Empowering the body’s natural defenses against life-threatening cancers.
We are creating therapies using the natural biology of T cells to treat patients with solid tumors.
TAC, our proprietary T cell Antigen Coupler, is a multi-domain chimeric molecule that works directly with the T cell receptor (TCR) to help a T cell recognize and attack cancer cells. The use of an intracellular co-receptor sequence as one of its domains is completely unique to Triumvira. This non-gene edited strategy is designed to retain the T cell’s natural control and internal feedback mechanisms.
We believe TAC will become an essential tool for safely and effectively treating patients with liquid and solid malignancies. The initial target of our TAC-based programs is HER2, a surface cancer antigen frequently over-expressed in a broad range of solid tumors.
No one else has created a technology that so closely mirrors a T cell’s natural biology and functions.
Jonathan Bramson, PhD, Scientific Co-Founder, and Chair of the Scientific Advisory Board
The modular structure of a TAC molecule.
Antigen Binding Domain
Binds to a specific tumor target on a cancer cell.
CD3 Binding Domain
Interacts with and co-opts the natural TCR.
CD4 Co-Receptor Domain (Unique to Triumvira)
Unique feature that anchors the TAC in the cell membrane and either activates or silences the T cell depending on the presence of a cancer antigen, critical in activating the immune response.
Advanced Antigen Targeting
TAC can redirect T cells to any tumor antigen of choice, independently from MHC molecules, enabling selective tumor recognition with broad applicability across tumor types.
Normal Immune Synapse
The TAC receptor has no signaling capacity in itself. Signaling is solely mediated by the endogenous TCR once the TAC interacts with both the cancer antigen and the TCR, which minimizes the risk of tonic signaling and leads to a normal immune synapse, as observed in natural T cells.
Controlled Cytokine Release
Through a low, controlled release of cytokines, TAC signals the T cell to stop cell killing once the tumor cell is eliminated, potentially reducing the risk of side effects.
Deep Tumor Penetration
TAC-T cells have been shown to effectively penetrate and expand in tumor tissues grown in mice, which may translate to safer, more efficacious tumor regression in patients.
T Cell Durability & Persistence
While lacking signs of premature exhaustion and showing retention of a desirable, mostly memory cell phenotype, TAC-T cells may be able to overcome the hostile tumor microenvironment to attack solid tumor cells.
Strong preclinical safety and efficacy.
Working with independent pharma and biotechnology companies, as well as contract services organizations, we have conducted multiple preclinical studies of our TAC platform in different liquid and solid tumor models.
Preclinical data reveals TAC’s ability to induce more efficient anti-tumor responses than other treatments, such as chimeric antigen receptors (CARs) and other active agents.
Our lead product candidate.
We are developing an autologous TAC program, TAC101-CLDN18.2, which co-opts a patient’s own T cell receptor and redirects the T cells to CLDN18.2-expressing cells in tumors. This approach requires apheresis of a patient’s blood sample and genetic engineering in the lab to create the TAC-T cell product.
Vast potential across manufacturing approaches and targets.
Our technology is highly versatile and can be readily combined with both existing and novel targets, including HER2, Claudin 18.2, GPC3 and GUCY2C. We are investigating both autologous and/or allogeneic applications of TAC-T cells to these targets.
While our autologous approach requires apheresis of a patient’s blood sample and genetic engineering in the lab to create the TAC-T cell product, our allogeneic approach employs an “off-the-shelf” cell bank of non-gene edited gamma delta (γδ) T cells, which are a subset of T cells. They are extracted from a healthy donor and genetically engineered with TAC technology.