Pipelines

Target ID
Hit-ID
Hit-to-Lead
Lead-ID
Lead Opt
Pre-IND
Dual RAF-MEK
Target ID
Hit-ID
Hit-to-Lead
Lead-ID
Lead Opt
Pre-IND

Title

90%
Trifecta MEK
Target ID
Hit-ID
Hit-to-Lead
Lead-ID
Lead Opt
Pre-IND

Title

70%
pan-KRAS
Target ID
Hit-ID
Hit-to-Lead
Lead-ID
Lead Opt
Pre-IND

Title

42%
RASi
IMM-1811901
Target ID
Hit-ID
Hit-to-Lead
Lead-ID
Lead Opt
Pre-IND

Title

42%
Metastasis Pathway
IMM-1352012
Target ID
Hit-ID
Hit-to-Lead
Lead-ID
Lead Opt
Pre-IND

Title

28%
Metabolism
IMM-2018512
Target ID
Hit-ID
Hit-to-Lead
Lead-ID
Lead Opt
Pre-IND

Title

28%
Additional Programs
Target ID
Hit-ID
Hit-to-Lead
Lead-ID
Lead Opt
Pre-IND

Title

13%

Immuneering is advancing a pipelines of drug programs focused on treating aspects of disease that have eluded conventional drug discovery.

Oncology – Select Therapies

  IMM-1611441

IMM-1611441 BODY showing digestive systemImmuneering is developing its lead candidate IMM-1611441 as a dual RAF-MEK inhibitor, 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.

IMM-1611441 is entering IND-enabling studies with a Clinical Candidate.

  IMM-2019611

IMM-2019611 BODY showing skeletonImmuneering is developing IMM-2019611 as 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

IMM-2019611 is currently in lead optimization stage of drug development.

  IMM-1811900

IMM-1811900 BODY showing organsImmuneering is developing IMM-1811900 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.

IMM-1811900 is currently in the lead optimization stage of drug development.