Pathios Therapeutics to Present Preclinical Data Highlighting Potential of GPR65 Inhibition as a Powerful Anti-Tumour Immunotherapy Strategy at SITC 2022

On November 3, 2022 Pathios Therapeutics Limited ("Pathios"), a biotech company focused on the development of first-in-class therapies for cancer, reported that new preclinical data highlighting the therapeutic potential of the company’s novel GPR65 inhibition platform will be the focus of a poster presentation at the upcoming 37th Annual Meeting of the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) (SITC 2022) (Press release, Pathios Therapeutics, NOV 3, 2022, View Source [SID1234622943]). Presented results will showcase the company’s unique approach to "macrophage conditioning" with novel GPR65 inhibitors as a means to reversing the immunosuppression that results from an acidic tumour microenvironment, and, in turn, driving anti-tumour activity. SITC (Free SITC Whitepaper) 2022 is being held November 8-12, 2022, in Boston, Massachusetts.

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Details of the company’s presentation at SITC (Free SITC Whitepaper) 2022 are as follows:

Poster Presentation #1324:

Title: Inhibition of Acid Sensing by GPR65 Normalizes Gene Expression in Macrophages, Increases Immune Cell Infiltration in Tumours, and Restrains Subcutaneous MC38 Growth in Mice
Presenting Author: Alastair Corbin, DPhil, senior scientist at Pathios
Date/Time: Friday, November 11, 2022, 9:00 a.m. – 8:30 p.m. Eastern Time
Location: Poster Hall C
Additional information on the 37th Annual Meeting of SITC (Free SITC Whitepaper) is available through the conference website at: View Source

About Acidity in the Tumour Microenvironment

The acidic tumor microenvironment, inherent to many cancers, causes a profound immunosuppression of infiltrating immune cells. This environment disarms the anti-cancer immune response and negates the effectiveness of current immunotherapies. This is particularly evident in tumour associated macrophages (TAM), where acidity is sensed by the cell-surface receptor GPR65, leading to the widespread suppression of a host of pro-inflammatory mediators and anti-tumourigenic genes as well as the up-regulation of several tissue repair genes and angiogenic factors.