-19-2138
4 DOI: 10.1155/2010/150960
5 DOI: 10.1007/s10147-017-1156-4
For most Alzheimer’s patients, there is no clear trajectory of disease progression or worsening symptoms. In fact, even clinical presentation can be widely different from individual to individual, suggesting that Alzheimer’s is less of a disease and more of a syndrome. Integrating brain gene expression and Alzheimer’s marker data offers the potential to stratify patients into subgroups with unique biology and identify targets specific to these subgroups.