Reprogramming Immunity to Rewrite the Future of ALK+ Cancer Care
Harnessing next-generation immuno-therapies to outsmart treatment resistance, eliminate ALK-positive cancer cells at their root, and restore the hope of long-term remission.
Scientific approach
At ALKemist Bio, we are developing novel immuno-therapies specifically designed to recognize the ALK oncogene—a known driver of several aggressive and treatment-resistant cancers. Anaplastic Lymphoma Kinase (ALK) is a receptor tyrosine kinase normally active only during embryonic development, where it plays a role in the formation of the nervous system. In healthy adult tissues, ALK expression is minimal to absent. In cancer, ALK becomes aberrantly activated through genetic alterations such as: - Gene fusions (e.g., EML4–ALK), which lead to the expression of intracellular oncogenic fusion proteins - Point mutations, particularly in neuroblastoma - Gene amplification or overexpression, resulting in abnormal ALK signaling These alterations drive tumor growth and survival, making ALK a well-validated and highly specific target for precision therapies. Depending on the tumor type, ALK may be found either as an intracellular fusion protein or as a transmembrane receptor on the cell surface—a distinction that informs our therapeutic approach.
Our strategy harnesses the immune system to deliver highly selective, potent therapies tailored to the biology of ALK-positive tumors.
Depending on how ALK is expressed—either as an intracellular fusion protein or as a full-length transmembrane receptor—ALKemist has designed a dual approach to maximize therapeutic efficacy.
CAR-T
For tumors - such as neuroblastoma - that express ALK as a membrane-bound receptor, we develop chimeric antigen receptor (CAR) T cells specifically targeting the extracellular domain of ALK. This approach enables direct recognition and elimination of tumor cells via surface antigen engagement, independent of HLA type.

TCR-T
For tumors - such as NSCLC - where ALK is presented intracellularly and processed into peptides bound to HLA molecules, we engineer patient-derived T cells with high-affinity T cell receptors (TCRs). These TCR-T cells are capable of recognizing and killing ALK-positive tumor cells across a wide range of solid cancers with defined HLA backgrounds.

Together, our CAR-T and TCR-T platforms form a comprehensive and adaptable therapeutic arsenal to selectively eliminate ALK-positive cancer cells across diverse tumor types and patient populations.