Cinnamomum cassia · PhytoNexus

01 Identity and provenance

Accepted binomial: Cinnamomum cassia
Common names: Cassia Cinnamon
Family (APG IV): Lauraceae
Part used: Bark
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): Abraham K et al. (coumarin bioavailability from cinnamon matrix) | PMC4913087 (coumarin intake and hepatotoxicity, Japanese Kampo) | PMC3373703 (negative RCT) | VERIFIED 2026 (batch 6) - 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
Volatile oil	Cinnamaldehyde Bark	No drug analogue. Coumarin (the toxic constituent) is unrelated to warfarin’s anticoagulant 4-hydroxycoumarins despite the shared name - a common and consequential confusion.

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: Culinary spice and traditional warming remedy. Marketed for glycaemic control, but a randomised trial of Cinnamonforce found NO significant improvement in fasting glucose, insulin or lipids over 13 weeks in type 2 diabetes.
Reported adverse effects: SPECIES DETERMINES THE RISK. Cassia contains 2,000-4,000 mg/kg coumarin (some sources up to 7,000); Ceylon cinnamon (C. verum, entry 21) contains under 200 mg/kg - a difference of two orders of magnitude. Coumarin is hepatotoxic; the EFSA/BfR tolerable daily intake is 0.1 mg/kg body weight. CONCRETE THRESHOLDS: a 60 kg adult reaches the TDI at about 2 g of cassia per day; A 15 KG CHILD REACHES IT AT ABOUT 0.5 G. BfR has shown that coumarin in the cinnamon matrix is absorbed comparably to isolated coumarin, so the "it’s bound in the plant" argument does not hold. Case reports link heavy cassia use to reversible transaminase rises. IN POWDER FORM THE TWO SPECIES CANNOT BE TOLD APART - only the stick cross-section (multi-layered for Ceylon, single thick roll for cassia) or a species declaration on the label distinguishes them.

04 Interaction matrix

Source column, verbatim: CLINICAL: caution in liver disease and with hepatotoxic or liver-metabolised drugs. The often-quoted warfarin interaction is mechanistically weak - coumarin is not an anticoagulant - but supplement labels rarely make that distinction.
Normalised onto 3 canonical drug classes below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Anticoagulants (vitamin-K antagonists, DOACs) Haemostasis	3Major	PD-additive + PK-CYP2C9	curated A	INR destabilisation in either direction; ecchymosis, epistaxis, gum bleed…	why ▾
Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose. Class mechanism. Coumarin-, salicylate- and coumestan-bearing botanicals add to vitamin-K-antagonist effect; several also compete for CYP2C9 and CYP3A4, raising S-warfarin exposure. Botanicals rich in vitamin K1 act in the opposite direction and blunt anticoagulation. Expected INR destabilisation in either direction; ecchymosis, epistaxis, gum bleeding, GI or intracranial haemorrhage. Management Do not start or stop the botanical without INR cover. Check INR at 3-5 days and again at 2 weeks. Document the product, batch and dose in the anticoagulation record. Onset rapid Evidence A - human data with a cited source Matched on “anticoagulant” Find evidence for this pair Map this mechanism
Hepatotoxic drugs Organ toxicity	3Major	Organ-toxicity additive	curated A	Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acu…	why ▾
Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose. 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” Find evidence for this pair Map this mechanism
Iron, calcium and mineral supplements Nutrition	2Moderate	PK-chelation	curated A	Failure of iron-deficiency correction, unexplained non-response to oral i…	why ▾
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 A - human data with a cited source Matched on “supplement” 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
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. Volatile terpenes are lipophilic, cross membranes readily and induce or inhibit CYP2B6 and CYP3A4 depending on the constituent. 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
Antiplatelet agents Haemostasis	3Major	PD-additive	predicted D	Prolonged bleeding time, surgical and post-procedural bleeding, bruising,…	why ▾
Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose. 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
NSAIDs Analgesia	3Major	PD-additive	predicted D	Peptic ulceration, upper GI bleeding, acute kidney injury in volume-deple…	why ▾
Chemistry of this pair. Phenylpropanoids inhibit platelet aggregation and thromboxane synthesis and are direct mucosal irritants; some deplete hepatic glutathione at high dose. Class mechanism. Salicylate-, coumarin- and eugenol-bearing botanicals add both antiplatelet activity and direct gastric mucosal irritation to cyclo-oxygenase inhibition; several also reduce renal prostaglandin-dependent perfusion. Expected Peptic ulceration, upper GI bleeding, acute kidney injury in volume-depleted patients. Management Avoid in ulcer history. Add gastroprotection where the combination is unavoidable, and monitor renal function in the elderly. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
Topical antiseptics, keratolytics and irritants Dermatology	2Moderate	PD-additive local	predicted D	Contact dermatitis, chemical burn, photoirritation, unexpected systemic a…	why ▾
Chemistry of this pair. Volatile terpenes are lipophilic, cross membranes readily and induce or inhibit CYP2B6 and CYP3A4 depending on the constituent. Class mechanism. Essential-oil terpenes, capsaicinoids and phorbol-type diterpenes add to the barrier disruption caused by topical antiseptics, retinoids and keratolytics, and increase percutaneous absorption of anything applied with them. Expected Contact dermatitis, chemical burn, photoirritation, unexpected systemic absorption from broken skin. Management Patch test first. Never apply undiluted essential oils to broken or freshly shaved skin, or with occlusion. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism

05 Hazard register

species confusion - Cassia vs Ceylon differ ~100-fold in coumari

06 Confusable material

These entries could be mistaken for this one in trade, in the herbarium, or in a prescription. Powdered material is often indistinguishable, so the check is macroscopic, microscopic and chromatographic rather than nominal.

Cinnamomum camphora Camphor Tree	Lauraceae	Same genus (Cinnamomum)
Cinnamomum verum Cinnamon	Lauraceae	Same genus (Cinnamomum)

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
Ocimum tenuiflorum Tulsi	Lamiaceae	6	0.67
Thymus vulgaris Thyme	Lamiaceae	6	0.86
Origanum vulgare Oregano	Lamiaceae	6	0.86
Myristica fragrans Nutmeg	Myristicaceae	6	0.75
Curcuma longa Turmeric	Zingiberaceae	5	0.56
Arnica montana Arnica	Asteraceae	5	0.63

10 References and notes

Source column: BfR opinion on coumarin in cassia cinnamon and FAQ

BfR opinion on coumarin in cassia cinnamon and FAQ

manual

BibTeX for all 1 records

@article{anon,
  title = {BfR opinion on coumarin in cassia cinnamon and FAQ},
}

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