Clinical Trials

Date: 2017-02-28

Type of information: Presentation of results at a congress

phase: preclinical

Announcement: presentation of results at Clinical Epigenetics International Meeting

Company: 4SC (Germany)

Product: resminostat (oral pan-histone deacetylase (HDAC) inhibitor)

Action mechanism: histone deacetylase inhibitor (HDAC inhibitor). Resminostat is an oral pan-histone-deacetylase (HDAC) inhibitor with an innovative, epigenetic mechanism of action that enables this compound to be deployed as a novel, targeted tumour therapy for a broad spectrum of oncological indications, particularly in combination with other anti-cancer drugs. Like other epigenetic therapies, resminostat has been shown to modify transcription of genes in cancer cells and, thereby, to reprogram the phenotypes of such cancer cells. Resminostat is therefore assumed to be able to halt tumour progression and induce tumour regression. Furthermore, due to its epigenetic mode of action resminostat is supposed to develop additional synergetic effects when combined with classical cancer therapies and thus also fight the development of tumour cell resistance. 4SC is currently enrolling advanced-stage cutaneous T-cell lymphoma patients in the RESMAIN pivotal study in 11 European countries to evaluate resminostat as maintenance therapy.

Disease: advanced-stage cutaneous T-cell lymphoma (CTCL)

Therapeutic area: Cancer - Oncology

Country:

Trial details:

Latest news:

• • On February 28, 2017,  4SC announced the presentation of supportive preclinical data on the potential of the histone deacetylase (HDAC) inhibitor resminostat as maintenance therapy for advanced-stage cutaneous T-cell lymphoma (CTCL) at two conferences. The data presented at the following two conferences highlight the mechanistic rationale for pursuing a maintenance indication. Progression of CTCL appears to be associated with a transition from Th1 to Th2 T-helper cell status that is related to altered expression of STAT4/STAT6. Resminostat’s ability to induce apoptosis in several CTCL cell lines and impact on STAT4/STAT6 expression were evaluated in preclinical experiments. Resminostat demonstrated anti-tumor activity in CTCL cells at clinically relevant doses. Resminostat also increased STAT4 expression and decreased STAT6 expression, suggesting a stabilization of the less advanced CTCL stage (Th1) or even a reconversion of the advanced Th2 to the Th1 phenotype.
• (Epigenetics in Drug Discovery Session, Advances in Drug Discovery Conference. Poster: Resminostat – an epigenetic approach for CTCL maintenance treatment.
• Clinical Epigenetics International Meeting. Poster: Resminostat – an epigenetic approach for CTCL maintenance treatment)

Is general: Yes