ReviewChannels (Austin, Tex.)2021
Selective Targeting of Nav1.7 with Engineered Spider Venom-Based Peptides.
Review in Channels (Austin, Tex.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed.
- A Systemically Administered Humanized Anti-Nav1.7 Antibody with Long-Lasting Analgesic Activity and Preserved Physiological Nociception.Pharmaceutics · 2026Article
- Scorpion Venom Peptides: From Structural Scaffolds to Therapeutic Applications-A Focus on Antioxidant Mechanisms and Translational Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Preclinical Animal Models to Investigate the Role of NaLife (Basel, Switzerland) · 2025Review
- Venom-derived peptides for breaking through the glass ceiling of drug development.Frontiers in chemistry · 2024Review
- Computational design of peptides to target NaeLife · 2022Article
- The Tarantula Venom Peptide Eo1a Binds to the Domain II S3-S4 Extracellular Loop of Voltage-Gated Sodium Channel NaFrontiers in pharmacology · 2021Article
- Strategies for Heterologous Expression, Synthesis, and Purification of Animal Venom Toxins.Frontiers in bioengineering and biotechnology · 2021Review
- Pain-related toxins in scorpion and spider venoms: a face to face with ion channels.The journal of venomous animals and toxins including tropical diseases · 2021Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A fundamental mechanism that drives the propagation of electrical signals in the nervous system is the activation of voltage-gated sodium channels. The sodium channel subtype Nav1.7 is critical for the transmission of pain-related signaling, with gain-of-function mutations in Nav1.7 resulting in various painful pathologies. Loss-of-function mutations cause complete insensitivity to pain and anosmia in humans that otherwise have normal nervous system function, rendering Nav1.7 an attractive target for the treatment of pain. Despite this, no Nav1.7 selective therapeutic has been approved for use as an analgesic to date. Here we present a summary of research that has focused on engineering peptides found in spider venoms to produce Nav1.7 selective antagonists. We discuss the progress that has been made on various scaffolds from different venom families and highlight the challenges that remain in the effort to produce a Nav1.7 selective, venom-based analgesic.
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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 Socratic graph.