Products: Resminostat

Summary

Resminostat is an orally administered histone deacetylase (HDAC) inhibitor that potentially represents a novel therapy for a broad spectrum of oncology indications, both in monotherapy and particularly in combination with other anti-cancer drugs.

In preclinical models, resminostat has shown selectivity for class I, IIB and IV HDAC enzymes with a particular specificity toward inhibiting the protein HDAC6, which is active in metastasis. Resminostat has the potential to provide significant benefit to patients by inhibiting tumor progression and metastasis, inducing tumor regression and enhancing the body’s own immune response to cancer.

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Clinical development profile

The clinical development of resminostat is currently focused on cutaneous T-cell lymphoma (CTCL). Resminostat was also investigated by 4SC and its Japanese partner Yakult Honsha in several other cancer indications.

The compound’s safety profile has been assessed in more than 300 patients to date and studies have shown that resminostat is well tolerated in various indications in both monotherapy and in combination with other drugs. The most frequent adverse events are gastrointestinal disorders (i.e. nausea, vomiting and diarrhea), fatigue, and thrombocytopenia (low platelet count in the blood). The majority of adverse events are mild to moderate, manageable and reversible.

Clinical Trials

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Partnering

Yakult Honsha Co., Ltd. (Yakult Honsha, Tokyo, Japan)

In April 2011, 4SC AG granted Yakult Honsha an exclusive license for the development and marketing of resminostat in Japan.

Partnering and Collaborations

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Scientific background

Resminostat is a potent inhibitor of class I, IIb and IV HDACs, including a pronounced activity against HDAC6. In pharmacology studies, resminostat dose-dependently inhibited HDACs and induced acetylation of histone and non-histone proteins resulting in changes in gene expression levels in tumor cells and the deregulation of pathways involved in cell differentiation, such as WNT signaling. Changes in cell differentiation are very often the cause for tumor progression, metastasis and acquired resistance to anti-cancer treatment.

In cutaneous T-cell lymphoma (CTCL) cell lines, resminostat up-regulated the expression of Th1 and reduced Th2 lineage associated genes. An imbalance between Th1 and Th2 cells is considered to contribute to pathogenesis of CTCL; especially an increased expression of Th2 related genes is associated with disease progression.

In addition to these important effects on the differentiation of tumor cells, resminostat also increases the immunogenicity of tumors by enhancing natural killer (NK) cell recognition and killing, increasing expression and presentation of tumor-associated antigens (that support T-cell functions), and reducing unspecific immunosuppressive mechanisms.

In vivo, resminostat has demonstrated significant anti-tumor activity in various human xenograft mice tumor models, and in combination with established therapies – such as irinotecan or sorafenib – generated additive, synergistic anti-tumor effects.

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