Our proprietary platform
T3 Pharma has developed a proprietary cancer therapy platform based on regulating and harnessing the natural behaviours of live bacteria.
The genetically engineered bacteria selectively target solid tumors, where they deliver chosen protein payloads into the cells.
We have generated and tested several hundred different bacterial strains and selected the most promising for further development, including our lead program, T3P-Y058-739.
T3 Pharma’s bacteria efficiently and selectively colonize solid tumors.
We achieve tumor selectivity by removing key bacterial virulence factors which are responsible for protecting them against the human immune system. In healthy tissues, our immune cells rapidly clear out the engineered bacteria, while in solid tumors the bacteria are able to survive and colonize.
Removing these key virulence factors not only contributes to highly specific tumor targeting and colonization, but also provides our live bacterial platform an attractive safety profile.
T3 Pharma has harnessed the bacterial type 3 (T3) secretion system to deliver bioactive proteins.
The T3 secretion system is part of the bacteria’s natural machinery. It functions like a nano-syringe to inject specific effector proteins into human target cells. Our proprietary techniques enable us to hijack this machinery so that we can replace the bacterial effector proteins with bioactive proteins of our choice.
Our engineered bacteria therefore act as highly specific and efficient delivery vehicles, injecting target cells with bioactive proteins. This can be used to activate dedicated signalling cascades and trigger an immune response, e.g. immune cell activation or cell death.
The ease of genetically engineering bacteria makes our platform into an extremely versatile tool to target therapeutically promising pathways in oncology and beyond.
The technology has been published in The Journal for Cell Biology: “A bacterial type III secretion-based protein delivery tool for broad applications in cell biology”
(Ittig et al. 211 (4): 913, JCB, 2015)