Identifying new mechanisms of action is vital for pre-clinical and clinical trials.
- Trabectedin and lurbinectedin
Trabectedin and Lurbinectedin are two selective inhibitors of trans-activated RNA polymerase II transcription. They selectively block the elongation phase of messenger RNA synthesis performed by RNA polymerase II. They do not inhibit RNA polymerase I or mitochondrial RNA polymerase, nor do they affect basal transcription: their action mechanism very selectively inhibits RNA polymerase II transcription. This is reflected in clinical results, since some tumors present transcriptional addiction (e.g. translocation-related sarcomas, small cell lung cancer, and triple negative breast cancer). These are clear examples of tumors that are sensitive to lurbinectidin.
Another of our drugs specifically inhibits a protein called eEF1A2. Inhibiting this cell target induces higher oxidative stress in tumor cells and triggers enzymes that accelerate cell death.
This compound inhibits tubulin polymerization. These proteins form part of the cell’s skeleton (the cytoskeleton). As a result, the cytoskeleton becomes degraded and the tumor cells lose the capacity to mobilize and divide.