01 Identity and provenance
- Accepted binomial
- Saraca asoca
- Common names
- Ashoka
- Family (APG IV)
- Fabaceae
- Part used
- Bark
- Verification tier
- Tier 2 · Unverified Clinical columns are populated but no primary reference was supplied. Treat the interaction list as a hypothesis to be checked against literature.
02 Constituent chemistry
| Chemical class | Marker compound | Synthetic analogue in use |
|---|---|---|
| Tannins | catechin, epicatechin
Bark
|
Tranexamic acid |
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.
03 Stated application
- Reported activity
- menstrual disorders, dysmenorrhea, uterine tonic
- Marketed in
- Dabur - Ashokarishta syrup, Himalaya wellness - tablets
- Reported adverse effects
- nausea, stomach upset, allergic reaction
04 Interaction matrix
Source column, verbatim: anti coagulant, anti platelets, hormonal therapy
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 ▾ |
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.
| |||||
|
Antiplatelet agents
Haemostasis
|
3Major | PD-additive | curated A | 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.
| |||||
|
Hormonal therapy, oral contraceptives and HRT
Endocrine
|
3Major | PK-CYP3A4 induction + PD-oestrogenic | curated A | Breakthrough bleeding and contraceptive failure; unpredictable effect in … | why ▾ |
Class mechanism. CYP3A4-inducing botanicals accelerate ethinylestradiol and progestin clearance. Separately, isoflavone, lignan and coumestan phyto-oestrogens bind oestrogen receptors and may add to or compete with prescribed hormones.
| |||||
Predicted from constituent chemistry
| 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. 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.
| |||||
|
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. 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.
| |||||
|
Antacids, PPIs and H2 blockers
Gastrointestinal
|
2Moderate | PK-absorption | predicted D | Reduced or erratic absorption of alkaloids; heartburn and reflux from pre… | why ▾ |
Chemistry of this pair. Polyphenolic tannins precipitate proteins and chelate di- and trivalent cations in the gut lumen. 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.
| |||||
|
Antibacterials and anthelmintics
Infection
|
2Moderate | PK-chelation + PK-CYP | predicted D | Treatment failure from subtherapeutic antibiotic concentrations, or raise… | why ▾ |
Chemistry of this pair. Polyphenolic tannins precipitate proteins and chelate di- and trivalent cations in the gut lumen. 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.
| |||||
|
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. Polyphenolic tannins precipitate proteins and chelate di- and trivalent cations in the gut lumen. 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.
| |||||
|
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.
| |||||
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.
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.
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 | Weight | Jaccard |
|---|---|---|---|---|
| Phyllanthus amarus
Bhui Amla |
Phyllanthaceae | 9 | 0.75 | |
| Vaccinium myrtillus
Bilberry |
Ericaceae | 8 | 0.80 | |
| Silybum marianum
Milk Thistle |
Asteraceae | 6 | 0.55 | |
| Ficus religiosa
Peepal |
Moraceae | 7 | 0.78 | |
| Senegalia catechu
Katha |
Fabaceae | 7 | 0.78 | |
| Psidium guajava
Guava |
Myrtaceae | 7 | 0.78 |
10 References and notes
Source column: Ayurvedic Pharmacopoeia of India; PubMed
Ayurvedic Pharmacopoeia of India
PubMed
BibTeX for all 2 records
@article{anon,
title = {Ayurvedic Pharmacopoeia of India},
}
@article{anon,
title = {PubMed},
}
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