EVO756 poster PR.pdf

EVO756: A Novel MRGPRX2 Antagonist

EVO756 is a novel MRGPRX2 antagonist that potently inhibits human mast cell degranulation in response to multiple agonists – a potential treatment for CSU and beyond.

Authors

Jamie L. Harden, Jelle Folkerts, See-Ying Tam, Stefan Frischbutter, Magda Babina, Hans E. Hofland*, Jeegar P. Patel, Marcus Maurer, and Stephen J. Galli
*1. Evommune, Palo Alto, CA
2. Department of Pathology, Stanford University School of Medicine, Stanford, CA
3. Institute of Allergology, Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Berlin, Germany
4. Fraunhofer Institute for Translational Medicine and Pharmacology ITMP, Immunology and Allergology, Berlin, Germany

Background

MRGPRX2 is highly promiscuous and activated by a variety of endogenous and exogenous agonists including neuropeptides (e.g., substance P) and pharmaceuticals (e.g., codeine). Activation of MRGPRX2 on mast cells results in rapid degranulation and release of inflammatory mediators such as histamine and tryptase, and is considered a key pathway in non-IgE-mediated mast cell degranulation. EVO756 is a novel, orally administered, small molecule antagonist of MRGPRX2. Here, we describe the in-vitro pharmacological characterization of EVO756 in a variety of MRGPRX2-expressing cells, including MRGPRX2-transfected cell lines, transformed human mast cell lines, and primary human mast cells.

Materials and Methods

Primary human mast cells

LAD2 human mast cells

Inhibition of Degranulation in Human Mast Cells

Agonist EVO756 IC50
Ciprofloxacin 16.6 nM
C48/80 6.67 nM
Substance P 5.25 nM
PAMP 9.2 nM
Icatibant 12.9 nM

EVO756 potently inhibits degranulation of human mast cells lines (LAD2 and ROSA) to multiple MRGPRX2 ligands, but not to IgE mediated degranulation.

EVO756 potently and dose-dependently inhibits the response of MRGPRX2 transfected CHO cells to multiple MRGPRX2 ligands.

Results

Response of Primary Mast Cells

Agonist EVO756 IC50
Cortistatin-14 15.1 nM
Substance P 12.5 nM
Codeine 22.7 nM

Primary human mast cells isolated from human skin were treated with EVO756 at increasing concentrations in conjunction with stimulation with (A) 0.3 uM cortistatin-14, 10 μg/mL codeine, or 1 μM substance P. Percent of degranulation was determined by β-hexosaminidase release. (B). Calculated IC50 values for EVO756 at inhibition of MRGPRX2 agonists in primary human mast cells (C) Primary human mast cells were treated with EVO756 in the absence of stimulation. Normalized (to no EVO756 treatment) caspase-3 and zombie staining data is shown.

Conclusions