SXL01 is the most advanced molecule in SeleXel’s portfolio. This molecule is a small interfering RNA (siRNA) that prevents the synthesis of the androgen receptor, master gene of prostate cancers. SXL01 is a first-in-class molecule to treat prostate cancer. After demonstrating its effectiveness and lack of toxicity in extensive laboratory studies, the first clinical trial of this innovative molecule will begin in 2016.
Mode of action of SXL01 and therapeutic indication
Unlike conventional hormonal treatments, which aim to remove hormones or block their binding to the androgen receptor, SXL01 acts by inhibiting the production of androgen receptor, whether normal or mutated. SXL01 has indeed been selected to degrade the mRNAS coding for all forms of the receptor identified in tumors, even in the more advanced stages.
Recent studies show that conventional hormone treatments, including the most recently developed, foster production in tumor cells of Androgen Receptor variants, said AR-V7, having the same activity as the normal receptor but no longer needing the presence of testosterone to be activated. The synthesis of these AR-V7 variants is inhibited by SXL01.
Laboratory studies show that SXL01 inhibits the growth of all types of prostate cancer: androgen dependent, castration-resistant, tumors expressing the AR-V7 variant.
The demand for new therapeutic solutions being particularly important at that stage, as a first therapeutic intention SXL01 is designed to treat the most aggressive prostate cancers, which no longer respond to conventional hormonal treatments including the most recently approved drugs. This indication will be further expanded to less aggressive cancers.
State of development
SXL01 preclinical studies are now completed. An application for authorisation of clinical trials will be filed beginning 2016 at the french National Agency for Health and Therapeutic drugs. Clinical trials will be carried out at the Institut Claudius Regaud /Institut Universitaire du Cancer de Toulouse (IUCT), under the direction of Professor Jean-Pierre Delord.