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BOTOX® May Be the First Neurotoxin Approved to Treat Detrusor Hyperactivity in Children

Allergan, an AbbVie company, announced that the U.S. Food and Drug Administration (FDA) has accepted the company’s supplemental biologics license application (sBLA) to expand the BOTOX® prescribing information for the treatment of signs and symptoms of detrusor (bladder muscle) overactivity associated with an underlying neurologic condition (e.g., spina bifida, spinal cord injuries) in pediatric patients (5 -17 years of age) who have an inadequate response to, or are intolerant of, or for any reason unwilling to continue anticholinergic medication.

The sBLA is based on data from a randomized, double-blind Phase 3 study evaluating the safety and efficacy of BOTOX® in more than 100 pediatric patients with neurogenic detrusor overactivity and a long-term extension study. The Prescription Drug User Fee Act date is expected to be in the first quarter of 2021 following a standard 10-month review.

“The FDA acceptance of this application underscores our ongoing commitment to pursuing the full potential of BOTOX® to serve patients across a wide spectrum of diseases and clinical needs,” said Mitchell F. Brin, M.D., Senior Vice President, Chief Scientific Officer, BOTOX® & Neurotoxins, AbbVie. “Children living with neurogenic detrusor overactivity currently have limited options when they fail anticholinergic medications and prior to surgical intervention. If approved, BOTOX® will be the first neurotoxin treatment approved for use in treating detrusor overactivity in pediatric patients with an underlying neurologic condition who are not adequately managed by anticholinergic medications.”

BOTOX® is the first and only neurotoxin approved for the treatment of leakage of urine (incontinence) due to overactive bladder caused by a neurologic condition in adults who still have leakage or cannot tolerate the side effects after trying an anticholinergic medication. BOTOX® temporarily reduces muscle contractions by blocking the transmission of nerve impulses to the muscle, in this case, the bladder muscle, by selectively preventing the release of the neurotransmitter acetylcholine at the neuromuscular junction.

Photo by aestheticmed.co.uk

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