Botulinum toxin type A (BoNT/A) is a well-established treatment for conditions characterized by muscle and autonomic nerve terminal overactivity, such as cervical dystonia and blepharospasm, and hyperhidrosis, respectively. BoNT/A is not digested in the gastrointestinal tract as it forms a complex with several proteins that protect and stabilize the neurotoxin. However, the pure neurotoxin is solely responsible for the therapeutic effect, and the complexing proteins have been shown to exhibit immunostimulating activity. The complexing proteins are not required for the stabilization of the neurotoxin in a formulation; the complexing proteins immediately dissociate from the neurotoxin at a physiologic pH, so they do not influence the spread of the neurotoxin. Xeomin is the only botulinum toxin that is free from complexing proteins and is stable at room temperature for a period of 4 years. When injected directly into muscles, Xeomin inhibits local neuromuscular cholinergic transmission, causing focal weakness. It binds to motor nerve terminal pre-synaptic receptors, is internalized via receptor-mediated endocytosis and then selectively cleaves a protein called SNAP-25. This is one of several so-called 'SNARE' proteins involved in exocytosis. Cleavage of SNAP-25 inhibits the secretion of acetylcholine causing the paralysis of the muscle. The clinical effects begin 24-72 h after injection, peak at approximately 4-6 weeks and are sustained for several months.