Syntaxin’s inflammation programme is focusing on the inhibition of mast cell mediators in disease areas such as allergic rhinitis (AR), asthma, rheumatoid arthritis and inflammatory bowel disease.
Syntaxin’s non-steroidal anti-inflammatory technology delivers multiple mast cell stabilisers with greater efficacy and longer duration of action in comparison to single mediator antagonists thus drastically improving symptom control.
By selectively inhibiting stimulated mast cell secretion, our technology can couple specificity with breadth of efficacy. Receptor choice allows targeting of multiple mechanisms with a single molecule.
The current focus is to complete allergic rhinitis proof of concept to demonstrate efficacy in a disease where the mast cell is a precedented mechanism.
Disease |
Mast Cell Function |
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| Allergic rhinitis and allergic skin diseases | AR patients have increased numbers of nasal mast cells during active disease Mast cell mediators have been shown to play a role in the early and late responses Efficacy of anti-histamines |
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| Asthma (including severe asthma) | Mast cells are increased in smooth muscle and epithelial layers Number of mast cells correlates with AHR to methacholine Mast cell mediators in asthmatic BAL Efficacy of mast cell antagonists Anti-IgE efficacy |
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| Rheumatoid Arthritis | Mast cells represent up to 5% of all cells in the RA synovium Mast cells are a major source of TNF and other inflammatory mediators linked to disease Mast cells shown to play a critical role in the development of inflammation in murine models of disease |
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| Inflammatory Bowel Disease | Effectors of the Brain-Gut axis Translate stress signals into the release of pro-inflammatory mediators Tryptase activation of PAR-2 receptors results in increased mucosal permeability |