Our Pipeline
As we evolve with our science, our multifaceted approach builds a robust pipeline of patient direct therapies.
At Ikena®, we are advancing a portfolio of targeted therapies intended to enable a personalized approach for every patient with cancer.
Our Pipeline
Discovery
IND Enabling
Phase 1
Late-Stage
Development
Partnerships & Rights
Targeted Oncology
Hippo Signaling Pathway
TEAD
Hippo-altered Cancers
Monotherapy & Multiple Combinations
Undisclosed
Hippo-altered Cancers
IK-595
MEK-RAF
RAS-mutated Cancers
Undisclosed
RAS-mutated Cancers
AHR Signaling
AHR
Monotherapy & Nivolumab Combination
Nivolumab Combination
EP4 Signaling
IK-007
EP4
MSS-CRC, PGEM Enriched
Pembrolizumab Combination
Targeted Oncology Programs in the Hippo and RAS Signaling Pathways
Our targeted oncology discovery efforts include programs that target the Hippo and RAS pathways, emphasizing our philosophy of designing treatments for tailored patient populations that are identified through the genetic makeup of their tumors. Our lead program, IK-930, targets the key TEAD transcription factor in the Hippo pathway. Across IK-930 and our preclinical pipeline, extensive translational data accompany our strategic development for each target, and we continue to generate data to identify biomarker-defined, underserved cancer patient populations.
The Hippo Signaling Pathway
As a key driver of cancer pathogenesis, the Hippo pathway regulates cell fate, proliferation, and survival. The pathway is genetically altered in approximately 10% of all human cancers. In certain tumors, the genetic alterations in the Hippo pathway can be as frequent as 40%, for example as in malignant Mesothelioma, and in epithelioid hemangioendothelioma (EHE), a rare type of soft tissue sarcoma, where 100% of patients have key Hippo pathway fusion genes.
The Hippo pathway is also implicated in therapeutic resistance, potentially providing compensatory growth and survival signals in tumors when patients are treated with other therapies. Resistance to multiple targeted therapies and tumor recurrence can be linked to YAP/TEAD activation. Overcoming resistance mechanisms can deepen and prolong responses.
Hippo Signaling Pathway Alterations and Activity Trigger Tumor Growth
IK-930: TEAD Inhibitor
IK-930 binds to TEAD transcription factors near the end of the Hippo pathway and prevents the expression of multiple target genes that drive cancer progression, metastases, and therapeutic resistance. We are exploring the potential of IK-930 both as a monotherapy in patients with Hippo pathway-mutated cancers and in combination with other targeted therapies.
The RAS Signaling Pathway
The RAS pathway is a well-known cancer-driving pathway that is mutated in approximately 30% of all human cancers. For decades, the RAS pathway was considered undruggable. Despite advancements in recent years targeting RAS-mutated cancers, approximately 85% of RAS mutations are not addressed by current product candidates or approved therapies. We believe that the key to addressing the unmet need for patients with these mutations is to target the pathway on multiple levels and understand the resistance mechanism to achieve deep and sustained responses.
Exploring Addressable Targets in the RAS Signaling Pathway
IK-595: MEK-CRAF Inhibitor
Ikena’s development candidate, IK-595, traps MEK and RAF in an inactive complex, more completely inhibiting RAS signals than existing inhibitors. IK-595’s ability to complex CRAF, in particular, prevents a well-recognized signaling bypass mechanism that cancer cells employ to drive therapeutic resistance to other drugs in this class. In addition, trapping CRAF in an inactive complex prevents the kinase independent anti-apoptotic function in RAS and RAF mutant cancers, a mechanism that cannot be addressed with first generation MEK inhibitors or pan-RAF inhibitors. IK-595 is being developed as an oral therapy, with a half-life enabling a pharmacokinetic profile potentially superior to other drugs, with the goal of developing an optimal therapeutic window for patients.
Immune Signal Targeting Programs in Tumor Microenvironment Modulation
AHR Inhibition
AHR Signaling
