ArticleChemMedChem2009
Structurally minimized mu-conotoxin analogues as sodium channel blockers: implications for designing conopeptide-based therapeutics.
Article in ChemMedChem, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- Exploring the Pain-Relieving Potential: Unveiling Antinociceptive Properties in Animal Venoms and Toxins.Toxins · 2026Review
- Conotoxins Targeting Voltage-Gated Sodium Ion Channels.Pharmacological reviews · 2024Review
- Review
- Identification of sodium channel toxins from marine cone snails of the subgenera Textilia and Afonsoconus.Cellular and molecular life sciences : CMLS · 2023Article
- Coagulation Factor XIIIa Inhibitor Tridegin: On the Role of Disulfide Bonds for Folding, Stability, and Function.Journal of medicinal chemistry · 2019Article
- Snails In Silico: A Review of Computational Studies on the Conopeptides.Marine drugs · 2019Review
- Sodium channels and pain: from toxins to therapies.British journal of pharmacology · 2018Review
- The Role of Individual Disulfide Bonds of μ-Conotoxin GIIIA in the Inhibition of NaMarine drugs · 2016Article
- Early engineering approaches to improve peptide developability and manufacturability.The AAPS journal · 2015Review
- Article
- Article
- Structure and function of μ-conotoxins, peptide-based sodium channel blockers with analgesic activity.Future medicinal chemistry · 2014Review
- Interactions of disulfide-deficient selenocysteine analogs of μ-conotoxin BuIIIB with the α-subunit of the voltage-gated sodium channel subtype 1.3.The FEBS journal · 2014Article
- Discovery, synthesis, and structure-activity relationships of conotoxins.Chemical reviews · 2014Review
- Expanding chemical diversity of conotoxins: peptoid-peptide chimeras of the sodium channel blocker μ-KIIIA and its selenopeptide analogues.European journal of medicinal chemistry · 2013Article
- Strategies for the development of conotoxins as new therapeutic leads.Marine drugs · 2013Review
- Distinct disulfide isomers of μ-conotoxins KIIIA and KIIIB block voltage-gated sodium channels.Biochemistry · 2012Article
- Conotoxins targeting neuronal voltage-gated sodium channel subtypes: potential analgesics?Toxins · 2012Review
- Design of bioactive peptides from naturally occurring μ-conotoxin structures.The Journal of biological chemistry · 2012Article
- A novel µ-conopeptide, CnIIIC, exerts potent and preferential inhibition of NaV1.2/1.4 channels and blocks neuronal nicotinic acetylcholine receptors.British journal of pharmacology · 2012Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Disulfide bridges that stabilize the native conformation of conotoxins pose a challenge in the synthesis of smaller conotoxin analogues. Herein we describe the synthesis of a minimized analogue of the analgesic mu-conotoxin KIIIA that blocks two sodium channel subtypes, the neuronal Na(V)1.2 and skeletal muscle Na(V)1.4. Three disulfide-deficient analogues of KIIIA were initially synthesized in which the native disulfide bridge formed between either C1-C9, C2-C15, or C4-C16 was removed. Deletion of the first bridge only slightly affected the peptide's bioactivity. To further minimize this analogue, the N-terminal residue was removed and two nonessential serine residues were replaced by a single 5-amino-3-oxapentanoic acid residue. The resulting "polytide" analogue retained the ability to block sodium channels and to produce analgesia. Until now, the peptidomimetic approach applied to conotoxins has progressed only modestly at best; thus, the disulfide-deficient analogues containing backbone spacers provide an alternative advance toward the development of conopeptide-based therapeutics.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.