TMEkine™

TMEkine™ is designed to target the tumor microenvironment(TME) and re-activate the immune system at the tumor site, where the activated immune system will eradicate malignant cancer cells. TMEkine™ molecules are composed of a TME targeting arm and a cytokine arm, the TME targeting arm directs the molecule to the TME for minimized systemic immune responses for a wide therapeutic window. Potent single agent activity is expected and synergistic effects can be achieved when used with other cancer immunotherapies such as immune checkpoint inhibitors.

KNP-101 (IL-12-Anti-Target A for solid tumors): Bi-specific antibody with an engineered IL-12 mutant arm that has minimized binding to normal cells, combined with Target A, a target highly expressed in TME of solid tumors

KNP-102 (IL-12-Anti-Target B for hematologic cancers): Bi-specific antibody with an engineered IL-12 mutant arm that has minimized binding to normal cells, combined with Target B, a well validated target for hematologic cancers

Cytokine X-Anti-Target A and Cytokine X-Anti-Target B: Bi-specific antibody with Cytokine X, a cytokine that induces migration of various immune cells and formation of lymphoid-like structures

Auto-Immune Disease Targeting Large Molecules

Specifically inhibiting the alternative pathway of the complement system, Kanaph's bispecific Fc-fusions can be used to treat a number of complement-mediated diseases in both the retinal and systemic fields.

KNP-301 (C3b inhibitor-VEGF binder): Bi-specific Fc-fusion protein that inhibits C3b and VEGF simultaneously for treatment of complement-mediated and angiogenesis driven retinal diseases

KNP-302 (C3b inhibitor-CD59): Bi-specific Fc-fusion protein that targets both the upstream and downstream of the complement cascade for a more complete inhibition of the alternative pathway

Cancer-targeting Small Molecules

Kanaph is building an oncology portfolio of best-in-class small molecules for areas with high unmet medical needs.

KNP-501 (4th generation EGFR Inhibitor): Targeting sub-populations that demonstrate specific mutational resistance to osimertinib

KNP-502 (EP2/4 dual antagonist): Molecule that removes suppressive immune cells and increases effector immune cells in the tumor microenvironment