Conium maculatum · PhytoNexus

01 Identity and provenance

Accepted binomial: Conium maculatum
Common names: Hemlock
Family (APG IV): Apiaceae
Part used: Fruit
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): Scatizzi A et al. Nephrol Dial Transplant 1993;6:939-43 (rhabdomyolysis/ATN series) | Boskabadi J et al. Clin Case Rep 2021;9:e4509 | Cureus 2025 (two-case series) | VERIFIED 2026 (batch 4) - synthetic analogue, application, interactions, side effects and references populated from retrieved primary/regulatory sources. Interactions labelled CLINICAL vs THEORETICAL. Marketed-formulation column intentionally blank. | IDENTITY

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Piperidine alkaloids	Coniine Fruit	No therapeutic analogue. Coniine is a nicotinic agonist producing depolarising neuromuscular blockade - functionally curare-like.

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: NO ACCEPTED THERAPEUTIC USE. Historically a sedative and antispasmodic. Retained for toxicological reference.
Reported adverse effects: MISIDENTIFICATION IS THE MAIN ROUTE - an Apiaceae member confused with parsley, celery leaf, wild carrot / Queen Anne’s lace and parsnip root by foragers. Piperidine alkaloids (coniine, gamma-coniceine) act at autonomic ganglia and the neuromuscular junction: ataxia, headache, salivation, mydriasis, then rapidly progressive muscle weakness, biphasic tachycardia-then-bradycardia, and DEATH FROM RESPIRATORY PARALYSIS. NON-NEUROLOGICAL FEATURES ARE RECENT AND UNDER-RECOGNISED: rhabdomyolysis with myoglobinuria and acute tubular necrosis was found in 17 of 18 coniine-poisoned patients in one series - check CK and renal function, do not treat as purely neurological. Highest alkaloid content in seed. SECONDARY POISONING is reported from eating meat of animals that grazed the plant. Teratogenic in animals. Survival is high with prompt respiratory support.

04 Interaction matrix

Source column, verbatim: CLINICAL: additive neuromuscular blockade with depolarising and non-depolarising blocking agents; additive with other nicotinic agents.
Normalised onto 0 canonical drug classes below.

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
Cytotoxic and targeted anticancer drugs Oncology	4Contraindicated	PK-CYP3A4/UGT + PD-antagonistic	predicted D	Neutropenic sepsis and severe diarrhoea from over-exposure, or reduced an…	why ▾
Chemistry of this pair. Piperine inhibits CYP3A4, UGT and P-glycoprotein and increases intestinal permeability, raising the exposure of many co-administered drugs. Class mechanism. Botanical CYP3A4 and UGT1A1 modulation alters exposure to irinotecan, taxanes, vinca alkaloids and kinase inhibitors. High-dose antioxidant botanicals may also oppose the oxidative mechanism of some cytotoxics and of proteasome inhibitors. Expected Neutropenic sepsis and severe diarrhoea from over-exposure, or reduced antitumour effect; boronic-acid proteasome inhibitors are directly antagonised by polyphenols. Management No botanical should be taken during active cytotoxic therapy without oncology sign-off. Record all supplements in the chemotherapy chart. 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. Piperine inhibits CYP3A4, UGT and P-glycoprotein and increases intestinal permeability, raising the exposure of many co-administered drugs. 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
Antiepileptics CNS	3Major	PK-CYP induction + PD-antagonistic	predicted D	Breakthrough seizures, status epilepticus, or additive sedation and ataxi…	why ▾
Chemistry of this pair. Piperine inhibits CYP3A4, UGT and P-glycoprotein and increases intestinal permeability, raising the exposure of many co-administered drugs. Class mechanism. Enzyme-inducing botanicals lower plasma anticonvulsant concentrations, while GABAergic constituents add sedation and a few (thujone, camphor, beta-asarone, pinene-rich oils) are directly proconvulsant and lower seizure threshold. Expected Breakthrough seizures, status epilepticus, or additive sedation and ataxia. Management Measure anticonvulsant levels before and 2-4 weeks after any change. Avoid proconvulsant essential oils entirely in epilepsy. Onset delayed Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Antacids, PPIs and H2 blockers Gastrointestinal	2Moderate	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

05 Hazard register

misidentification - foraged as parsley, celery or wild carrot. A

06 Confusable material

No same-genus or shared-common-name entry in the corpus.

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.

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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
Piper longum Long Pepper	Piperaceae	4	0.67
Strychnos nux-vomica Nux Vomica	Loganiaceae	4	0.44
Lobelia inflata Indian Tobacco	Campanulaceae	4	1.00
Piper nigrum Black Pepper	Piperaceae	3	0.50
Ginkgo biloba Ginkgo	Ginkgoaceae	3	0.33
Hypericum perforatum St. John's Wort	Hypericaceae	3	0.25

10 References and notes

Source column: Vetter J. Food Chem Toxicol 2004

Vetter J. Food Chem Toxicol 2004

Vetter J 2004 manual

BibTeX for all 1 records

@article{VetterJ2004,
  title = {Vetter J. Food Chem Toxicol 2004},
  author = {Vetter J},
  year = {2004},
}

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