01 Identity and provenance
- Accepted binomial
- Phyllanthus amarus
- Common names
- Bhui Amla
- Family (APG IV)
- Phyllanthaceae
- Part used
- Whole plant
- Verification tier
- Tier 2 · Verified Clinical columns reviewed and a source is on record.
- Reviewer note (2026 audit)
- CORRECTED - F:M: Chemical class cell duplicated the plant part; every field from composition onward sat one column right of its header
Reference not supplied - claim unverified against primary literature.
02 Constituent chemistry
| Chemical class | Marker compound | Synthetic analogue in use |
|---|---|---|
| Phyllanthin, Hypophyllanthin, Lignans, Flavonoids, Tannins | Phyllanthin
Whole plant
|
Silymarin (similar hepatoprotective activity) |
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
- Hepatoprotective (liver protector)
- Marketed in
- Liv.52, Bhumyamalaki Churna/Capsules
- Reported adverse effects
- Mild stomach upset, Diarrhea, Dizziness
04 Interaction matrix
Source column, verbatim: Antidiabetic drugs, Antihypertensive drugs, Anticoagulants
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 B | 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.
| |||||
|
Antidiabetic drugs (insulin, sulfonylureas, biguanides, GLP-1, SGLT2)
Endocrine
|
3Major | PD-additive | curated B | Symptomatic hypoglycaemia, sweating, tremor, confusion; severe events rep… | why ▾ |
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.
| |||||
|
Antihypertensives
Cardiovascular
|
2Moderate | PD-additive | curated B | Orthostatic hypotension, dizziness, syncope and falls; or loss of blood-p… | why ▾ |
Class mechanism. Vasodilator, diuretic, ACE-inhibitory and calcium-antagonist activity in botanical extracts adds to prescribed blood-pressure lowering. A minority (ephedrine-, glycyrrhizin- and caffeine-bearing) act in the opposite direction and antagonise control.
| |||||
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. Isoflavone and lignan aglycones bind oestrogen receptor beta with measurable affinity and inhibit aromatase and sulfotransferase. 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.
| |||||
|
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.
| |||||
|
Hormonal therapy, oral contraceptives and HRT
Endocrine
|
3Major | PK-CYP3A4 induction + PD-oestrogenic | predicted D | Breakthrough bleeding and contraceptive failure; unpredictable effect in … | why ▾ |
Chemistry of this pair. Isoflavone and lignan aglycones bind oestrogen receptor beta with measurable affinity and inhibit aromatase and sulfotransferase. 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.
| |||||
|
Thyroid hormones and antithyroid drugs
Endocrine
|
3Major | PK-absorption + PD-modulation | predicted D | Iatrogenic hyper- or hypothyroidism, unexplained TSH drift, loss of euthy… | why ▾ |
Chemistry of this pair. Isoflavone and lignan aglycones bind oestrogen receptor beta with measurable affinity and inhibit aromatase and sulfotransferase. 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.
| |||||
|
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
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.
| Phyllanthus emblica
Amla |
Phyllanthaceae | Same genus (Phyllanthus) |
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 |
|---|---|---|---|---|
| Silybum marianum
Milk Thistle |
Asteraceae | 8 | 0.67 | |
| Vaccinium myrtillus
Bilberry |
Ericaceae | 9 | 0.75 | |
| Saraca asoca
Ashoka |
Fabaceae | 9 | 0.75 | |
| Camellia sinensis
Green Tea |
Theaceae | 8 | 0.53 | |
| Echinacea purpurea
Echinacea |
Asteraceae | 8 | 0.50 | |
| Vaccinium macrocarpon
Cranberry |
Ericaceae | 7 | 0.58 |
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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