Our clinical pipeline of
kinase inhibitors includes
tumor-targeted therapies
and immuno-targeted
Immuno-Targeted Therapies

Macrophages play key pro-tumoral roles in the tumor microenvironment including driving immunosuppression that protects tumor cells from immune system attack, as well as stimulating tumor proliferation and invasiveness. Combined targeting of the tumor killing T-cell and and the immune suppressing macrophage has become a new frontier in the development of immuno-oncology targets. Deciphera has developed a pipeline of immune- therapies targeting immunokinases. These therapies target macrophage checkpoints to increase therapeutic response rates when used in combination with T-cell checkpoint inhibitors, such as anti-PD-1 and anti-PD-L1 therapies.

Part 1: Kinases direct cell signaling activity to control cellular processes and are regulated by switches to adopt active or inactive kinase states.

Part 2: Deciphera’s switch control inhibitors restore the immune system to a strong cancer fighting state by blocking immunosuppressive kinase activation.


DCC-3014 is a potent and highly-selective immunokinase inhibitor targeting colony stimulating factor receptor 1 (CSF1R), also known as FMS. DCC-3014 is entering clinical development for the treatment of multiple solid tumors both as an adjuvant tumor microenvironment agent and in combination with immunotherapy and other modalities.

DCC-3014 has demonstrated a compelling preclinical profile including preventing tumor invasion in vivo with nanomolar potency and ultra-selectivity. Importantly, DCC-3014 has also demonstrated potent macrophage checkpoint inhibition as a single agent and in combination with PD1/PDL1 checkpoint inhibitors by blocking macrophage immunosuppressive function.


Rebastinib is a first-in-class TIE2 inhibitor targeting TIE2 expressing macrophages (TEMs), in clinical development for the treatment of multiple solid tumors as a single-agent and in combination with immuno-oncology agents.

Rebastinib has demonstrated in vivo activity blocking TEM macrophage checkpoint mechanisms and evasive tumor growth and vascularization in the tumor microenvironment.

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