President and CEO
Ikena Oncology
Ikena Oncology develops targeted therapies that focus on the Hippo and RAS signaling pathways to address cancer growth and resistance. Their biomarker-driven approach aims to provide effective treatment options for specific patient populations with high unmet medical needs.
- Biotechnology
Updated 7 months ago
Funding
Raised to date
$75MRaised to date based on public sources. This may differ from the amount the company actually raised and is based only on what is publicly available on the internet.
Funding rounds are not available yet.
Founders
Product
Problem
Approximately 30% of all human cancers are driven by mutations in the RAS pathway, but current therapies and product candidates do not address roughly 85% of these mutations. Many existing RAS pathway inhibitors are also limited by cancer cells' ability to develop therapeutic resistance through signaling bypass mechanisms.
Solution
Ikena Oncology develops targeted oncology therapies focused on the RAS signaling pathway, employing a tumor-directed approach. Their lead development candidate, IK-595, is a MEK-RAF molecular glue that traps MEK and RAF in an inactive complex, inhibiting RAS signals more completely than existing inhibitors. By complexing the RAFs, including CRAF, IK-595 prevents a signaling bypass mechanism that cancer cells use to drive therapeutic resistance. Trapping CRAF in an inactive complex also prevents the kinase-independent anti-apoptotic function in RAS and RAF mutant cancers. IK-595 is designed as an oral therapy with a pharmacokinetic profile that aims for a superior therapeutic window.
Target Audience
The primary target audience includes patients with RAS and RAF altered cancers, as well as the physicians who treat them.
Features
- IK-595: MEK-RAF molecular glue development candidate
- Traps MEK and RAF in an inactive complex
- Inhibits RAS signals more completely than existing inhibitors
- Complexes RAFs, including CRAF, to prevent signaling bypass
- Prevents kinase-independent anti-apoptotic function in RAS and RAF mutant cancers
- Oral therapy with a half-life enabling a potentially superior pharmacokinetic profile