The study, led by authors Nix and Gourisankar with Crabtree, Gray, Hinshaw, and Green as senior authors, was published online in Cell on July 20, 2026, according to Stanford Medicine.
Stanford Medicine reports that diffuse large B-cell lymphoma is frequently driven by BCL6.
In healthy immune cells, BCL6 temporarily suppresses genes that would trigger cell death, allowing cells to multiply during an immune response. In BCL6-driven lymphomas, this switch remains permanently on. Researchers used a technique called chemically-induced proximity, which brings molecules that rarely interact together through chemical bonds. According to Nix, one side of TCIP3 binds to BCL6 while the other binds to p300 or CBP; acetylation by these enzymes blocks BCL6's suppression. Nix explained that the approach lifts the suppression while simultaneously driving active expression of cell-death genes, accounting for the compound's high effectiveness.
The mouse trial and its limitations
Mice received TCIP3 injections twice daily, according to Stanford Medicine. The treated animals showed no obvious signs of toxicity and no sharp increase in inflammatory signals in the blood, although TCIP3 simultaneously dissolved germinal centers in immune cells, the cell type that becomes dysregulated in lymphomas.
More potent and gentler than p300/CBP comparison drugs in cell tests
In cell culture experiments using SUDHL5 lymphoma cells, TCIP3 was 238 times more potent than A-485 and 12 times more potent than dCBP-1, both of which also target p300/CBP. At the same time, TCIP3 damaged B and T cells from tonsil tissue of two donors and primary human fibroblasts far less than SUDHL5 cells, and was gentler than the comparison drugs. For cell lines with low BCL6 levels, TCIP3 performed as well as a combination of GNE-781 and BI-3812; the advantage became clear especially at high BCL6 levels. These comparisons come from a study version that had not yet been peer-reviewed at the time of publication; the source page now references a peer-reviewed version in Cell.
What broader application still needs
As of August 19, 2026, researchers were already searching for other cancer-driving proteins suitable for the same approach, according to Stanford Medicine. They suspected that molecules like TCIP3 could in the future also work against autoimmune diseases such as rheumatoid arthritis and myasthenia gravis, since germinal center cells also drive these diseases. Crabtree and Gray were co-founders and advisors of Shenandoah Therapeutics, which at the time held a license to the TCIP technology from Stanford, according to Stanford Medicine as of August 19, 2026.