Tussilago farfara · PhytoNexus

01 Identity and provenance

Accepted binomial: Tussilago farfara
Common names: Coltsfoot
Family (APG IV): Asteraceae
Part used: Leaf, Flower
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): Roulet M et al. J Pediatr 1988;112:433-6 (index case) | Adamczak A et al. 2013 (PA variability) | Systematic review of borage/coltsfoot/comfrey case reports, 2020 | VERIFIED 2026 (batch 3) - 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 | substitution (also COMPOSITION

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Mucilage, pyrrolizidine alkaloids	Tussilagone Leaf, Flower	No synthetic analogue. Mucilage acts as a demulcent; the pyrrolizidine alkaloids are contaminating toxins, not the therapeutic principle.

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: Traditional cough remedy (the name means "cough suppressant") in European and Chinese practice. Restricted in Austria and Germany.
Reported adverse effects: Contains hepatotoxic 1,2-unsaturated pyrrolizidine alkaloids (senkirkine, senecionine) - macrocyclic diesters associated with hepatic veno-occlusive disease. IMPORTANT CAVEAT ON THE CLASSIC CASE: the 1988 Swiss report of fatal neonatal hepatic VOD after maternal coltsfoot tea prompted the German withdrawal, but later investigation found the tea also contained Petasites (another PA source) and coltsfoot was probably NOT the cause. The PA class hazard is real; the attribution in that specific case is not secure. PA content varies widely (0.06-1.04 ug/g dry leaf) and is largely genetic; PA-free clones exist (registered variety "Wien").

04 Interaction matrix

Source column, verbatim: THEORETICAL: additive hepatotoxicity with other PA-containing herbs (comfrey, borage, Petasites) and with hepatotoxic drugs.
Normalised onto 1 canonical drug class below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Hepatotoxic drugs Organ toxicity	4Contraindicated	Organ-toxicity additive	curated A	Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acu…	why ▾
Chemistry of this pair. Pyrrolizidine alkaloids are bioactivated by CYP3A4 to pyrrolic esters that alkylate sinusoidal endothelium. Class mechanism. Pyrrolizidine alkaloids, high-dose anthraquinones, kava constituents and germander-type diterpenes cause hepatocellular or sinusoidal injury that adds to the risk from paracetamol, isoniazid, methotrexate, azoles and statins. Expected Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acute liver failure. Management Baseline and 4-weekly ALT and bilirubin. Stop the botanical at any transaminase rise above three times the upper reference limit. Onset unspecified Evidence A - human data with a cited source Matched on “hepatotoxic drugs” 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. Hydrocolloids raise luminal viscosity and physically entrap co-administered drug molecules, delaying and reducing absorption. 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
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
Antidiabetic drugs (insulin, sulfonylureas, biguanides, GLP-1, SGLT2) Endocrine	3Major	PD-additive	predicted D	Symptomatic hypoglycaemia, sweating, tremor, confusion; severe events rep…	why ▾
Chemistry of this pair. Hydrocolloids raise luminal viscosity and physically entrap co-administered drug molecules, delaying and reducing absorption. Class mechanism. Hypoglycaemic botanicals act through insulin secretagogue, insulin-sensitising, alpha-glucosidase-inhibiting or glucose-transport routes. Added to a titrated pharmacological regimen the effects summate rather than plateau. Expected Symptomatic hypoglycaemia, sweating, tremor, confusion; severe events reported with insulin and sulfonylureas. Management Increase self-monitoring frequency for 2 weeks after starting or stopping. Anticipate a downward dose adjustment of insulin or sulfonylurea. Onset rapid 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
Antibacterials and anthelmintics Infection	2Moderate	PK-chelation + PK-CYP	predicted D	Treatment failure from subtherapeutic antibiotic concentrations, or raise…	why ▾
Chemistry of this pair. Hydrocolloids raise luminal viscosity and physically entrap co-administered drug molecules, delaying and reducing absorption. Class mechanism. Cation- and tannin-rich botanicals chelate tetracyclines and fluoroquinolones; efflux-pump-inhibiting and CYP-modulating constituents alter macrolide, rifamycin and azole exposure. Anthelmintic botanicals add to praziquantel and albendazole effect. Expected Treatment failure from subtherapeutic antibiotic concentrations, or raised toxicity of azoles and macrolides. Management Separate doses by 2-3 hours. Do not rely on botanical antimicrobials in place of an indicated antibiotic. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Iron, calcium and mineral supplements Nutrition	2Moderate	PK-chelation	predicted D	Failure of iron-deficiency correction, unexplained non-response to oral i…	why ▾
Chemistry of this pair. Hydrocolloids raise luminal viscosity and physically entrap co-administered drug molecules, delaying and reducing absorption. Class mechanism. Tannins, phytates, oxalates and mucilage form insoluble complexes with divalent and trivalent cations in the gut lumen, reducing absorption of both the mineral and any co-administered chelating drug. Expected Failure of iron-deficiency correction, unexplained non-response to oral iron or calcium. Management Separate mineral doses from tannin- and fibre-rich botanicals by at least 2 hours; take iron with ascorbate instead. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Thyroid hormones and antithyroid drugs Endocrine	2Moderate	PK-absorption + PD-modulation	predicted D	Iatrogenic hyper- or hypothyroidism, unexplained TSH drift, loss of euthy…	why ▾
Chemistry of this pair. Hydrocolloids raise luminal viscosity and physically entrap co-administered drug molecules, delaying and reducing absorption. Class mechanism. Guggulsterone stimulates thyroid function and T4-to-T3 conversion; goitrogenic glucosinolates and lithospermic acid suppress it; high-fibre and cation-rich botanicals bind levothyroxine in the gut and reduce absorption. Expected Iatrogenic hyper- or hypothyroidism, unexplained TSH drift, loss of euthyroid control. Management Separate levothyroxine from fibre and mineral products by 4 hours. Recheck TSH 6-8 weeks after any botanical change. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism

05 Hazard register

chemotype) - Petasites contamination confounds the classic case;

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.

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
Echinacea purpurea Echinacea	Asteraceae	7	0.54
Phyllanthus amarus Bhui Amla	Phyllanthaceae	6	0.43
Senna alexandrina Senna	Fabaceae	5	0.33
Senegalia senegal Gum Acacia	Fabaceae	5	0.63
Salvia hispanica Chia	Lamiaceae	5	0.63
Cyamopsis tetragonoloba Guar	Fabaceae	5	0.63

10 References and notes

Source column: Nedelcheva A et al. PA content in T. farfara

Nedelcheva A et al. PA content in T. farfara

Nedelcheva A et al. manual

BibTeX for all 1 records

@article{NedelchevaA,
  title = {Nedelcheva A et al. PA content in T. farfara},
  author = {Nedelcheva A et al.},
}

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