STAT3 as a target in cancer immunotherapy

Reference number
Coordinator Glactone Pharma Development AB
Funding from Vinnova SEK 300 000
Project duration March 2017 - July 2017
Status Completed
Venture Innovative Startups
Call Innovativa startups fas 1 Våren 2017

Purpose and goal

STAT3 is a protein that is activated in several types of cancer and is involved in uncontrolled growth of tumor cells, treatment resistance and downregulation of the immune system. However, only a few studies have shown that the function of STAT3 can be blocked by directly by drug-like small molecules. The project’s goal was to design and perform a study that could demonstrate that Glactone’s STAT3 inhibitor could block tumor induced effects on immune cells that act through STAT3 signalling.

Expected results and effects

The study demonstrated that Glactone’s STAT3 inhibitor could reduce the expression of immune modulating and tumor promoting factors and that the levels of immunosuppressive cells that are driven by STAT3 could be down regulated. These results support the continued characterization of STAT3 inhibitors in more advanced models and that Glactone’s compounds have the potential to be combined with immunotherapies. The project’s positive outcome increases the values of the company’s portfolio and offers the possibility of establishing the company in a very important therapeutic area.

Planned approach and implementation

The study was designed in consultation with leading experts in immuno-oncology and the study was conducted by a contract research organization that are specialists in the field. Data from the study was analyzed in collaboration with the contracted lab that performed the study and with the experts that participated in the design. No deviations from the original plan were necessary and the study could be performed as planned.

External links

The project description has been provided by the project members themselves and the text has not been looked at by our editors.

Last updated 25 November 2019

Reference number 2017-00278

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