Colchicum autumnale · PhytoNexus

01 Identity and provenance

Accepted binomial: Colchicum autumnale
Common names: Autumn Crocus
Family (APG IV): Colchicaceae
Part used: Corm, Seed
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): StatPearls NBK431102 | 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. | DOSE

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Tropolone alkaloids	Colchicine Corm, Seed	Colchicine itself is the marketed drug (plant-derived, not an analogue).

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: Acute gout flare and prophylaxis; familial Mediterranean fever; pericarditis. Increasingly used in cardiovascular inflammation.
Reported adverse effects: Diarrhoea, nausea, vomiting, abdominal pain (dose-related). Severe: rhabdomyolysis/myopathy, agranulocytosis, acute renal failure, hepatic failure, arrhythmia, multiorgan dysfunction, death. In FAERS reports that stated severity, 61% involved hospitalisation and 24% death.

04 Interaction matrix

Source column, verbatim: MAJOR - NARROW THERAPEUTIC INDEX. Colchicine is a CYP3A4 substrate and a P-glycoprotein substrate. FATAL interactions reported with clarithromycin (dual CYP3A4/P-gp inhibitor). Also erythromycin, verapamil, ciclosporin, atazanavir, grapefruit juice, statins. Combination is contraindicated in renal or hepatic impairment. Strongest FAERS signal: colchicine + atazanavir and rhabdomyolysis (ROR 35.4, 95% CI 12.8-97.6).
Normalised onto 3 canonical drug classes below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Immunosuppressants (ciclosporin, tacrolimus, mycophenolate) Transplant	4Contraindicated	PK-CYP3A4/P-gp + PD-antagonistic	curated A	Acute graft rejection with inducers; nephrotoxicity, neurotoxicity and hy…	why ▾
Chemistry of this pair. Colchicine is a tubulin-binding CYP3A4 and P-glycoprotein substrate with a very narrow margin between therapeutic and lethal exposure. Class mechanism. These are narrow-therapeutic-index CYP3A4 and P-glycoprotein substrates. Botanical induction collapses trough levels; inhibition causes toxic accumulation. Immunostimulant botanicals separately oppose the therapeutic goal. Expected Acute graft rejection with inducers; nephrotoxicity, neurotoxicity and hypertension with inhibitors; autoimmune flare with immunostimulants. Management Treat as contraindicated in transplant recipients. Any exposure requires immediate trough level measurement and transplant team notification. Onset unspecified Evidence A - human data with a cited source Matched on “ciclosporin” Find evidence for this pair Map this mechanism
Narrow-therapeutic-index CYP3A4 substrates Pharmacokinetic	4Contraindicated	PK-CYP3A4	curated A	Toxic accumulation or subtherapeutic failure of the co-prescribed drug, s…	why ▾
Chemistry of this pair. Colchicine is a tubulin-binding CYP3A4 and P-glycoprotein substrate with a very narrow margin between therapeutic and lethal exposure. 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 A - human data with a cited source Matched on “cyp3a4 substrate” Find evidence for this pair Map this mechanism
Statins and lipid-lowering drugs Cardiovascular	3Major	PK-CYP3A4/OATP	curated A	Myalgia, raised creatine kinase, rhabdomyolysis, hepatic transaminase ele…	why ▾
Class mechanism. CYP3A4 and OATP1B1 inhibition by furanocoumarin- and flavonoid-rich botanicals raises simvastatin, atorvastatin and lovastatin exposure. Some botanicals themselves contain monacolin K, which is chemically lovastatin. Expected Myalgia, raised creatine kinase, rhabdomyolysis, hepatic transaminase elevation. Management Ask specifically about red-yeast-rice type products. Check CK and ALT if muscle symptoms appear; prefer a non-3A4 statin. Onset unspecified Evidence A - human data with a cited source Matched on “statins” 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
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. Colchicine is a tubulin-binding CYP3A4 and P-glycoprotein substrate with a very narrow margin between therapeutic and lethal exposure. 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
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

05 Hazard register

narrow therapeutic index - CYP3A4/P-gp substrate, fatal interact

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
Gloriosa superba Glory Lily	Colchicaceae	4	0.80
Hypericum perforatum St. John's Wort	Hypericaceae	4	0.33
Echinacea purpurea Echinacea	Asteraceae	4	0.31
Uncaria tomentosa Cat's Claw	Rubiaceae	4	0.31
Sambucus nigra Elderberry	Adoxaceae	4	0.67
Ficus religiosa Peepal	Moraceae	4	0.50

10 References and notes

Source column: Gomez-Lumbreras A et al. Ann Pharmacother 2023. doi:10.1177/10600280221148031

Gomez-Lumbreras A et al. Ann Pharmacother 2023. doi:10.1177/10600280221148031

Gomez-Lumbreras A et al. Ann Pharmacother 2023 doi:10.1177/10600280221148031 manual

BibTeX for all 1 records

@article{GomezLumbre2023,
  title = {Gomez-Lumbreras A et al. Ann Pharmacother 2023. doi:10.1177/10600280221148031},
  author = {Gomez-Lumbreras A et al.},
  journal = {Ann Pharmacother},
  year = {2023},
  doi = {10.1177/10600280221148031},
}

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