Oncology

Discovery
IND-enabling
Phase 1
Phase 2
Phase 3
Trifecta MEK

Title

8%
KRAS4B

Title

8%
RAS induction

Title

8%
Covalent-MEK

Title

8%
PI3K-alpha

Title

8%

Neuroscience

IMM-ALL-01

Title

8%
IMM-ALL-03

Title

8%

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

Dual-MEK inh

Our MEK product candidate, IMM-1-104, is designed to be a highly selective inhibitor of ERK activation (i.e., phosphorylation), prevent MAPK pathway reactivation and have a short plasma half-life that reduces sustained pathway inhibition. Unlike MEK inhibitors approved by the U.S. Food and Drug Administration, or the FDA, IMM-1-104 is designed to prevent RAF-mediated activation of MEK by engagement of the RAF activation loop on MEK, such as CRAF-bypass. Additionally, with a short plasma half-life, IMM-1-104 can achieve deep cyclic inhibition of the MAPK pathway. As a result of these differentiating attributes, we plan to evaluate IMM-1-104 in RAS mutant solid tumors where a high unmet medical need currently exists.

MEK-io

Our MEK-immuno-oncology MEK-io program is focused on developing innovative allosteric MEK inhibitors to be administered in combination with select immune modulators (e.g., checkpoint inhibitors) for the treatment of “cold” solid tumors, which are immunologically inaccessible. Our investigational MEK-io, IMM-6-415, is designed with unique pharmacokinetic and pharmacodynamic profiles that may enhance cycle inhibition time of MEK and ERK to optimize the patient’s immune response and promote maximal antitumor responses when administered in combination with select immune modulators.

Alzheimer’s

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. We aim to be leaders in delivering effective precision medicines to patients suffering with Alzheimer’s disease globally.