Pasithea Therapeutics' New Preclinical Data Shows PAS-004 Provides Superior Inhibition Of ETS2-Driven Inflammatory Responses Compared To Selumetinib In Human Macrophage Model Of Chronic Inflammation In IBD

-- Demonstrates PAS-004's potential as a differentiated MEK inhibitor for immune-mediated inflammatory diseases such as IBD and ankylosing spondylitis –

-- Positions PAS-004 for potential expansion beyond MAPK pathway driven tumors into inflammatory diseases –

-- PAS-004 outperforms FDA-approved MEK inhibitor selumetinib in targeting ETS2 pathway –

-- Study conducted at Francis Crick Institute by lead author of 2024 Nature paper that identified ETS2 as a central regulator of macrophage-driven Inflammation in IBD --

MIAMI, May 20, 2025 (GLOBE NEWSWIRE) -- Pasithea Therapeutics Corp. (NASDAQ:KTTA) ("Pasithea" or the "Company"), a clinical-stage biotechnology company developing PAS-004, a next-generation macrocyclic MEK inhibitor, today announced new preclinical data demonstrating that PAS-004 provides superior inhibition of ETS2-driven inflammatory responses compared to selumetinib in a human macrophage model of chronic inflammation that mimics the inflammatory milieu seen in inflammatory bowel disease (IBD).

This study was conducted at the Francis Crick Institute in London, U.K. by Dr. James Lee, a gastroenterologist and Clinician Scientist Group Leader at the Genetic Mechanisms of Disease Laboratory. Dr. Lee was the lead author of a landmark 2024 Nature paper that identified ETS2 as a master regulator of inflammatory responses in IBD, and uncovered a novel genetic mechanism behind the disease, which pointed to a new, potentially effective treatment strategy through MEK inhibition.

In this new study RNA sequencing was used to measure gene expression, with PAS-004 consistently outperforming the FDA-approved MEK inhibitor selumetinib across all tested doses (0.01 μM, 0.1 μM, and 1 μM), showing greater downregulation of ETS2 target genes, as well as experimentally validated MEK1/2 pathway genes. These data suggest more robust and durable MEK inhibition by PAS-004 under inflammatory conditions.