FDA fast tracks DNA therapy for MS-related bladder issue
EG110A aims to treat neurogenic detrusor overactivity
The U.S. Food and Drug Administration (FDA) granted fast track designation to EG110A, EG 427‘s DNA-based therapy to treat neurogenic detrusor overactivity (NDO) — a bladder disorder that can arise from spinal cord injury or neurodegenerative conditions such as multiple sclerosis (MS).
The FDA gives fast track status to experimental treatments that have the potential to address serious conditions with limited therapeutic options. The designation is intended to speed the development and regulatory review of a therapy, providing benefits such as more frequent FDA interactions and potential eligibility for priority review once a marketing application is submitted.
“The FDA’s decision to grant Fast Track designation to EG110A demonstrates the urgent need for more effective therapies for individuals living with neurogenic detrusor overactivity,” Philippe Chambon, MD, PhD, CEO at EG 427, said in a company press release. “We welcome the opportunity to work more closely with the FDA as we advance EG110A through clinical development.”
NDO occurs when nerve damage, such as that caused by a spinal cord injury or MS, disrupts signals that control bladder function, causing the detrusor muscle around the bladder to contract uncontrollably.
This increases pressure inside the bladder and reduces the amount of urine it can hold, leading to urinary urgency, frequent urination, and urine leakage — symptoms that can significantly affect physical comfort, social engagement, and psychological well-being. Over time, it can also increase the risk of urinary tract infections and kidney damage.
DNA treatment aims to avoid common side effects
While several medications can help decrease detrusor muscle activation, these are usually limited by tolerability issues or short-term benefits.
EG110A is designed to address those limitations by targeting the sensory neurons that detect bladder filling and send signals to the spinal cord to initiate bladder muscle contractions.
The treatment uses a harmless form of the herpes simplex virus type 1 (HSV-1) to deliver DNA instructions to these neurons that enable them to produce a modified fragment of botulinum toxin type F. This toxin blocks the release of chemical messengers by nerve cells that drive muscle contraction.
Due to its ability to selectively target sensory neurons, EG110A may offer a long-term treatment option that avoids common side effects of current therapies, the company said.
In preclinical studies using rat models of overactive bladder, treatment with EG110A safely reduced urinary frequency and increased bladder capacity. Its safety and efficacy profiles were comparable to botulinum toxin type A, but without affecting bladder function and voiding.
The therapy’s safety and early efficacy are being evaluated in a Phase 1b/2a clinical trial (NCT06596291). The study aims to enroll up to 16 adults with NDO associated with spinal cord injury who continue to experience incontinence despite standard treatments. It is being conducted at centers in California, Michigan, Pennsylvania, and Texas.
Participants will receive increasing doses of EG110A, administered through multiple small injections into the bladder wall during a single treatment session.
Early top-line data from the first patients who received the lowest dose showed that EG110A reduced urinary incontinence episodes by more than 88% after 12 weeks, with improvements seen as early as week 4. The therapy was well tolerated, with no treatment-related safety concerns.
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