Echinacea purpurea · PhytoNexus

01 Identity and provenance

Accepted binomial: Echinacea purpurea
Common names: Echinacea
Family (APG IV): Asteraceae
Part used: Root
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): Reference not supplied - claim unverified against primary literature.

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Caffeic acid derivatives, Alkylamides, Polysaccharides, Glycoproteins, Flavonoids	Chicoric acid, Echinacoside, Caftaric acid, Dodecatetraenoic acid isobutylamide Root	Imiquimod (immune stimulation), Levamisole (historical immunomodulator), Interferon inducers (functional similarity rather than structural similarity)

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: Immune support, prevention of upper respiratory tract infections, wound healing, anti-inflammatory
Marketed in: Capsules, tablets, syrups, lozenges, herbal teas, immune boosters, topical creams
Reported adverse effects: Allergic reactions (especially Asteraceae-sensitive individuals), rash, gastrointestinal upset, fever (rare), asthma exacerbation (rare)

04 Interaction matrix

Source column, verbatim: Immunosuppressants, corticosteroids, chemotherapy agents, hepatotoxic drugs, CYP1A2/CYP3A4 substrates
Normalised onto 5 canonical drug classes below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Cytotoxic and targeted anticancer drugs Oncology	4Contraindicated	PK-CYP3A4/UGT + PD-antagonistic	curated B	Neutropenic sepsis and severe diarrhoea from over-exposure, or reduced an…	why ▾
Chemistry of this pair. Flavonoids inhibit CYP3A4, CYP1A2, OATP1B1 and UGT to a variable extent and have measurable antiplatelet activity. 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 B - reviewed clinical column, source pending Matched on “chemotherapy agents” Find evidence for this pair Map this mechanism
Immunosuppressants (ciclosporin, tacrolimus, mycophenolate) Transplant	4Contraindicated	PK-CYP3A4/P-gp + PD-antagonistic	curated B	Acute graft rejection with inducers; nephrotoxicity, neurotoxicity and hy…	why ▾
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 B - reviewed clinical column, source pending Matched on “immunosuppressants” Find evidence for this pair Map this mechanism
Narrow-therapeutic-index CYP3A4 substrates Pharmacokinetic	4Contraindicated	PK-CYP3A4	curated B	Toxic accumulation or subtherapeutic failure of the co-prescribed drug, s…	why ▾
Chemistry of this pair. Flavonoids inhibit CYP3A4, CYP1A2, OATP1B1 and UGT to a variable extent and have measurable antiplatelet activity. 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 B - reviewed clinical column, source pending Matched on “cyp3a4 substrates” Find evidence for this pair Map this mechanism
Corticosteroids Endocrine	3Major	PD-additive + PK-CYP3A4	curated B	Pseudohyperaldosteronism: hypertension, hypokalaemia, oedema, myopathy; C…	why ▾
Class mechanism. Glycyrrhizin inhibits 11-beta-hydroxysteroid dehydrogenase type 2 and prolongs cortisol half-life, potentiating mineralocorticoid effect. Anthraquinone laxatives compound steroid-driven potassium loss, and CYP3A4 inhibition raises systemic corticosteroid exposure. Expected Pseudohyperaldosteronism: hypertension, hypokalaemia, oedema, myopathy; Cushingoid features at unchanged steroid dose. Management Restrict licorice-containing products. Check potassium and blood pressure. Reduce steroid dose if features of excess appear. Onset rapid Evidence B - reviewed clinical column, source pending Matched on “corticosteroids” Find evidence for this pair Map this mechanism
Hepatotoxic drugs Organ toxicity	3Major	Organ-toxicity additive	curated B	Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acu…	why ▾
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 B - reviewed clinical column, source pending 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
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
Antiplatelet agents Haemostasis	3Major	PD-additive	predicted D	Prolonged bleeding time, surgical and post-procedural bleeding, bruising,…	why ▾
Chemistry of this pair. Flavonoids inhibit CYP3A4, CYP1A2, OATP1B1 and UGT to a variable extent and have measurable antiplatelet activity. Class mechanism. Organosulfur compounds, gingerols, salicylates, ginkgolides and eugenol inhibit thromboxane A2 synthesis, platelet aggregation and PAF-mediated activation, duplicating the pharmacology of aspirin and P2Y12 blockers. Expected Prolonged bleeding time, surgical and post-procedural bleeding, bruising, haematuria. Management Stop the botanical 7-14 days before elective surgery or neuraxial anaesthesia. Record it on the pre-operative medicines list. Onset rapid 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
Statins and lipid-lowering drugs Cardiovascular	2Moderate	PK-CYP3A4/OATP	predicted D	Myalgia, raised creatine kinase, rhabdomyolysis, hepatic transaminase ele…	why ▾
Chemistry of this pair. Flavonoids inhibit CYP3A4, CYP1A2, OATP1B1 and UGT to a variable extent and have measurable antiplatelet activity. 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 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

The audit recorded no hazard beyond the interaction profile. The controlled-vocabulary field reads not assessed, which means the assessment has not been done rather than that it came back clear.

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
Senna alexandrina Senna	Fabaceae	8	0.50
Phyllanthus amarus Bhui Amla	Phyllanthaceae	8	0.50
Rubia cordifolia Manjistha	Rubiaceae	6	0.35
Hypericum perforatum St. John's Wort	Hypericaceae	6	0.35
Vaccinium myrtillus Bilberry	Ericaceae	7	0.50
Tussilago farfara Coltsfoot	Asteraceae	7	0.54

10 References and notes

No citation is on record for this entry. That is itself the finding: the audit flagged it, and it is why the entry does not carry an A evidence grade.

Curator notes

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