
EG 427’s Clinical Data Showing Sustained Incontinence Episode Reduction with EG110A DNA Therapy Maintained at 6 Months Timepoint
6.1.2026 07:00:00 CET | GlobeNewswire by notified | Press release
Paris, Jan. 06, 2026 (GLOBE NEWSWIRE) --
- 88% reduction in urinary incontinence episodes in patients with neurogenic bladder sustained through 24 weeks
- Good tolerability maintained
- Enrollment and dosing of Cohort 2 in progress
- Results demonstrate the ability to modulate very specifically the activity of subset of neurons and hence validate EG 427’s HERMES nrHSV-1 technology platform
Paris, France, January 06, 2026 – EG 427, a biotechnology company leading the development of pinpoint DNA medicines for prevalent chronic diseases in neurology, announced today that the promising clinical efficacy of EG110A, an 88% reduction in urinary incontinence episodes by week 12, was consistently maintained at week 24 follow-up. EG110A is being evaluated in an ongoing Phase 1b/2a, open-label, dose-escalation study for the treatment of neurogenic detrusor overactivity (NDO) in people with spinal cord injury (SCI). A good safety profile in all patients was also maintained with no new safety signals. Dosing of the second cohort in the study is currently ongoing.
“Following the very promising initial clinical results at 12 weeks, we are seeing the first patients maintaining a highly clinically relevant reduction in urinary incontinence episodes at 24 weeks, a major milestone in EG110A’s clinical development,” said Cornelia Haag-Molkenteller, MD, PhD, Chief Medical Officer at EG 427. “For patients, this drop in incontinence episodes combined with a long-term effect could dramatically improve quality of life. We are continuing to follow these patients up to 52 weeks then will ask them to enroll into a long-term observational study. At this time we are evaluating EG110A in the next cohort at a higher dose, although these remarkable results were already achieved with the lowest dose tested.”
EG110A is a non-replicating HSV-1 vector designed to selectively silence the signals of type C sensory neurons responsible for the bladder muscle overactivity, whilst preserving other bladder controls. NDO is a common urinary bladder dysfunction caused by SCI and other neurodegenerative diseases, such as multiple sclerosis or Parkinson’s disease.
“We continue to be very encouraged with the clinical effect seen with administration of EG110A and the strong safety profile. What is truly remarkable, is that by targeting a very small number of sensory neurons, we are able to achieve such a dramatic improvement for the patients,” said Philippe Chambon, MD, PhD, Chief Executive Officer at EG 427. “These stellar initial clinical results with EG110A to date are only at the beginning of realizing the potential of our novel approach and our goal of safe and precise DNA medicines for patients with chronic diseases.”
The Phase 1b/2a, open-label, dose-escalation study (ClinicalTrials.gov ID: NCT06596291) is currently enrolling the second cohort of 6 adult participants with NDO following SCI, who have persistent urinary incontinence after standard of care therapy and who perform clean intermittent catheterization on a regular basis. Participants receive a single treatment course consisting of multiple intradetrusor injections of EG110A. The study is being conducted at four leading US institutions located in California, Michigan, Pennsylvania and Texas.
NDO causes uncontrolled urinary incontinence, risk of kidney damage as well as urinary tract infections than can lead to death in 5-10% of the SCI population. NDO affects most (70-84%) patients living with SCI, an estimated total of 300,000-400,000 worldwide. Altogether, NDO affects at least 2 million patients suffering from SCI, multiple sclerosis, Parkinson’s and other neurodegenerative diseases, across the seven major markets and has a significant impact on their quality of life. The European Association of Urology recently estimated that incontinence caused by NDO and other indications, such as overactive bladder, represents a growing economic burden of over €69.1 billion in 2023 in Europe1.
This research was supported, in part, by the Assistant Secretary of Defense for Health Affairs endorsed by the Department of Defense, in the amount of $3,165,836, through the Spinal Cord Injury Research Program under Award No. HT9425-25-1-0505. Opinions, interpretations, conclusions, and recommendations are those of the author and are not necessarily endorsed by the Department of Defense.
About EG 427
EG 427 is the global leader in non-replicating HSV-1 (nrHSV-1) vector technology in neurology. EG 427 has started a phase 1/2 study in the US with its lead DNA medicine candidate, EG110A, in patients with neurogenic detrusor overactivity (neurogenic bladder)-related incontinence. This is the first human study of this type of a vector targeting sensory neuron-based diseases. EG110A is being developed to addresses multiple severe bladder diseases, including overactive bladder (OAB), and has the potential to be a major improvement over existing therapies, resulting in better care for patients and lower costs for healthcare systems. The company’s unique HERMES platform delivers pinpoint neurotherapeutics to treat prevalent diseases of the peripheral and central nervous system. Its vectors can achieve focal transduction in specific regions and then selective expression of transgenes in targeted subsets of neurons thanks to the control of sophisticated regulatory elements. With demonstrated clinical safety and possible repeated dosing, the large payload capacity of
nrHSV-1 vectors allows for versatile DNA delivery for smarter DNA medicine.
For more information:
- Check our website at www.eg427.com
- Follow us on www.linkedin.com/company/eg427/
Contacts:
| EG 427 | Media Relations: Rose Piquante Consulting |
| Philippe Chambon, M.D., Ph.D., | Sophie Baumont |
| Founder and CEO | sophie.baumont@rosepiquante-consulting.com |
| pchambon@eg427.com | +33 6 27 74 74 49 |
[1] https://d56bochluxqnz.cloudfront.net/media/Socio-economic_report_UrgetoAct.pdf#asset:4080543@1
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