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Selective Targeting of Nav1.7 with Engineered Spider Venom-Based Peptides
Robert A Neff1, Alan D Wickenden2
1Neuroscience Discovery, Janssen Research and Development, LLC , San Diego, CA, USA.
Channels (Austin, Tex.)
|January 11, 2021
Summary
Navigating pain signaling requires voltage-gated sodium channels (Nav1.7). Researchers are engineering spider venom peptides to create selective Nav1.7 blockers for novel pain therapeutics.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Voltage-gated sodium channels (Nav1.7) are crucial for pain signal transmission in the nervous system.
- Nav1.7 gain-of-function mutations cause pain, while loss-of-function mutations lead to pain insensitivity.
- Nav1.7 is a key target for developing new pain relief medications, but selective drugs are still lacking.
Purpose of the Study:
- To summarize research efforts in developing Nav1.7 selective antagonists.
- To explore the potential of engineering spider venom peptides as analgesics.
Main Methods:
- Reviewing studies on spider venom peptide scaffolds targeting Nav1.7.
- Analyzing progress and challenges in developing venom-based Nav1.7 inhibitors.
Main Results:
- Spider venom peptides offer promising scaffolds for Nav1.7 antagonist development.
- Progress has been made using various venom families.
Conclusions:
- Engineering spider venom peptides is a viable strategy for creating Nav1.7 selective analgesics.
- Further research is needed to overcome challenges in developing these venom-based therapeutics.
