Molecular target
Voltage-Gated Sodium Channel
Action-potential-generating channel in neurons. Use-dependent inhibition is the mechanism of phenytoin, carbamazepine, lamotrigine, and other anti-seizure drugs. Several plant compounds modulate Na channels (eugenol, kavalactones).
Educational use only. This page summarizes published research and traditional-use records for educational purposes. It does not diagnose, treat, cure, or prevent any disease. Do not start, stop, or change medications based on this information. Discuss any decisions about therapies — pharmaceutical or botanical — with a qualified clinician who knows your medical history.
No PHI / HIPAA notice: Do not share Protected Health Information (PHI) of any patient on this site — including names, dates of birth, addresses, MRNs, or any identifying information. Use abstract case framing only. Sharing PHI with non-covered entities risks HIPAA violation regardless of platform capability.
Pharmaceutical agents
Drugs that act on Voltage-Gated Sodium Channel
These medications have Voltage-Gated Sodium Channel among their molecular targets. Sharing a target is a mechanistic relationship — it does not make any plant below an alternative to, or substitute for, these drugs.
Botanical connections
Plants whose compounds act on Voltage-Gated Sodium Channel
Each plant below contains a named compound documented to act on Voltage-Gated Sodium Channel. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.
- QuinineQuinoline alkaloid
Research reports accumulation in the Plasmodium falciparum digestive vacuole where it is investigated as an inhibitor of haem polymerisation (haemozoin formation), disrupting parasite detoxification. Also investigated for membrane-stabilising and sodium-channel effects contributing to antispasmodic properties. Stereochemical configuration at C-9 (erythro orientation) reported to be critical for antiplasmodial potency.
- QuinidineQuinoline alkaloid (stereoisomer of quinine)
Shares the antiplasmodial haem polymerisation inhibition mechanism with quinine. As a pharmaceutical agent, quinidine is classified as a class Ia antiarrhythmic: studies describe blockade of voltage-gated sodium channels (prolonging action potential), L-type calcium channel antagonism, and α1-adrenergic blocking activity. These cardiac effects are relevant to drug interaction risk.
- AconitineDiterpenoid alkaloid
Aconitine binds voltage-gated sodium channels and causes prolonged, persistent activation, preventing channel inactivation. This mechanism underlies both the reported analgesic (topical, low-dose) effects and the highly toxic cardiovascular and neurotoxic profile documented in case reports. Studies also report interaction with voltage-gated calcium channels at higher concentrations.
- EugenolPhenylpropanoid
Preclinical studies report eugenol inhibits COX-1/COX-2 and NF-κB signalling, suppresses PGE2 synthesis, and modulates TRPV1 and voltage-gated sodium channels; proposed as the primary driver of observed analgesic and anti-inflammatory signals.