Ficus religiosa · PhytoNexus

01 Identity and provenance

Accepted binomial: Ficus religiosa
Common names: Peepal
Family (APG IV): Moraceae
Part used: Bark
Verification tier: Tier 1 · chemistry only Taxonomy, plant part and marker chemistry are populated and stable. The clinical columns are deliberately empty because no primary source has been retrieved for them yet. Interactions shown below are rule predictions from the constituent chemistry, not clinical findings.
Reviewer note (2026 audit): TIER 1 populated (name, family, part, constituent class, marker) - stable taxonomic/phytochemical facts. TIER 2 columns (analogue, application, brand, interactions, side effects) left blank BY DESIGN - populate only from retrieved primary literature. Do not use clinically until Tier 2 is filled and a reference is recorded.

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Alkaloids	PENDING VERIFICATION Bark	none listed

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

Left empty by design — this is a Tier 1 entry, and the clinical columns are only populated once a primary source has been retrieved for them.

04 Interaction matrix

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. 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. 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
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. 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. 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. 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
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. Expected Reduced or erratic absorption of alkaloids; heartburn and reflux from premature release of volatile-oil preparations. Management Separate administration by 2 hours. Avoid non-enteric peppermint oil in reflux disease. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
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. Expected Treatment failure from subtherapeutic antibiotic concentrations, or raised toxicity of azoles and macrolides. Management Separate doses by 2-3 hours. Do not rely on botanical antimicrobials in place of an indicated antibiotic. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
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. 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 D - in silico rule prediction only Find evidence for this pair Map this mechanism
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. Expected Myalgia, raised creatine kinase, rhabdomyolysis, hepatic transaminase elevation. Management Ask specifically about red-yeast-rice type products. Check CK and ALT if muscle symptoms appear; prefer a non-3A4 statin. Onset unspecified Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism

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.

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	7	0.58
Vaccinium myrtillus Bilberry	Ericaceae	7	0.78
Saraca asoca Ashoka	Fabaceae	7	0.78
Phyllanthus amarus Bhui Amla	Phyllanthaceae	7	0.58
Senegalia catechu Katha	Fabaceae	7	1.00
Psidium guajava Guava	Myrtaceae	7	1.00

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.

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