Camptotheca acuminata

01 Identity and provenance

Accepted binomial: Camptotheca acuminata
Common names: Happy Tree
Family (APG IV): Nyssaceae
Part used: Bark, Seed
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): PMC12114900 (UGT1A1 genotype and MTD, systematic review) | NCBI Medical Genetics Summaries NBK294473 (Irinotecan and UGT1A1) | Nature J Hum Genet 2013 (UGT1A1*6 in Japanese patients) | VERIFIED 2026 (batch 5) - synthetic analogue, application, interactions, side effects and references populated from retrieved primary/regulatory sources. Interactions labelled CLINICAL vs THEORETICAL. Marketed-formulation column intentionally blank. | HOST FACTOR

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Quinoline alkaloids	Camptothecin Bark, Seed	Irinotecan (CPT-11) and topotecan - semi-synthetic camptothecin analogues. Also sacituzumab govitecan (antibody-drug conjugate delivering SN-38).

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: Source of camptothecin, the parent topoisomerase I inhibitor. THE PARENT COMPOUND FAILED: camptothecin itself was WITHDRAWN from clinical trials for poor aqueous solubility and severe unpredictable toxicity. Irinotecan and topotecan - built by adding basic side chains to solve solubility - were approved in the 1990s and remain in use for colorectal, pancreatic, gastro-oesophageal, ovarian and small-cell lung cancer. A clear case where the plant molecule is NOT the drug.
Reported adverse effects: Dose-limiting: severe delayed diarrhoea (SN-38 excreted into bile then colon) and myelosuppression, especially neutropenia. Topotecan is chiefly haematologically toxic.

04 Interaction matrix

Source column, verbatim: PHARMACOGENOMIC, AND FORMALLY LABELLED. Irinotecan is a prodrug hydrolysed to SN-38, which is inactivated by UGT1A1 glucuronidation. UGT1A1*28 and UGT1A1*6 alleles reduce enzyme activity: homozygous *28 carriers had a 9.3-fold higher risk of grade 4 neutropenia. In one Japanese gynaecological-cancer series, *6 homozygosity or *6/*28 compound heterozygosity carried odds ratios of 16.0 and 31.3 for severe neutropenia or diarrhoea. FDA labels and EMA assessment reports recommend genotype-based dose reduction, though only for poor metabolisers, and dosing guidelines still lack consensus. NOTE: UGT1A1*6 is more prevalent in East Asian populations than *28 - genotyping panels validated on European cohorts may miss it.
Normalised onto 1 canonical drug class below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Cytotoxic and targeted anticancer drugs Oncology	4Contraindicated	PK-CYP3A4/UGT + PD-antagonistic	curated A	Neutropenic sepsis and severe diarrhoea from over-exposure, or reduced an…	why ▾
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 A - human data with a cited source Matched on “irinotecan” 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. Alkaloidal bases have pH-dependent absorption and commonly interact with hepatic CYP isoenzymes and efflux transporters. 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
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. Alkaloidal bases have pH-dependent absorption and commonly interact with hepatic CYP isoenzymes and efflux transporters. 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

05 Hazard register

pharmacogenomic - UGT1A1*28/*6 determine irinotecan toxicity; *6

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
Piper longum Long Pepper	Piperaceae	3	0.50
Rauvolfia serpentina Sarpagandha	Apocynaceae	3	0.50
Colchicum autumnale Autumn Crocus	Colchicaceae	3	0.60
Gloriosa superba Glory Lily	Colchicaceae	3	0.75
Lobelia inflata Indian Tobacco	Campanulaceae	3	0.75
Conium maculatum Hemlock	Apiaceae	3	0.75

10 References and notes

Source column: Innocenti F et al. J Clin Oncol 2004

Innocenti F et al. J Clin Oncol 2004

Innocenti F et al. J Clin Oncol 2004 manual

BibTeX for all 1 records

@article{InnocentiF2004,
  title = {Innocenti F et al. J Clin Oncol 2004},
  author = {Innocenti F et al.},
  journal = {J Clin Oncol},
  year = {2004},
}

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