Verismo Therapeutics has created SynKIR™, a generation‑2.0 KIR‑CAR platform that uses a dual‑chain architecture modeled on killer immunoglobulin‑like receptors to prevent chronic T‑cell stimulation. By separating tumor binding from activation and employing a parallel DAP12 signaling pathway, the technology maintains long‑term T‑cell persistence and cytotoxicity in solid‑tumor micro‑environments, offering biopharma partners and researchers a next‑generation CAR‑T solution for hard‑to‑treat cancers.
Funding
$4M 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
Current CAR T cell therapies rely on a single-chain receptor design that leads to rapid T cell exhaustion and have demonstrated limited efficacy against solid tumors, leaving many patients without effective immunotherapy options.
Solution
Verismo Therapeutics has developed SynKIR™, a generation‑2.0 KIR‑CAR platform that mimics the natural architecture of killer immunoglobulin‑like receptors. The technology separates tumor binding from T cell activation with independent binding and signaling chains that remain uncoupled at rest, preventing chronic stimulation. When a tumor antigen is encountered, the chains couple to form a functional receptor, delivering a parallel DAP12 activation signal that bypasses the CD3‑ζ pathway and provides intrinsic co‑stimulation. This design sustains long‑term T cell persistence and cytotoxic activity in the hostile micro‑environment of solid tumors, achieving durable anti‑tumor responses in preclinical models where traditional CAR T cells fail.
Target Audience
Primary customers are biopharmaceutical companies and research institutions developing cellular immunotherapies for solid tumors, as well as oncology clinicians seeking next‑generation CAR T solutions.
Features
- Dual‑chain KIR‑CAR architecture that decouples at rest and couples upon tumor antigen engagement
- Parallel DAP12 signaling pathway providing activation and co‑stimulation independent of CD3‑ζ
- Enhanced surface stability with sustained receptor expression on both activated and resting T cells
- Demonstrated long‑term T cell functionality and complete tumor remissions in mesothelioma and glioblastoma mouse models
- Combines NK cell innate potency with T cell durability for prolonged anti‑cancer efficacy