Product Name:µ-conotoxin-GIIIB
Synonyms:Myotoxin II, Geographutoxin II, GTx-II
CAS No:140678-12-2
Purity:95%
Molar Mass:2640
Chemical Formula:C101H175N39O30S7
Storage:Store at -20 degrees Celsius
Sequence:RDCCTXXRKCKDRRCKXMKCCA
Target:NaV1.4 Na+ channels
Application:
µ-Conotoxin GIIIB is a highly selective peptide toxin derived from the venom of the marine cone snail Conus geographus. This toxin specifically targets voltage-gated sodium channels (Nav1.4) in skeletal muscle by blocking sodium ion flow through the channel, thus inhibiting action potentials in muscle fibers. µ-Conotoxin GIIIB is widely used in neurophysiological studies to investigate the function of sodium channels and their role in muscle contraction and excitability. Its high selectivity for Nav1.4 makes it a valuable tool for understanding muscle physiology and exploring potential therapeutic applications for neuromuscular disorders, such as myotonia and muscular dystrophy.
Current Research:
μ-Conotoxin GIIIB is a 22-amino-acid peptide derived from the venom of the marine cone snail Conus geographus. It functions as a potent and selective blocker of voltage-gated sodium channels, particularly the Naᵥ1.4 subtype predominantly found in skeletal muscle.
Structural Characteristics
The peptide's structure includes three disulfide bridges, which are crucial for its stability and bioactivity. These disulfide bonds contribute to the peptide's ability to effectively occlude the sodium channel pore, thereby inhibiting ion conductance.
Mechanism of Action
μ-Conotoxin GIIIB binds to site I on the α-subunit of voltage-gated sodium channels, physically blocking the channel pore. This action prevents sodium ion influx, thereby inhibiting action potential propagation in muscle cells. The peptide exhibits high specificity for the Naᵥ1.4 channel, with an affinity in the nanomolar range, making it a valuable tool for distinguishing between neuronal and muscle sodium channel subtypes.
Research Applications
Due to its specificity, μ-Conotoxin GIIIB is extensively used in neurophysiological studies to:
Investigate Sodium Channel Function: By selectively inhibiting Naᵥ1.4 channels, researchers can study the role of these channels in muscle physiology and related pathologies.
Develop Therapeutic Agents: Understanding the interaction between μ-Conotoxin GIIIB and sodium channels aids in the design of novel therapeutics targeting channelopathies.
Clinical Implications
The ability of μ-Conotoxin GIIIB to selectively block muscle-specific sodium channels positions it as a potential therapeutic candidate for conditions involving hyperexcitability of skeletal muscles, such as certain myotonias. However, its application is currently limited to research settings, and further studies are necessary to explore its therapeutic potential.
Conclusion
μ-Conotoxin GIIIB serves as a powerful tool in the study of voltage-gated sodium channels, offering insights into their function and paving the way for potential therapeutic developments targeting muscle-related disorders.
Reference:
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