Therapeutics Q&A: Abobotulinum Toxin in Clinical Practice

For more than 20 years, botulinum toxin—from one source in the US and from two elsewhere in the world—has dominated the landscape of neurotoxin therapy, while the numbers and variety of patients receiving the agent have expanded remarkably. Reflecting the prominence of botulinum toxin-A therapy, the Botox (onabotulinum toxin-A) trade name has become a household name, like Viagra or Lipitor. Another formulation, abobotulinum toxin-A (Dysport, Ipsen) was recently approved by the FDA for cervical dystonia and is already becoming well-known in the public sphere, potentially due to its simultaneously approved cosmetic indication. This form of botulinum toxin A has been readily available elsewhere in the world for nearly two decades. As the market expands in the US, clinicians will have questions. Here, a botulinum toxin expert helps navigate the changing field.

What are the most important differences between onabotulinum toxin type A and abobotulinum toxin type A?
Onabotulinum and abobotulinum toxin have unique dosing, as spelled out in each agent's prescribing information. It is important that physicians be familiar with the respective dosing guidelines for each agent and be prepared to make appropriate treatment decisions in any clinical setting.

Nonetheless, clinicians are inclined to ask about conversion from one agent to the other. There is no fixed factor for dose conversion between these agents. Perhaps as evidence of the importance of dosing each agent on its own terms rather than thinking in terms of conversion, the European literature offers only a confusing, wide range of conversion factors. It suggests numbers anywhere between 2.5 to 5 units of abobotulinum toxin per unit of onabotulinum toxin, according to Stephen Gollomp, MD, Chief of Neurology at Lankenau Hospital and Clinical Professor of Neurology at Thomas Jefferson University Hospital in Philadelphia. “However, it appears that the consensus is somewhere around 2.5 to 3 units. I have been using 2.75 with reasonable success,” he says.

On a molecular basis, how is abobotulinum toxin different from onabotulinum toxin and rimabotulinum toxin?
Abobotulinum's hemagglutinin complex is different than onabotulinum's, though the active botulinum toxin A molecule is identical, Dr. Gollomp says. Due to this difference, some have suggested that abobotulinum's zone of activity is wider than onabotulinum's. “If really true, that may be some therapeutic advan- tage in certain instances, i.e. in the limbs, and a disadvantage in others, i.e. particularly near the pharynx; it requires clinical judgment and knowledge of the purported differences between the formulations,” he says.

As for rimabotulinum, it is botulinum toxin B, a completely different serotype with a different, though closely related, site of physiologic action. “I am of the belief that rimabotulinum should be reserved for A- resistant patients and should not be used interchangeably with A,” Dr. Gollomp says. Rimabotulinum presents the potential issue of a much higher protein load with possible antibody formation.

What lessons can be learned from European experience with abobotulinum toxin?
“The formulation is clearly safe and effective, but must be used with a true knowledge of its differences from onabotulinum and rimabotulinum toxin,” Dr. Gollomp says. Neurologists must educate themselves about the specific dosing and application of this newcomer. “We will inevitably be forced to make conversions based on evolving, aggressive third party reimbursement tactics that are different, but analogous to those seen in Europe,” he adds.