Summary
Elevated rates of reactive oxygen species (ROS) have been detected in almost all cancers, where they promote many aspects of tumour development and progression. The radical generated, the location, as well as the local concentration, are essential for the cellular functions of ROS in cancer. Among redox modulating compounds, selenium derivatives have gained substantial attention due to their promising chemotherapeutic potential, which result from selenium’s ability to act as a pro-oxidant at high dosage. This proposal is intended to develop novel therapeutic agents based on selenium-containing dendrimers, which act as precision carriers with unparalleled structural perfection. These agents, with a plethora of internally queued selenium-selenium bridges will be activated upon the rupturing of the dendritic carriers by external stimuli. It is herein envisioned that RUPTURE can rise to the challenge, acting as cutting-edge prodrugs that will fine-tune intracellular ROS signalling to effectively deprive cells of ROS-induced tumour-promoting events, thereby tipping the balance to ROS-induced apoptotic signalling.
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| Web resources: | https://cordis.europa.eu/project/id/101064084 |
| Start date: | 01-02-2023 |
| End date: | 31-01-2025 |
| Total budget - Public funding: | - 206 887,00 Euro |
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Original description
Elevated rates of reactive oxygen species (ROS) have been detected in almost all cancers, where they promote many aspects of tumour development and progression. The radical generated, the location, as well as the local concentration, are essential for the cellular functions of ROS in cancer. Among redox modulating compounds, selenium derivatives have gained substantial attention due to their promising chemotherapeutic potential, which result from selenium’s ability to act as a pro-oxidant at high dosage. This proposal is intended to develop novel therapeutic agents based on selenium-containing dendrimers, which act as precision carriers with unparalleled structural perfection. These agents, with a plethora of internally queued selenium-selenium bridges will be activated upon the rupturing of the dendritic carriers by external stimuli. It is herein envisioned that RUPTURE can rise to the challenge, acting as cutting-edge prodrugs that will fine-tune intracellular ROS signalling to effectively deprive cells of ROS-induced tumour-promoting events, thereby tipping the balance to ROS-induced apoptotic signalling.Status
SIGNEDCall topic
HORIZON-MSCA-2021-PF-01-01Update Date
09-02-2023
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