Botulinum toxin
Neurotoxic protein produced by Clostridium botulinum / From Wikipedia, the free encyclopedia
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Botulinum toxin, or botulinum neurotoxin (commonly called botox), is a highly potent neurotoxic protein produced by the bacterium Clostridium botulinum and related species.[23] It prevents the release of the neurotransmitter acetylcholine from axon endings at the neuromuscular junction, thus causing flaccid paralysis.[24] The toxin causes the disease botulism.[25] The toxin is also used commercially for medical and cosmetic purposes.[26][27] Botulinum toxin is an acetylcholine release inhibitor and a neuromuscular blocking agent.[1][22]
Clinical data | |
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Trade names | Botox, Myobloc, Jeuveau, others |
Other names | BoNT, botox |
Biosimilars | abobotulinumtoxinA, daxibotulinumtoxinA, daxibotulinumtoxinA-lanm, evabotulinumtoxinA, incobotulinumtoxinA, letibotulinumtoxinA, letibotulinumtoxinA-wlbg,[1] onabotulinumtoxinA, prabotulinumtoxinA, relabotulinumtoxinA, rimabotulinumtoxinB |
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MedlinePlus | a619021 |
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Routes of administration | Intramuscular, subcutaneous, intradermal |
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KEGG | |
ECHA InfoCard | 100.088.372 |
Chemical and physical data | |
Formula | C6760H10447N1743O2010S32 |
Molar mass | 149323.05 g·mol−1 |
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Bontoxilysin | |||||||||
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EC no. | 3.4.24.69 | ||||||||
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IntEnz | IntEnz view | ||||||||
BRENDA | BRENDA entry | ||||||||
ExPASy | NiceZyme view | ||||||||
KEGG | KEGG entry | ||||||||
MetaCyc | metabolic pathway | ||||||||
PRIAM | profile | ||||||||
PDB structures | RCSB PDB PDBe PDBsum | ||||||||
Gene Ontology | AmiGO / QuickGO | ||||||||
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The seven main types of botulinum toxin are named types A to G (A, B, C1, C2, D, E, F and G).[26][28] New types are occasionally found.[29][30] Types A and B are capable of causing disease in humans, and are also used commercially and medically.[31][32][33] Types C–G are less common; types E and F can cause disease in humans, while the other types cause disease in other animals.[34]
Botulinum toxins are among the most potent toxins known to science.[35] Intoxication can occur naturally as a result of either wound or intestinal infection or by ingesting formed toxin in food. The estimated human median lethal dose of type A toxin is 1.3–2.1 ng/kg intravenously or intramuscularly, 10–13 ng/kg when inhaled, or 1000 ng/kg when taken by mouth.[36]