The science behind S.1.p
Given the role that it plays in the progression of tumors, angiogenesis has become one of the most attractive targets for developing treatments in the domain of oncology. However, the efficacy of antiangiogenic therapy remains questionable, and there is an accumulation of evidence indicating that inducing hypoxia in tumors favors the invasion processes leading in fine to metastasis. Hypoxia increases the glycolysis and pentose cycle, promotes epithelial to mesenchymal transition, increases metalloprotease activity, increases growth-factor expression and favors the occurrence of a protumoral immune microenvironment. Furthermore, it is clear that the vascular disruption of abnormal tumor vessels impairs the efficient delivery of chemotherapeutic agents, while decreasing tumor radiosensitivity and immunotherapy efficiency.
Along these lines, and based on clinical observations, the company has developed a paradigm-shifting approach – in contrast to the prevailing antiangiogenic doctrine – in the form of a neoadjuvant therapy using a proangiogenic molecule acting as a tumor vasculature normalizer.
A functional plasmatic biomarker has been identified, allowing the selection of a subpopulation of eligible patients for such therapy.
This strategy is under pre-clinical investigation in collaboration with a research team located at the University of Geneva (UNIGE).
Tumors are characterized by an abnormal vasculature both in terms of morphology and functionality
High-dosage antiangiogenic therapy inducing vascular disruption of abnormal tumor vessels impairs delivery of chemotherapeutic agents, decreases the tumor radiosensitivity and favor a protumoral immune micro-environment (Th2 response). Low-dosage antiangiogenic therapy or the use of tumor vasculature normalizers result in the improvement of drug delivery and radiotherapy efficiency, and favor the occurrence of antitumor immune micro-environments (Th1 response).
The science behind our CAP6
Our CAP6 belongs to a new generation of cancer drugs having few side effects and generally greater efficacy. It displays a dual mechanism of action, specifically targeting tubulin and membranes of tumor cells, with low toxicity for normal cells. CAP6s bind to cancer cells by electrostatic interaction, and this leads to cytotoxicity of cancer cells.
Originally developed for the treatment of non-Hodgkin lymphomas, our CAP6 has since been tested ex vivo for its anti-proliferative properties on 33 tumor cells, and has achieved the best scores in 17 instances. When tested in vivo it showed a significant improvement in terms of reduced lung tumor volume in mice when compared to Erlotinib. Based on the results of a pharmacological test initiated in March 2018, the protocol for the pre-clinical regulatory work will be drawn up, followed by a Phase I/II trial.
CAP 6 acts as a taxol-like molecule specifically on tumor cells
Effect of CAP6 on tubulin network in A 549 tumor cells (upper pictures) or normal human fibroblasts (lower pictures). A549 cells were incubated in the absence or the presence of 15 μM CAP6. Tubulin structures(green) were immunostained with an anti-α-tubulin.
Validation Stages and Timelines
The graphic below shows the stages and timelines for S.1.p and our CAP6.
