Exploring Venom Toxins as Molecular Models for Chronic Pain Treatment

Abstract


 
 
 The purpose of this project is to propose venomous animal toxins as molecular models for pain medication. Chronic pain is a prevalent health problem among the general population, and current pharmacological treatments are oftentimes ineffective or limited due to undesirable side-effects. This project explores the role of specific Voltage- Gated Sodium Channels, such as Sodium Channel 1.7 (NaV 1.7), in setting the stage for proposing analgesics with binding properties in peripheral pain-sensing neurons. Sodium Channels, notably NaV 1.7, play a major role in human pain signaling pathways that propagate action potentials in excitable cells. By inhibiting and blocking them, analgesic effects are known to be achievable. Through means of bioinformatic tools, we explore amino acid sequence alignments, Motif scans, tertiary structure modeling, and molecular docking of venomous animal toxins for in-silico new drug discovery research. Cysteine residues in toxins were reviewed as a possible link between acting upon the receptor and their analgesic effects. This led to the questioning of cysteine's role in the search for potential antagonists of NaV 1.7. Eventually, the attempt for a further investigation prompted the consideration for molecular docking between selected toxins and the receptor, aiming to seize chronic pain.