Kyn Therapeutics Rebrands as Ikena Oncology, Reflecting Next Phase of Growth
FDA Clearance of IND Application for Phase 1 Study of AHR Antagonist, IK-175
Anticipating Multiple Clinical and Regulatory Milestones in 2020, Including Report of
Preliminary Clinical Data on Its Lead Program IK-007, an EP4 Antagonist
Disclosing New Pipeline Program Modulating the Hippo Signaling Pathway
New Corporate Identity Aligned with Broadened Strategy on Novel, Patient-Directed,
Boston, Mass. – December 3, 2019 – Kyn Therapeutics, a clinical-stage biotechnology company, today announced it is rebranding to Ikena Oncology. The rebranding reflects the evolution of the Company beyond its continued achievements in immuno-metabolism, as well as its renewed commitment to biomarker-driven oncology drug development. The rebranding is accompanied by announcement of the clearance by the U.S. Food and Drug Administration (FDA) of the Company’s investigational new drug (IND) application for IK-175, a small molecule antagonist of AHR. In addition, Ikena unveiled a new discovery program aimed at modulating the Hippo signaling pathway for treatment of cancer. Ikena has five development and discovery programs with multiple clinical and regulatory milestones expected in 2020, including report of preliminary clinical data on its lead program IK-007, an EP4 antagonist.
Mark Manfredi, Ph.D., President and Chief Executive Officer of Ikena Oncology, commented, “Ikena Oncology represents the growth and evolution of our vision, strategy, capabilities and values. We look forward to leveraging these drivers to build on our efforts to become an industry leader in novel therapeutics for patients battling cancer.”
The new name “Ikena” is derived from the combination of “i” which refers to the individual patient and “ken” which means knowledge, thereby illustrating the Company’s focus on using its insights to identify patients most likely to benefit from its therapies.
Advancement and Expansion of Development Pipeline
The expanded Ikena Oncology development pipeline is composed of patient-directed programs addressing distinct molecular targets and biologic pathways within and outside of immuno-metabolism, including immunotherapies and tumor cell intrinsic product candidates:
- IK-007: A highly selective, first-in-class, oral EP4 receptor antagonist targeting the prostaglandin E2 (PGE2) immunosuppressive signaling pathway. IK-007 (formerly ARY-007) is being investigated in two ongoing Phase 1b/2 studies in combination with Merck’s anti-PD-1 therapy Keytruda® (pembrolizumab) in patients with advanced or progressive microsatellite stable colorectal cancer (MSS CRC) and in patients with advanced or metastatic PD-1/L-1 refractory non-small cell lung cancer (NSCLC). Ikena is employing a robust, biomarker strategy by analyzing blood, tumor and urine biomarkers relevant to T cell checkpoint inhibitors and EP4 signaling. Ikena expects to report preliminary data in 2020.
- IK-175: A selective oral AHR antagonist which prevents AHR-modulated tumor promotion through its influence on both the tumor and the immune system. The Company’s recently FDA-cleared IND enables the commencement of a first-in-human clinical study in which the anti-tumor activity of IK-175 (formerly KYN-175) will be evaluated as a single agent, and in combination with other therapies, in cancers with activated AHR. Ikena expects to initiate a clinical study evaluating IK-175 in early 2020. Ikena is employing a multi-assay AHR activation biomarker strategy to select lead cancer indications and enable prospective selection of patients believed most likely to benefit from IK-175. A patent application with claims directed to IK-175 has been deemed allowed by the United States Patent and Trademark Office. The AHR antagonist program is the subject of a global strategic collaboration with Celgene, now Bristol-Myers Squibb.
- IK-412: A highly potent and stable kynurenine-degrading enzyme (or “Kynase”) that may be able to overcome resistance to immune modulating agents. Ikena expects to file an IND for IK-412 (formerly KYN-412) in the second half of 2020. The first-in-human clinical study will be focused on patients with cancers that express high IDO1/TDO2. IK-412 is the subject of a global strategic collaboration with Bristol-Myers Squibb.
- Hippo Program: The Hippo signaling pathway is a key tumor suppressor axis with tumor cell intrinsic dependence and immune system mechanisms of action. It is highly mutated in several cancer types, providing a streamlined path to clinical proof-of-concept. For example, there is a high prevalence of NF2 loss of function mutations in mesothelioma and LATS1/2 in bladder and renal cancers. Currently in the lead optimization stage, Ikena expects to identify a development candidate during the second half of 2020.
“As we launch our new corporate identity, we anticipate an exciting 2020 that includes multiple clinical and regulatory milestones. We are encouraged by the ongoing studies investigating IK-007 in combination with Keytruda® in patients with MSS CRC and PD-1/L-1 refractory NSCLC, and look forward to continuing enrollment. Moreover, we aim to advance IK-175 into the clinic, file an IND for IK-412, and identify a development candidate for the Hippo program,” concluded Dr. Manfredi.
The Company’s website is now available at IkenaOncology.com.
About Ikena Oncology
Ikena Oncology is a clinical-stage biotechnology company that discovers and develops patient-directed, biomarker-driven therapies for cancer patients who need life-saving treatment, by understanding what drives their disease. Ikena is advancing five clinical, preclinical and discovery programs: IK-007, an EP4 receptor antagonist; IK-175, an AHR antagonist; IK-412, a kynurenine-degrading enzyme (“Kynase”); discovery-stage molecules targeting the Hippo signaling pathway; and a discovery-stage program against an undisclosed target. Ikena has entered into a global strategic collaboration with Bristol-Myers Squibb on the AHR antagonist and Kynase programs. Ikena has raised capital from top tier investors OrbiMed Advisors and Atlas Venture.