Incendia Therapeutics is a clinical‑stage biotech that develops fully human monoclonal antibodies to remodel the tumor microenvironment (TME) and enable immune cell infiltration. Its lead candidate, PRTH‑101, inhibits DDR1 to reduce collagen‑mediated barriers and is being tested in a Phase 1c trial alone and with PD‑1 blockade for PD‑L1‑negative NSCLC and ICI‑refractory thymic carcinoma, aiming to improve the efficacy of checkpoint inhibitors in solid tumors.
Funding
$65M raised to dateRaised to date based on public sources. This may differ from the amount the company actually raised and is based only on what is publicly available on the internet.
Founders
Product
Problem
Cancer cells create a hostile tumor microenvironment (TME) that blocks immune cell infiltration and reduces the efficacy of existing therapies, especially in solid tumors such as pancreatic, ovarian, colorectal, lung, breast, thymic and NSCLC.
Solution
Incendia Therapeutics develops monoclonal antibodies that target structural and biochemical components of the TME to normalize it and permit host immune cells to reach tumor cores. By inhibiting Discoidin Domain Receptor 1 (DDR1) with its lead candidate PRTH‑101, the company aims to dismantle collagen‑mediated barriers and enhance the activity of checkpoint inhibitors. PRTH‑101 is being evaluated in a Phase 1c trial both as monotherapy and in combination with PD‑1 blockade for PD‑L1‑negative NSCLC and ICI‑refractory thymic carcinoma, with plans for Phase 2 expansion. The approach seeks to convert immune‑excluded, treatment‑resistant tumors into responsive disease states, improving progression‑free survival and overall outcomes.
Target Audience
Primary customers are oncology pharmaceutical companies and clinical research organizations developing immunotherapies for solid tumors, as well as oncologists treating patients with immune‑excluded or checkpoint‑resistant cancers.
Features
- Fully human monoclonal antibody (PRTH‑101) that selectively binds and inhibits DDR1, a key driver of TME stiffness and immune exclusion
- Dual mechanism: physical remodeling of extracellular matrix and modulation of signaling pathways that suppress immune activation
- Designed for combination with existing immune‑checkpoint inhibitors to boost their efficacy
- Clinical program includes a Phase 1c trial with safety, pharmacokinetic, and early efficacy endpoints, followed by planned Phase 2 expansion in 2026
- Proprietary biomarker strategy to identify DDR1‑high solid tumors and monitor TME normalization during treatment