Ricinus communis · PhytoNexus

01 Identity and provenance

Accepted binomial: Ricinus communis
Common names: Castor
Family (APG IV): Euphorbiaceae
Part used: Seed
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): StatPearls NBK441948 (Ricin Toxicity) | CDC ricin chemical fact sheet | VERIFIED 2026 (batch 2) - synthetic analogue, application, interactions, side effects and references populated from retrieved primary/regulatory sources. Interactions labelled CLINICAL vs THEORETICAL. Marketed-formulation column intentionally blank. | PREPARATION

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Fixed oil (hydroxy fatty acid)	Ricinoleic acid Seed	Castor oil is itself the pharmacopoeial stimulant laxative; bisacodyl and sodium picosulfate are functional analogues.

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: CASTOR OIL (seed, cold-pressed) - stimulant laxative via ricinoleic acid, plus wide industrial and excipient use. THE OIL IS NOT THE SEED: ricin is a water-soluble protein and does NOT partition into the oil, so properly produced castor oil is safe. Toxicity belongs to the whole seed and the residual press cake.
Reported adverse effects: RICIN (whole seed / press cake) is a ribosome-inactivating toxalbumin, lethal at approx. 5-10 micrograms/kg by inhalation or injection. Seeds are up to 5% ricin. Ingestion of as few as 2 crushed seeds has proved toxic; reported fatal dose 5-10 crushed seeds or about 6 mg ricin, fatal period 2 days to several. INTACT UNBROKEN SEEDS ARE LARGELY NON-TOXIC - the seed coat must be breached, which is why paediatric ingestions vary so widely in outcome. Features: oral burning resembling alkali injury, vomiting, bloody diarrhoea, severe abdominal pain, haemolysis, convulsions, jaundice, collapse. Seed dust causes conjunctivitis, rhinitis, asthmatic bronchitis and dermatitis in processing workers. No antidote; management supportive. CDC Category B biothreat agent.

04 Interaction matrix

Source column, verbatim: Standard stimulant-laxative cautions: electrolyte loss with diuretics and cardiac glycosides; reduced absorption of co-administered drugs.
Normalised onto 3 canonical drug classes below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Cardiac glycosides (digoxin, digitoxin) Cardiovascular	4Contraindicated	PD-additive + PK-transporter + assay interference	curated A	Nausea, xanthopsia, bradyarrhythmia, AV block, ventricular tachycardia an…	why ▾
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 A - human data with a cited source Matched on “cardiac glycosides” Find evidence for this pair Map this mechanism
Diuretics Renal	4Contraindicated	PD-additive + electrolyte-mediated	curated A	Hypokalaemia, hyponatraemia, dehydration, muscle weakness, cramps, arrhyt…	why ▾
Class mechanism. Aquaretic and saluretic botanicals add to renal potassium and sodium loss. Anthraquinone laxatives compound this through colonic potassium loss, and glycyrrhizin causes mineralocorticoid-like retention of sodium with kaliuresis. Expected Hypokalaemia, hyponatraemia, dehydration, muscle weakness, cramps, arrhythmia; potentiation of digoxin toxicity through low potassium. Management Check potassium, sodium and creatinine 1-2 weeks after starting. Avoid the combination entirely in patients also on digoxin. Onset rapid Evidence A - human data with a cited source Matched on “diuretics” Find evidence for this pair Map this mechanism
Laxatives and antidiarrhoeals Gastrointestinal	3Major	PD-additive	curated A	Cramping, diarrhoea, electrolyte loss, melanosis coli with chronic anthra…	why ▾
Class mechanism. Anthraquinone and mucilage botanicals add to stimulant and bulk laxative action; tannin-rich astringents oppose it. Expected Cramping, diarrhoea, electrolyte loss, melanosis coli with chronic anthraquinone use; or constipation and obstruction risk with astringents plus inadequate fluid. Management Limit stimulant laxative botanicals to under 2 weeks. Ensure adequate fluid intake with any bulk-forming product. Onset rapid Evidence A - human data with a cited source Matched on “laxative” 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. Ribosome-inactivating toxalbumins depurinate 28S rRNA and halt protein synthesis at extremely low doses. 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
Hepatotoxic drugs Organ toxicity	4Contraindicated	Organ-toxicity additive	predicted D	Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acu…	why ▾
Chemistry of this pair. Ribosome-inactivating toxalbumins depurinate 28S rRNA and halt protein synthesis at extremely low doses. 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 D - in silico rule prediction only Find evidence for this pair Map this mechanism
Nephrotoxic drugs Organ toxicity	4Contraindicated	Organ-toxicity additive	predicted D	Rising creatinine, tubulointerstitial nephritis, urothelial carcinoma wit…	why ▾
Chemistry of this pair. Ribosome-inactivating toxalbumins depurinate 28S rRNA and halt protein synthesis at extremely low doses. Class mechanism. Aristolochic acid, high oxalate loads and anthraquinone-driven volume depletion add to aminoglycoside, NSAID, contrast and calcineurin-inhibitor nephrotoxicity. Expected Rising creatinine, tubulointerstitial nephritis, urothelial carcinoma with aristolochic acid, oxalate nephropathy. Management Check creatinine and urinalysis. Aristolochia-containing material must never be dispensed; verify identity of any Fangchi or Mu Tong substitute. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism

05 Hazard register

processing-dependent - ricin does not enter the oil. Oil safe, s

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	4	0.29
Rubia cordifolia Manjistha	Rubiaceae	4	0.31
Hypericum perforatum St. John's Wort	Hypericaceae	3	0.21
Echinacea purpurea Echinacea	Asteraceae	3	0.20
Cassia fistula Amaltas	Fabaceae	3	0.43
Rheum emodi Rhubarb	Polygonaceae	3	0.43

10 References and notes

Source column: Worbs S et al. Toxins 2011;3:1332-72. PMC3210461

Worbs S et al. Toxins 2011

Worbs S et al. Toxins 2011 manual

3:1332-72. PMC3210461

manual

BibTeX for all 2 records

@article{WorbsSeta2011,
  title = {Worbs S et al. Toxins 2011},
  author = {Worbs S et al.},
  journal = {Toxins},
  year = {2011},
}

@article{anon,
  title = {3:1332-72. PMC3210461},
}

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