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Press Release: 4SC presents new immunotherapeutic activity data of its epigenetic cancer drug resminostat at the ECCO ITOC conference 2015 - Seite 2
rendering the tumor microenvironment sensitive against immune cell based
anti tumor activities. In clinical treatment practice this could increase
the number of patients responding to immunotherapeutic treatments, in
particular check inhibitors like PD1 and CTLA4 inhibitors. Additionally,
resminostat considerably enhanced the expression of several cancer antigens
and MHC class I molecules, on several tumor cell lines thus making tumour
cells more visible for recognition by the T cells of the immune system
which in consequence leads to a more efficacious elimination of the tumour
cells. Finally, upregulation of NK cell ligands and a strong boost of NK
cells (natural killer cells of the immune system) by resminostat completes
the new discoveries on epigenetic impact on immunotherapy.
Ends
Details of the Presentation:
Presentation Title: Immunomodulatory characteristics of Resminostat, a
novel HDAC inhibitor in phase II clinical development
Time/location: Thursday, 26 March 2015, 11:00am - 12:15pm CET, Technical
University of Munich,
Type: Oral presentation and Poster
Session: PLENARY SESSION 4: IMMUNOMODULATORY AGENTS
Presenter: Svetlana Hamm
About resminostat
Resminostat (4SC-201) is an oral protein-deacetylase (HDAC) inhibitor with
an innovative epigenetic mechanism of action that potentially enables the
compound to be deployed as a novel, targeted tumour therapy for a broad
spectrum of oncological indications, both in monotherapy and, in
particular, in combination with other 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. Additionally, resminostat has
immunotherapeutic effects by activating NK cells, restoring MHCI and MHCII
proteins and suppression of unspecific immunosuppression. Resminostat is
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. For example, in preclinical trials, resminostat has shown that
it effectively inhibits epithelial-mesenchymal transition (EMT). EMT, which
may be promoted through the administration of certain conventional cancer
therapies, leads to the formation of particularly aggressive tumour cells,
Presentation Title: Immunomodulatory characteristics of Resminostat, a
novel HDAC inhibitor in phase II clinical development
Time/location: Thursday, 26 March 2015, 11:00am - 12:15pm CET, Technical
University of Munich,
Type: Oral presentation and Poster
Session: PLENARY SESSION 4: IMMUNOMODULATORY AGENTS
Presenter: Svetlana Hamm
About resminostat
Resminostat (4SC-201) is an oral protein-deacetylase (HDAC) inhibitor with
an innovative epigenetic mechanism of action that potentially enables the
compound to be deployed as a novel, targeted tumour therapy for a broad
spectrum of oncological indications, both in monotherapy and, in
particular, in combination with other 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. Additionally, resminostat has
immunotherapeutic effects by activating NK cells, restoring MHCI and MHCII
proteins and suppression of unspecific immunosuppression. Resminostat is
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. For example, in preclinical trials, resminostat has shown that
it effectively inhibits epithelial-mesenchymal transition (EMT). EMT, which
may be promoted through the administration of certain conventional cancer
therapies, leads to the formation of particularly aggressive tumour cells,
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