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Scientific Background

Enhancing the host defence response to inhaled pathogens

We are dedicated to improving the lives of those affected by chronic respiratory diseases with our new oral treatment, glasmacinal.

Our approach

Our research into macrolides led to our hypothesis that lung epithelium plays a central role in macrolides' beneficial effects

A growing body of evidence supports the clinical efficacy of off-label use of antibiotic macrolides for COPD in reducing exacerbations due to their immunomodulatory activity rather than their direct antimicrobial activity . However, chronic use contributes to the development of antimicrobial resistance (AMR), limiting their widespread, long-term use.

Our lead asset, glasmacinal, built on the knowledge from macrolides, is an oral, anti-inflammatory drug without clinically relevant AMR potential designed to address chronic respiratory diseases such as COPD.

EpiEndo's clinical program is aimed at bringing glasmacinal to patients with the ultimate goal of exacerbation reduction.

The name glasmacinal is inspired by its origins in Iceland, referring to glaciers (glas-) and using the WHO designated suffix -macinal, which means a non-antibacterial macrolide agent with anti-inflammatory activity. This is an entirely new drug class, making glasmacinal a first-in-class drug.

Therapeutic focus

A fresh perspective on chronic respiratory disease treatment with EpiEndo's glasmacinal

  1. An Oral Option
  2. Improvement Over Azithromycin
  3. Our Preclinical Data
  4. Our Clinical Results

Most therapeutic options for COPD are either inhaled or injectable, our treatment will be a simple, oral treatment.

Our preclinical studies have demonstrated equivalent or better efficacy than azithromycin in models of smoke exposure, air pollution, endotoxin and virus. Unlike azithromycin, glasmacinal has negligible antibiotic activity and does not impact the lung or gut microbiome in clinical studies – thus eliminating concerns about antimicrobial resistance.

In models of both neutrophilic (lipopolysaccharide, cigarette smoke, respiratory syncytial virus) and eosinophilic inflammation (ovalbumin, house-dust mite), we show that glasmacinal (EP395) can reduce neutrophilic and eosinophilic inflammation.

  • Barriolides: Non-antibacterial compounds with epithelial barrier enhancing properties and anti-inflammatory effects in vitro.
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  • Inhibition of neutrophilic inflammation by targeting the airway epithelial barrier with EP395.
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  • The new macrolide EP395 reduces airway eosinophilic inflammation.
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  • EP395 effect on cell diapedesis measured by intravital microscopy.
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In our four clinical studies that have been conducted to date, glasmacinal (EP395) has been shown to be well tolerated. In a clinical LPS challenge study glasmacinal treatment increased the host defense response to inhaled LPS, including the epithelial response, whilst inhibiting inflammatory site pro-inflammatory mediators. In stable COPD patients glasmacinal treatment for 12 weeks reduced sputum neutrophil elastase and MPO.