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4SC-205
4SC-205 is an anti-cancer compound that inhibits the kinesin spindle protein Eg5 (KIF11), which plays a key role in cell division and growth of tumor cells. Cell division inhibitors have been successful cancer therapies, however, they have serious side effects on the peripheral nervous system. Due to 4SC-205’s special mechanism of action, the compound does not cause such adverse side effects.
4SC-205 is the only orally administered Eg5 inhibitor currently in clinical development to the best of the Company’s knowledge. 4SC-205 is administered orally in low doses to maintain a steady bioavailability and exhibit continuous therapeutic effect. The anti-tumor efficacy of 4SC-205 was demonstrated in diverse pre-clinical models. In a Phase I clinical study (AEGIS) the drug demonstrated good safety and was well-tolerated; initial indications of efficacy were also determined.
4SC-205 is so far licensed for China, Hong Kong, Taiwan and Macao to Guangzhou Link Health Pharma Co., Ltd (Link Health).
AEGIS – First-in-human study of 4SC‑205 in solid tumors
The AEGIS study was a first-in-human, multi-center, open label, dose escalation Phase I first-in-human study of oral 4SC 205 in patients with advanced malignancies.
| Recruitment status | Completed |
| Study phase | Phase I |
| Enrollment | 60 |
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Poster presentations
| 30 May 2015 2015 Annual Meeting of the American Society of Clinical Oncology (ASCO) Chicago, USA |
Overcoming the proliferation rate paradox: Clinical evaluation of a continuous dosing scheme of the novel oral Eg5 inhibitor 4SC-205 |
| 1 June 2014 2014 Annual Meeting of the American Society of Clinical Oncology (ASCO) Chicago, USA |
First-in-human study of 4SC-205 (AEGIS), a novel oral inhibitor of Eg5 kinesin spindle protein |
Kv1.3 Inhibitors
Kv1.3 is a voltage-gated ion channel which has diverse functions in various cell types and cellular mechanisms but plays an essential role in the activation and proliferation of T-cells. 4SC’s family of Kv1.3 ion channel inhibitors are designed to act on chronically stimulated cell populations whilst sparing “normal” immune cells, thus addressing an underlying pathogenic principle in a multitude of autoimmune diseases.