| Candidate ID: | R0025 |
| Source ID: | DB00083 |
| Source Type: | approved; investigational |
| Compound Type: |
biotech
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| Compound Name: |
Botulinum toxin type A
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| Synonyms: |
AbobotulinumtoxinA; Botulinum A neurotoxin; Botulinum antitoxin type A; Botulinum toxin A; Botulinum toxin type A; BTX-A; EvabotulinumtoxinA; IncobotulinumtoxinA; OnabotulinumtoxinA; Prabotulinumtoxin A
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| Molecular Formula: |
--
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| SMILES: |
--
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| DrugBank Description: |
In 2002, botulinum toxin A, also known as onabotulinumtoxinA or Botox, was the first type A botulism toxin to be introduced into the market for cosmetic use. With a wide variety of applications and favourable safety profile, Botulinum toxin A injection is a minimally invasive and promising treatment for cosmetic imperfections, muscle spasms, and other conditions. A popular use for Botox is the treatment of facial wrinkles and lines, however, there are many uses for the botulinum toxin A in the treatment of dystonia, incontinence, migraine, blepharospasm, and hyperhidrosis.
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| CAS Number: |
93384-43-1
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| Molecular Weight: |
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| DrugBank Indication: |
Botulinum toxin A is indicated for a variety of conditions, depending on the preparations. Cosmetically, it is used for the treatment of facial fine lines and wrinkles, specifically for upper facial rhytides, including forehead, lateral canthus, and glabellar lines.
In addition to the above indications, botulinum toxin A is used for the following conditions: treatment of adults with symptomatic overactive bladder with or without incontinence, treatment of incontinence in adult patients who are not candidates for anticholinergic therapy, treatment of Neurogenic Detrusor Overactivity (NDO) in patients over 5 years who cannot undergo anticholinergic therapy. Botulinum toxin A is indicated for the prevention of chronic migraines, for the treatment of muscle spasms, cervical dystonia, axillary hyperhidrosis, strabismus, and disorders of the 7th cranial nerve.
Off-label, botulinum toxin A is used for a variety of conditions such as temporomandibular joint (TMJ) disorders and myofascial pain, neurogenic thoracic outlet syndrome, epicondylitis, post-stroke pain, post-herpetic neuralgia, diabetic neuropathy, trigeminal neuralgia, neuropathic pain, spinal cord injury, and bladder pain.
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| DrugBank Pharmacology: |
Botulinum toxin A inhibits the release of acetylcholine, relieving muscle contraction and spasm associated with many conditions, such as incontinence and dystonia. Cosmetically, botulinum toxin A paralyses muscles in the face to temporarily treat wrinkles. The maximum effects of muscle paralysis occur four to seven days after a dose. When injected at therapeutic doses, botulinum toxin A causes partial chemical denervation of muscle tissue, causing local reduction of muscle activity. Muscle atrophy may result, axonal sprouting may begin, and extrajunctional acetylcholine receptors can be formed. Reinnervation of the muscle may occur, reversing muscle denervation caused by botulinum toxin A.
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| DrugBank MoA: |
Botulinum toxin is a 150-kDa molecular weight protein consisting of a light chain (50 kDa) and heavy chain (100 kDa) linked by a single disulfide bond. The crystal structure reveals 3 lobes - the light chain, the amino-terminal portion of the heavy chain, and the carboxyl-terminal portion of the heavy chain.
Botulinum toxin type A blocks neuromuscular transmission on motor or sympathetic nerve terminals, inhibiting the release of acetylcholine. Botulinum toxins have actions on various regions: the neuromuscular junction, autonomic ganglia, and both postganglionic sympathetic and parasympathetic nerve endings. The heavy chain of the toxin binds selectively at the presynaptic surface of cholinergic neurons in an irreversible fashion. After binding, the toxin-receptor complex is transported into the cell by endocytosis. The disulfide bond between the two chains is cleaved and the botulism toxin enters the cytoplasm. The light chain specifically interacts with SNAP-25 in the nerve terminals to block binding of acetylcholine vesicles with the cell membrane. SNAP-25 is required for successful binding and release of acetylcholine from vesicles in nerve endings.
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| Targets: |
Synaptosomal-associated protein 25 inhibitor; Rho-related GTP-binding protein RhoB inhibitor
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| Inclusion Criteria: |
Indication associated
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