Acorus calamus · PhytoNexus

01 Identity and provenance

Accepted binomial: Acorus calamus
Common names: Vacha
Family (APG IV): Acoraceae
Part used: Rhizome
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): EMA/HMPC position on beta-asarone | Chamorro G / PMC4335289 (infant hepatotoxicity) | 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. | COMPOSITION

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Phenylpropanoids	beta-Asarone Rhizome	No therapeutic analogue. beta-Asarone is a phenylpropanoid structurally related to safrole and estragole - the same genotoxic-carcinogen class.

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 use (Vacha) for cognition, epilepsy and digestive complaint. REGULATORY POSITION CONFLICTS WITH TRADITIONAL USE - see side effects.
Reported adverse effects: beta-ASARONE IS GENOTOXIC AND CARCINOGENIC IN RODENTS. Because a genotoxic mechanism is assumed, NO acceptable daily intake can be derived. The US FDA bans calamus oil and A. calamus preparations from food entirely; the EU prohibits beta-asarone as a flavouring; EMA set a temporary exposure limit of approx. 2 micrograms/kg body weight/day from herbal products. beta-Asarone content is chemotype- and ploidy-dependent and Indian material is generally high - SOURCE AND ASSAY THE CHEMOTYPE, do not assume. Also reported: hepatotoxicity, cardiotoxicity, reproductive toxicity; prolonged vomiting in human consumers.

04 Interaction matrix

Source column, verbatim: THEORETICAL: sedative and CNS-active drugs. Case of hepatotoxicity in a 3-month-old infant linked to a paediatric herbal product with high beta-asarone content - avoid entirely in infants.
Normalised onto 1 canonical drug class below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Sedatives, hypnotics and benzodiazepines CNS	3Major	PD-additive	curated A	Excess sedation, psychomotor and driving impairment, falls, respiratory d…	why ▾
Class mechanism. Valepotriate, kavalactone, apigenin, sesquiterpene and alkaloid constituents act at GABA-A, adenosine and histamine sites, summating with prescribed CNS depression. Some also inhibit CYP3A4 and raise benzodiazepine exposure. Expected Excess sedation, psychomotor and driving impairment, falls, respiratory depression when combined with opioids. Management Warn against driving and machine operation. Avoid triple combinations with opioids. Reduce hypnotic dose in older adults. Onset rapid Evidence A - human data with a cited source Matched on “sedative” 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
Anticoagulants (vitamin-K antagonists, DOACs) Haemostasis	3Major	PD-additive + PK-CYP2C9	predicted D	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 D - in silico rule prediction only Find evidence for this pair Map this mechanism
Antiepileptics CNS	3Major	PK-CYP induction + PD-antagonistic	predicted D	Breakthrough seizures, status epilepticus, or additive sedation and ataxi…	why ▾
Chemistry of this pair. Volatile monoterpenes are GABA-A antagonists at higher exposure, lowering seizure threshold, and are metabolised to reactive intermediates. Class mechanism. Enzyme-inducing botanicals lower plasma anticonvulsant concentrations, while GABAergic constituents add sedation and a few (thujone, camphor, beta-asarone, pinene-rich oils) are directly proconvulsant and lower seizure threshold. Expected Breakthrough seizures, status epilepticus, or additive sedation and ataxia. Management Measure anticonvulsant levels before and 2-4 weeks after any change. Avoid proconvulsant essential oils entirely in epilepsy. Onset delayed 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
Hepatotoxic drugs Organ toxicity	3Major	Organ-toxicity additive	predicted D	Transaminase elevation, cholestasis, sinusoidal obstruction syndrome, acu…	why ▾
Chemistry of this pair. Volatile monoterpenes are GABA-A antagonists at higher exposure, lowering seizure threshold, and are metabolised to reactive intermediates. 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
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	3Major	PD-additive local	predicted D	Contact dermatitis, chemical burn, photoirritation, unexpected systemic a…	why ▾
Chemistry of this pair. Volatile monoterpenes are GABA-A antagonists at higher exposure, lowering seizure threshold, and are metabolised to reactive intermediates. 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

chemotype - beta-asarone content is ploidy/chemotype dependent.

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
Achillea millefolium Yarrow	Asteraceae	6	0.46
Artemisia absinthium Wormwood	Asteraceae	5	0.56
Myristica fragrans Nutmeg	Myristicaceae	5	0.56
Thymus vulgaris Thyme	Lamiaceae	5	0.63
Origanum vulgare Oregano	Lamiaceae	5	0.63
Cinnamomum cassia Cassia Cinnamon	Lauraceae	5	0.56

10 References and notes

Source column: Uebel T et al. J Appl Toxicol 2021;41:1166-79. doi:10.1002/jat.4112

Uebel T et al. J Appl Toxicol 2021

Uebel T et al. J Appl Toxicol 2021 manual

41:1166-79. doi:10.1002/jat.4112

doi:10.1002/jat.4112 manual

BibTeX for all 2 records

@article{UebelTeta2021,
  title = {Uebel T et al. J Appl Toxicol 2021},
  author = {Uebel T et al.},
  journal = {J Appl Toxicol},
  year = {2021},
}

@article{anon,
  title = {41:1166-79. doi:10.1002/jat.4112},
  doi = {10.1002/jat.4112},
}

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