The problem

The tumor ecosystem sends overlapping signals that shut CAR-T cells down.

Across solid tumors, tumor cells, immune cells, stroma, and local chemistry create overlapping routes to dysfunction. Even after CAR-T cells reach and recognize the tumor, those pressures can act together and erode function.

Blocking one route can leave the others active.

A CAR-T cell engages a solid-tumor cell while suppressive pressure from surrounding tumor, immune, stromal, and metabolic components converges on the T cell.

Close-up of an engineered CAR-T membrane where suppressive signals remain outside the cell but selected receptor-mediated routes are absent, while CAR-driven tumor recognition continues.

Our approach

Build resistance into the cell.

We use multiplex base editing to knock out selected receptors in the same CAR-T cell. The combination is designed to interrupt several routes to dysfunction at once while leaving CAR-driven tumor recognition intact.

The signals remain. Selected routes to dysfunction are disconnected.

Across solid tumors

The pressure profile changes by tumor. So should the resistance design.

Different solid tumors rely on different combinations of suppressive pressure. We use disease-specific human biology to tailor the resistance design to each context. Externally sponsored studies are already evaluating this approach across CNS and non-CNS tumors.

Two engineered CAR-T cells operate in distinct CNS and non-CNS tumor environments, each facing a different pattern of suppressive pressure. — Different pressure profiles. Disease-specific resistance designs.