Incendia Therapeutics is developing PRTH-101, a monoclonal antibody that inhibits Discoidin Domain Receptor 1 (DDR1) to disrupt collagen alignment in the tumor microenvironment, facilitating immune cell access to tumors. This approach targets immune-excluded tumors in recalcitrant cancers, enhancing the efficacy of immunotherapies and traditional treatments.
Funding
Funding not disclosed
Founders
Product
Problem
Many cancers create a hostile microenvironment that prevents immune cells from reaching and attacking tumor cells effectively. This immune exclusion contributes to the resistance of these tumors to both immunotherapies and traditional treatments.
Solution
Incendia Therapeutics is developing PRTH-101, a monoclonal antibody that inhibits Discoidin Domain Receptor 1 (DDR1), a collagen receptor highly expressed by cancer cells. By blocking DDR1, PRTH-101 disrupts the alignment of collagen fibers in the tumor microenvironment, creating gaps in the barrier and allowing T cells to infiltrate and attack the tumor cells. This approach aims to enhance the efficacy of immunotherapies, modified T cell therapies, chemotherapies, and radiation by improving immune cell access and reducing tumor hypoxia. PRTH-101 represents a novel strategy for stimulating immune-based antitumor activity in recalcitrant cancers.
Target Audience
The primary target audience includes patients with recalcitrant cancers characterized by immune-excluded tumors, as well as oncologists and researchers seeking to improve the efficacy of cancer immunotherapies and traditional treatments.
Features
- PRTH-101 is a monoclonal antibody targeting Discoidin Domain Receptor 1 (DDR1).
- DDR1 inhibition disrupts collagen fiber alignment in the tumor microenvironment.
- Disruption of collagen alignment facilitates T cell infiltration into tumors.
- PRTH-101 is being evaluated in a Phase 1 clinical trial (NCT05753722) as a monotherapy and in combination with PD-1 inhibitors.
- Preclinical studies demonstrate that PRTH-101 promotes immune-based antitumor activity.
- Addressing aligned collagen may allow modified T cell therapies to enter solid tumors more easily.
- May decrease tumor bed oncotic pressure allowing the diffusion of chemotherapies into the tumor at higher concentrations.
- PRTH-101 may decrease hypoxia in the tumor microenvironment allowing radiation to work more effectively.