Aconitum napellus · PhytoNexus

01 Identity and provenance

Accepted binomial: Aconitum napellus
Common names: Monkshood
Family (APG IV): Ranunculaceae
Part used: Root
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): Coulson JM et al. Clin Toxicol 2017;55:313-21 | VERIFIED 2026 - synthetic analogue, application, interactions, side effects and references populated from retrieved primary/regulatory sources (see References). Interaction entries are labelled CLINICAL (case reports or trials in humans) vs THEORETICAL (in-vitro or animal only). Marketed-formulation column intentionally left blank. | PREPARATION

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Diterpene alkaloids	Aconitine Root	None. Aconitine persistently activates voltage-gated Na+ channels; there is no therapeutic synthetic counterpart.

The analogue column is what makes the interaction reasoning tractable: where a constituent has a marketed structural counterpart, the counterpart's interaction profile is the starting hypothesis for the plant.

Looking up structures and physicochemical properties from PubChem…

03 Stated application

Reported activity: Historically analgesic and antipyretic. Used in TCM and Ayurveda only after processing/detoxification (shodhana). The margin between analgesic and toxic dose is very low. NOT for unprocessed use.
Reported adverse effects: LIFE-THREATENING. Ventricular tachycardia, bidirectional VT and ventricular fibrillation; hypotension, cardiogenic shock. Paraesthesia, GI and neurotoxic effects. No specific antidote; management supportive - amiodarone and flecainide are reasonable first line, with cardiopulmonary bypass in refractory cases. Aconitine half-life approx. 3 hours.

04 Interaction matrix

Source column, verbatim: CLINICAL: additive risk with any Na+-channel-active or antiarrhythmic drug. Aconite-induced ventricular arrhythmia is often refractory to cardioversion and to standard antiarrhythmics.
Normalised onto 1 canonical drug class below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Antiarrhythmics Cardiovascular	4Contraindicated	PD-additive + electrolyte-mediated	curated A	Proarrhythmia, QT prolongation, torsade de pointes, ventricular arrhythmi…	why ▾
Chemistry of this pair. Aconitine binds persistently to the open state of voltage-gated sodium channels in myocardium and neurons. Class mechanism. Botanicals that shift potassium or magnesium, block sodium or potassium channels, or prolong repolarisation add to class I and class III antiarrhythmic effects on an already unstable myocardium. Expected Proarrhythmia, QT prolongation, torsade de pointes, ventricular arrhythmia. Management Avoid. If unavoidable, baseline and follow-up ECG with QTc measurement plus potassium and magnesium correction. Onset rapid Evidence A - human data with a cited source Matched on “antiarrhythmics” Find evidence for this pair Map this mechanism

Predicted from constituent chemistry

These edges are not clinical findings. Each one is a rule inference: a constituent class in this plant is known to act on a target that the drug class also acts on. They are shown because a blank cell reads as “safe”, and for a Tier 1 entry a blank cell only means “not yet looked at”. Treat them as a literature-search agenda, not as a warning.

