Kbi-110 -

"Then we need to go somewhere they can't follow," she replied.

The face that filled the screen was unremarkable. A woman in her mid-thirties, tired eyes, short hair. Her name was listed as "Subject 110." But the designation beneath her name made Elias’s blood run cold. KBI-110

In the hallway, the boots were getting closer. The handlers were coming to reset her manually. "Then we need to go somewhere they can't

The pyridyl‑urea arm of KBI‑110 weakly recruits the E3 ligase CRBN . While the affinity is insufficient for robust degradation on its own, in cells where BRD9 is over‑expressed (e.g., AML blasts), the ternary complex forms long enough to ubiquitinate and partially degrade BRD9. This results in a dose‑dependent, partial knock‑down (≈ 30‑40 % reduction at 100 nM), which is enough to blunt pathogenic transcription without fully erasing the protein’s physiological function. Her name was listed as "Subject 110

Solid tumors (pancreatic, ovarian, colorectal) are often "cold"—they hide from the immune system. By physically tethering a T-cell to the tumor, KBI-110 doesn't wait for the immune system to find the cancer; it drags the two together. This could unlock resistant tumors that don't respond to PD-1 inhibitors.