For the treatment of cervical dystonia in adults to decrease the severity of abnormal head position and neck pain associated with cervical dystonia. Also for the treatment of severe primary axillary hyperhidrosis that is inadequately managed with topical agents and for the treatment of strabismus and blepharospasm associated with dystonia, including benign essential blepharospasm or VII nerve disorders in patients 12 years of age and above. Also used cosmetically to temporarily improve the appearance of moderate-to-severe frown lines between the eyebrows (glabellar lines) as well as for the treatment of excessive underarm sweating.
Examples of Clinical Use:
Cervical dystonia, severe primary axillary hyperhidrosis, strabismus and blepharospasm
A 150 kDa neurotoxic protein produced from fermentation of Hall strain Clostridium botulinum type A grown in a medium containing casein hydrolysate, glucose and yeast extract. It is purified from the culture solution by dialysis and a series of acid precipitations to a complex consisting of the neurotoxin, and several accessory proteins. The product is not expected to be present in the peripheral blood at measurable levels following IM or intradermal injection at the recommended doses. The recommended quantities of neurotoxin administered at each treatment session are not expected to result in systemic, overt distant clinical effects, i.e. muscle weakness, in patients without other neuromuscular dysfunction. However, sub-clinical systemic effects have been shown by single-fiber electromyography after IM doses of botulinum toxins appropriate to produce clinically observable local muscle weakness.
Mechanism of action:
Botulinum Toxin Type A blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings.
Humans and other mammals
Target 1. Synaptosomal-associated protein 25; Target 2. Rho-related GTP-binding protein RhoB
Botulinum Toxin Type A, commonly known as Botox, is an impressively powerful neurotoxin, structurally and functionally versatile, influencing various medical treatments and research paths.
Background of Botulinum Toxin Type A
Botulinum Toxin Type A was first discovered in the late 19th century by a German scientist named Emile van Ermengem. He isolated the toxin from a bacteria named Clostridium botulinum, following an outbreak of food poisoning. Unlike other pathogenic bacterial toxins, Botulinum Toxin Type A is encoded within the bont/A gene locus located on the bacterial plasmid. The protein structure of this bacterium demonstrates a complex dichain molecule, composed of a 50 kDa light chain and a 100 kDa heavy chain, connected by a disulphide bond.
Botulinum Toxin Type A Function
The primary function of Botulinum Toxin Type A is blocking the release of acetylcholine at the neuromuscular junction, leading to flaccid paralysis. The heavy chain aids the toxin's entry into the neuron. Simultaneously, the light chain, a zinc-dependent protease, cleaves the SNARE complex proteins, disrupting the neurotransmitter fusion mechanism. This disruption inhibits muscle contraction and leads to muscle relaxation.
Botulinum Toxin Type A-related Signaling Pathways
Botulinum Toxin impacts several signaling pathways, notably the SNAP-25 dependent pathways, central to synaptic vesicle fusion and neurotransmitter release. Once this pathway is blocked, the nerve signals cannot stimulate muscle contraction, leading to localized, temporary muscle paralysis. Furthermore, the toxin influences the vesicle associated membrane proteins (VAMP) and syntaxin pathways by their selective cleavage. Each of these pathways plays a crucial role in regulating critical cellular processes like cell growth, differentiation, and gene expression.
Botulinum Toxin Type A related Diseases and Role in Diseases
Botulinum Toxin Type A, due to its unique neuron blocking ability, plays a significant role in the treatment of various neurological diseases, including Cervical dystonia, Blepharospasm, and Strabismus. Botulism, a rare but severe paralytic illness, is caused by botulinum toxin, leading to varying degrees of paralysis. Moreover, the toxin’s functional versatility extends to treating conditions like chronic migraine, excessive sweating, overactive bladder, and certain muscle disorders.
The Application of Botulinum Toxin Type A in Medicine
Medical applications of Botulinum Toxin Type A are vast, ranging from aesthetics to therapeutics. It is most popularly known for its use in cosmetic procedures for reducing fine lines and wrinkles. But it's not limited to that. Botox has been proven to be significantly effective in managing various movement disorders caused by muscle hyperactivity. It also offers notable benefits in treating conditions like excessive sweating, chronic migraines, or even bladder control problems.
List of Drug Candidates related to Botulinum Toxin Type A
Several drugs have been developed based on the properties of Botulinum Toxin Type A, with Botox (OnabotulinumtoxinA) and Dysport (AbobotulinumtoxinA) being at the forefront. Xeomin (IncobotulinumtoxinA), another formulation, is used in the treatments of cervical dystonia and blepharospasm. Additionally, newer vehicles for delivering the toxin are under trial, including the transdermal application and nasal sprays. In summary, Botulinum Toxin Type A, since its discovery, has remarkably influenced medical science with its distinct properties and versatile applications. While it began as a threat to public health, it has gradually transformed into a therapeutic ally, fostering a range of medical treatments. However, like any potent substance, it requires highly controlled and skilled use. As researchers continue to unravel its potential, Botulinum Toxin Type A remains a central interest in medical and scientific advancements.
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