PittsburghV1, Main, Exploration, bibRecord, 007B72

New calcium channel agonists as potential therapeutics in Lambert–Eaton myasthenic syndrome and other neuromuscular diseases

Identifieur interne : 007B72 ( Main/Exploration ); précédent : 007B71; suivant : 007B73

New calcium channel agonists as potential therapeutics in Lambert–Eaton myasthenic syndrome and other neuromuscular diseases

Auteurs : Tyler B. Tarr ; Guillermo Valdomir [États-Unis] ; Mary Liang [États-Unis] ; Peter Wipf [États-Unis] ; Stephen D. Meriney

Source :

Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2012-12.

RBID : ISTEX:665B58589622DF1BB46866A4E324C74E7B7E233A

Descripteurs français

Wicri :
- topic : Calcium, Thérapeutique.

English descriptors

Abstract

Lambert–Eaton myasthenic syndrome (LEMS) causes neuromuscular weakness as a result of an autoimmune attack on the calcium channels that normally regulate chemical transmitter release at the neuromuscular junction. Currently there are limited treatment options for patients with this and other forms of neuromuscular weakness. A novel, first‐in‐class calcium channel agonist that is selective for the types of voltage‐gated calcium channels that regulate transmitter release at neuromuscular synapses has recently been developed. This compound (GV‐58) slows deactivation (closing) of the channel, resulting in a large increase in total calcium entry during motor nerve action potential activity. This new calcium channel agonist is currently being evaluated for the treatment of neuromuscular weakness. Potential applications include development as single therapeutics, or for combination treatments.

Url:

https://api.istex.fr/document/665B58589622DF1BB46866A4E324C74E7B7E233A/fulltext/pdf

DOI: 10.1111/nyas.12001

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Istex, to step Corpus: 001759
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to stream Istex, to step Checkpoint: 001523
to stream Main, to step Merge: 008050
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Le document en format XML

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<term>Neuromuscular junction</term>
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<term>Novel calcium channel agonists</term>
<term>Open time</term>
<term>Open time distribution</term>
<term>Passive transfer</term>
<term>Potassium channel blocker</term>
<term>Potential therapeutics</term>
<term>Potential therapeutics tarr</term>
<term>Presynaptic</term>
<term>Roscovitine</term>
<term>Roscovitine analogs</term>
<term>Side chains</term>
<term>Side effects</term>
<term>Symptomatic relief</term>
<term>Symptomatic treatments</term>
<term>Synaptic</term>
<term>Syndrome</term>
<term>Tarr</term>
<term>Therapeutics</term>
<term>Transmitter release</term>
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<term>Calcium</term>
<term>Calcium channel</term>
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<term>Calcium channel agonists</term>
<term>Calcium channel gating</term>
<term>Calcium channels</term>
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<term>Congenital myasthenic syndromes</term>
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<front><div type="abstract" xml:lang="en">Lambert–Eaton myasthenic syndrome (LEMS) causes neuromuscular weakness as a result of an autoimmune attack on the calcium channels that normally regulate chemical transmitter release at the neuromuscular junction. Currently there are limited treatment options for patients with this and other forms of neuromuscular weakness. A novel, first‐in‐class calcium channel agonist that is selective for the types of voltage‐gated calcium channels that regulate transmitter release at neuromuscular synapses has recently been developed. This compound (GV‐58) slows deactivation (closing) of the channel, resulting in a large increase in total calcium entry during motor nerve action potential activity. This new calcium channel agonist is currently being evaluated for the treatment of neuromuscular weakness. Potential applications include development as single therapeutics, or for combination treatments.</div>
</front>
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New calcium channel agonists as potential therapeutics in Lambert–Eaton myasthenic syndrome and other neuromuscular diseases

New calcium channel agonists as potential therapeutics in Lambert–Eaton myasthenic syndrome and other neuromuscular diseases

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri