Abstract
Since its introduction as a treatment for strabismus, botulinum toxin (BoNT) has had a phenomenal journey and is now recommended as first-line treatment for focal dystonia, despite short-term clinical benefits and the risks of adverse effects. To cater for the high demand across various medical specialties, at least six US Food and Drug Administration (FDA)-approved formulations of BoNT are currently available for diverse labelled indications. The toxo-pharmacological properties of these formulations are not uniform and thus should not be used interchangeably. Synthetic BoNTs and BoNTs from non-clostridial sources are not far from clinical use. Moreover, the study of mutations in naturally occurring toxins has led to modulation in the toxo-pharmacokinetic properties of BoNTs, including the duration and potency. We present an overview of the toxo-pharmacology of conventional and novel BoNT preparations, including those awaiting imminent translation from the laboratory to the clinic.
Highlights
There has been a surge of research into botulinum toxins, which has led to the addition of newer formulations with an increasing range of indications
In the of BoNT, botulinum toxin interferes with the steps of release thereafter
We have described the structure and molecular function of BoNTs
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Botulinum toxin essentially blocks the release of ACh post-synaptic membrane [17].[17]. At this stage, in the of BoNT, botulinum toxin interferes with the steps of release thereafter. The light the vesicles are ready to fuse with the presynaptic membrane and release ACh into the synaptic cleft. The free and active light chain cleaves and deactivates various proteins such as VAMP, SNAP25, and syntaxin, which are essential for the release of ACh. The free and active light chain cleaves and deactivates various proteins such as VAMP, SNAP25, and syntaxin, which are essential for the release of ACh These proteins (SNARE proteins) are essential for the fusion of vesicles with the presynaptic membrane and subsequent release of the toxins into the synaptic cleft. Large dense core vesicles carry cargo including proteins and receptors (e.g., transient receptor potential cation channel subfamily V member 1 (TRPV1), transient receptor potential cation channel subfamily A member 1 (TRPA1), purinergic receptor P2X ligand-gated ion channel 3 (P2 × 3), etc.), whose insertion into the lipid bilayer of the synaptic membrane is critical to nociception [24]
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