Aesculus hippocastanum

01 Identity and provenance

Accepted binomial: Aesculus hippocastanum
Common names: Horse Chestnut
Family (APG IV): Sapindaceae
Part used: Seed
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): Diehm C et al. Lancet 1996;347:292-4 | VERIFIED 2026 - synthetic analogue, application, interactions, side effects and references populated from retrieved primary/regulatory sources (see References). Interaction entries are labelled CLINICAL (case reports or trials in humans) vs THEORETICAL (in-vitro or animal only). Marketed-formulation column intentionally left blank. | INTERACTION

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Triterpenoid saponins	Escin Seed	Diosmin/Hesperidin, Oxerutins (FUNCTIONAL venotonic). No structural analogue.

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: Chronic venous insufficiency - reduces lower-leg volume, calf and ankle circumference, leg pain, pruritus and calf spasm. Cochrane-reviewed. One RCT found it equivalent to compression stockings for oedema. Also used for haemorrhoids.
Reported adverse effects: Generally mild - pruritus, nausea, headache, dizziness, gastrointestinal upset. Escin has strong haemolytic activity in vitro. Insufficient safety data in pregnancy. Raw seed is unsafe to eat.

04 Interaction matrix

Source column, verbatim: CLINICAL: escin impairs platelet function - caution with anticoagulants and antiplatelets and in bleeding disorders. (Note: flower extracts showed only negligible anticoagulant effect; the caution applies to seed extract.)
Normalised onto 2 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. 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 A - human data with a cited source Matched on “anticoagulants” Find evidence for this pair Map this mechanism
Antiplatelet agents Haemostasis	3Major	PD-additive	curated A	Prolonged bleeding time, surgical and post-procedural bleeding, bruising,…	why ▾
Chemistry of this pair. Triterpene and steroidal saponins alter membrane permeability, inhibit platelet aggregation and show weak steroid-receptor affinity. 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 A - human data with a cited source Matched on “antiplatelets” 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
Antidiabetic drugs (insulin, sulfonylureas, biguanides, GLP-1, SGLT2) Endocrine	3Major	PD-additive	predicted D	Symptomatic hypoglycaemia, sweating, tremor, confusion; severe events rep…	why ▾
Chemistry of this pair. Triterpene and steroidal saponins alter membrane permeability, inhibit platelet aggregation and show weak steroid-receptor affinity. 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. Expected Symptomatic hypoglycaemia, sweating, tremor, confusion; severe events reported with insulin and sulfonylureas. Management Increase self-monitoring frequency for 2 weeks after starting or stopping. Anticipate a downward dose adjustment of insulin or sulfonylurea. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
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. Triterpene and steroidal saponins alter membrane permeability, inhibit platelet aggregation and show weak steroid-receptor affinity. 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. Expected Breakthrough bleeding and contraceptive failure; unpredictable effect in hormone-sensitive malignancy. Management Advise a second, non-hormonal contraceptive method. Avoid phyto-oestrogens in oestrogen-receptor-positive breast cancer without oncology advice. Onset delayed Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism

05 Hazard register

additive - antiplatelet action of escin.

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
Panax ginseng Ginseng	Araliaceae	4	0.40
Panax quinquefolius American Ginseng	Araliaceae	4	0.67
Silybum marianum Milk Thistle	Asteraceae	4	0.50
Chlorophytum borivilianum Safed Musli	Asparagaceae	4	0.57
Phyllanthus amarus Bhui Amla	Phyllanthaceae	4	0.33
Serenoa repens Saw Palmetto	Arecaceae	3	0.75

10 References and notes

Source column: Pittler MH & Ernst E. Cochrane Database Syst Rev 2012;11:CD003230. doi:10.1002/14651858.CD003230.pub4

Pittler MH & Ernst E. Cochrane Database Syst Rev 2012

Systematic review / meta-analysis Pittler MH 2012 manual

11:CD003230. doi:10.1002/14651858.CD003230.pub4

doi:10.1002/14651858.CD003230.pub4 manual

BibTeX for all 2 records

@article{PittlerMH2012,
  title = {Pittler MH & Ernst E. Cochrane Database Syst Rev 2012},
  author = {Pittler MH},
  year = {2012},
}

@article{anon,
  title = {11:CD003230. doi:10.1002/14651858.CD003230.pub4},
  doi = {10.1002/14651858.CD003230.pub4},
}

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