Vinca minor · PhytoNexus

01 Identity and provenance

Accepted binomial: Vinca minor
Common names: Lesser Periwinkle
Family (APG IV): Apocynaceae
Part used: Herb
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): PMC9161525 (colchicine and Vinca alkaloid review, distinguishes vincamine from vincristine) | ScienceDirect, Vinca minor / vinpocetine | 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. | IDENTITY

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Indole alkaloids	Vincamine Herb	Vinpocetine - a semi-synthetic derivative of vincamine, used in Hungary, Germany, Poland and Japan for cerebrovascular disease and sold in the USA as a nootropic supplement.

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 vincamine, a cerebral vasodilator studied for cerebrovascular insufficiency and cognitive decline. Evidence for the nootropic claim is limited.
Reported adverse effects: NOMENCLATURE HAZARD - THE MAIN REASON THIS ENTRY MATTERS. Vinca minor (lesser periwinkle) yields VINCAMINE, a vasodilator. Catharanthus roseus (Madagascar periwinkle, entry 44) - formerly named Vinca rosea, and still loosely called "periwinkle" - yields VINCRISTINE and VINBLASTINE, cytotoxic antimitotics with dose-limiting neurotoxicity, SIADH and fatal outcomes if given intrathecally. TWO GENERA, ONE COMMON NAME, AND DRUGS THAT ARE NOT INTERCHANGEABLE IN ANY RESPECT. The obsolete synonym Vinca rosea appears throughout older literature and patents, so a literature search on "Vinca" will return both. Any database or search pipeline keyed on common name or genus alone will conflate them.

04 Interaction matrix

Source column, verbatim: THEORETICAL: additive with antihypertensives and anticoagulants (vinpocetine has reported antiplatelet activity). Not well characterised clinically.
Normalised onto 3 canonical drug classes below.

Curated from the reviewed source

Drug class	Severity	Mechanism type	Provenance	Expected effect
Antihypertensives Cardiovascular	4Contraindicated	PD-additive	curated A	Orthostatic hypotension, dizziness, syncope and falls; or loss of blood-p…	why ▾
Chemistry of this pair. Indole and beta-carboline alkaloids act on monoamine storage, reuptake and oxidation, and several are tubulin poisons. 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. Expected Orthostatic hypotension, dizziness, syncope and falls; or loss of blood-pressure control with pressor botanicals. Management Home BP log for 2 weeks after any change. Warn about postural symptoms; review in the elderly and in those on multiple agents. Onset rapid Evidence A - human data with a cited source Matched on “antihypertensives” Find evidence for this pair Map this mechanism
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 ▾
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 “antiplatelet” 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
Antidepressants (SSRI, SNRI, TCA) CNS	4Contraindicated	PD-additive serotonergic + PK-CYP2D6	predicted D	Serotonin syndrome (agitation, clonus, hyperthermia, autonomic instabilit…	why ▾
Chemistry of this pair. Indole and beta-carboline alkaloids act on monoamine storage, reuptake and oxidation, and several are tubulin poisons. Class mechanism. Hypericin- and hyperforin-type constituents inhibit monoamine reuptake and induce CYP3A4/2C19 and P-glycoprotein; others inhibit CYP2D6, raising tricyclic and SSRI concentrations. Expected Serotonin syndrome (agitation, clonus, hyperthermia, autonomic instability) or loss of antidepressant effect on withdrawal of an inducer. Management Screen for serotonergic burden before adding. Taper rather than stop abruptly. Consider therapeutic drug monitoring for tricyclics. Onset rapid Evidence D - in silico rule prediction only Find evidence for this pair Map this mechanism
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. Indole and beta-carboline alkaloids act on monoamine storage, reuptake and oxidation, and several are tubulin poisons. 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
Monoamine oxidase inhibitors CNS	4Contraindicated	PD-additive	predicted D	Hypertensive crisis, hyperpyrexia, serotonin syndrome, intracranial haemo…	why ▾
Chemistry of this pair. Indole and beta-carboline alkaloids act on monoamine storage, reuptake and oxidation, and several are tubulin poisons. Class mechanism. Beta-carboline (harmine, harmaline) and related botanical alkaloids are themselves reversible MAO-A inhibitors. Combined with a prescribed MAOI, or with tyramine-rich food or sympathomimetics, the pressor and serotonergic reserve is abolished. Expected Hypertensive crisis, hyperpyrexia, serotonin syndrome, intracranial haemorrhage. Management Absolute contraindication. Apply the full MAOI dietary and drug restriction list to the botanical as well. Onset rapid 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. 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

nomenclature - "periwinkle" and the synonym Vinca rosea conflate

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.

Catharanthus roseus

Periwinkle

Apocynaceae

Shares the common name "periwinkle"

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
Uncaria tomentosa Cat's Claw	Rubiaceae	8	0.67
Rauvolfia serpentina Sarpagandha	Apocynaceae	6	0.75
Catharanthus roseus Periwinkle	Apocynaceae	6	0.75
Alstonia scholaris Saptaparna	Apocynaceae	6	0.75
Physostigma venenosum Calabar Bean	Fabaceae	6	0.60
Peganum harmala Syrian Rue	Nitrariaceae	6	0.60

10 References and notes

Source column: StatPearls NBK557842 (Vinca alkaloid toxicity)

StatPearls NBK557842 (Vinca alkaloid toxicity)

manual

BibTeX for all 1 records

@article{anon,
  title = {StatPearls NBK557842 (Vinca alkaloid toxicity)},
}

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