Drug class	Severity	Mechanism type	Provenance	Expected effect
Cardiac glycosides (digoxin, digitoxin) Cardiovascular	4Contraindicated	PD-additive + PK-transporter + assay interference	predicted D	Nausea, xanthopsia, bradyarrhythmia, AV block, ventricular tachycardia an…	why ▾
Chemistry of this pair. Aconitine binds persistently to the open state of voltage-gated sodium channels in myocardium and neurons. Class mechanism. Cardenolide- and bufadienolide-bearing plants are themselves Na+/K+-ATPase inhibitors, so co-administration is pharmacological overdose. Several also inhibit intestinal P-glycoprotein, raising digoxin exposure, and cross-react with digoxin immunoassays so that serum levels become uninterpretable. Expected Nausea, xanthopsia, bradyarrhythmia, AV block, ventricular tachycardia and death; falsely reassuring or falsely high assay results. Management Treat as an absolute contraindication. If exposure has occurred, manage on ECG and clinical grounds, not on assay values, and consult toxicology about digoxin-specific Fab. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Cardiotoxic drugs Organ toxicity	4Contraindicated	Organ-toxicity additive	predicted D	Arrhythmia, reduced ejection fraction, myocarditis-like presentation.	why ▾
Chemistry of this pair. Aconitine binds persistently to the open state of voltage-gated sodium channels in myocardium and neurons. Class mechanism. Aconitine-type alkaloids, cardenolides and high-dose ephedrine add to anthracycline, trastuzumab and antiarrhythmic myocardial toxicity. Expected Arrhythmia, reduced ejection fraction, myocarditis-like presentation. Management Avoid during cardiotoxic chemotherapy. Baseline and follow-up echocardiography where exposure has occurred. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Narrow-therapeutic-index CYP3A4 substrates Pharmacokinetic	4Contraindicated	PK-CYP3A4	predicted D	Toxic accumulation or subtherapeutic failure of the co-prescribed drug, s…	why ▾
Chemistry of this pair. Alkaloidal bases have pH-dependent absorption and commonly interact with hepatic CYP isoenzymes and efflux transporters. Class mechanism. Furanocoumarins, bergamottin, piperine, glabridin and berberine inhibit CYP3A4; hyperforin, andrographolide and several diterpenes induce it through PXR. Because CYP3A4 handles roughly half of marketed drugs, the affected list is broad and the direction is product-specific. Expected Toxic accumulation or subtherapeutic failure of the co-prescribed drug, sometimes fatal for antiarrhythmics, immunosuppressants and oncology agents. Management Screen the full regimen for 3A4 substrates. Where the substrate has a narrow index, avoid rather than monitor. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Antacids, PPIs and H2 blockers Gastrointestinal	3Major	PK-absorption	predicted D	Reduced or erratic absorption of alkaloids; heartburn and reflux from pre…	why ▾
Chemistry of this pair. Alkaloidal bases have pH-dependent absorption and commonly interact with hepatic CYP isoenzymes and efflux transporters. Class mechanism. Gastric pH elevation alters the dissolution and ionisation of alkaloidal and enteric-coated botanical products; menthol- and peppermint-oil products lose their enteric protection at high pH and can be released prematurely. Expected Reduced or erratic absorption of alkaloids; heartburn and reflux from premature release of volatile-oil preparations. Management Separate administration by 2 hours. Avoid non-enteric peppermint oil in reflux disease. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Topical antiseptics, keratolytics and irritants Dermatology	3Major	PD-additive local	predicted D	Contact dermatitis, chemical burn, photoirritation, unexpected systemic a…	why ▾
Chemistry of this pair. Volatile terpenes are lipophilic, cross membranes readily and induce or inhibit CYP2B6 and CYP3A4 depending on the constituent. Class mechanism. Essential-oil terpenes, capsaicinoids and phorbol-type diterpenes add to the barrier disruption caused by topical antiseptics, retinoids and keratolytics, and increase percutaneous absorption of anything applied with them. Expected Contact dermatitis, chemical burn, photoirritation, unexpected systemic absorption from broken skin. Management Patch test first. Never apply undiluted essential oils to broken or freshly shaved skin, or with occlusion. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism

05 Hazard register

processing-dependent - requires shodhana. Analgesic-to-toxic mar

06 Confusable material

These entries could be mistaken for this one in trade, in the herbarium, or in a prescription. Powdered material is often indistinguishable, so the check is macroscopic, microscopic and chromatographic rather than nominal.

Aconitum ferox

Vatsanabha

Ranunculaceae

Same genus (Aconitum)

07 Mechanism map

Chemistry sorts to the left, pharmacology to the right. Dashed edges are predicted. Drag nodes, scroll to zoom, export at 3× for a figure.

species

chemical class

marker compound

drug class

expected effect

hazard

08 Open literature

Abstract-scoped query built from this binomial, its common names and its marker compounds, run live against Europe PMC, PubMed and OpenAlex, then ranked locally against an evidence hierarchy.

Checking openFDA spontaneous reports…

09 Isomechanistic neighbours

Species whose interaction profile overlaps this one, ranked by shared severity weight rather than by count — a shared contraindication counts for more than a shared minor signal. Practical use: these are the plants you should not stack with this one, because the mechanisms summate.

Species	Family	Shared classes	Jaccard
Aconitum ferox Vatsanabha	Ranunculaceae	6	1.00
Ephedra gerardiana Himalayan Ephedra	Ephedraceae	5	0.45
Citrus aurantium Bitter Orange	Rutaceae	5	0.63
Senna alexandrina Senna	Fabaceae	4	0.29
Ephedra sinica Ephedra	Ephedraceae	4	0.40
Carapichea ipecacuanha Ipecac	Rubiaceae	4	0.50

10 References and notes

Source column: Chan TYK. Clin Toxicol 2009;47:279-85. doi:10.1080/15563650902904407

Chan TYK. Clin Toxicol 2009

Chan TYK 2009 manual

47:279-85. doi:10.1080/15563650902904407

doi:10.1080/15563650902904407 manual

BibTeX for all 2 records

@article{ChanTYK2009,
  title = {Chan TYK. Clin Toxicol 2009},
  author = {Chan TYK},
  year = {2009},
}

@article{anon,
  title = {47:279-85. doi:10.1080/15563650902904407},
  doi = {10.1080/15563650902904407},
}

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