Uncaria tomentosa · PhytoNexus

01 Identity and provenance

Accepted binomial: Uncaria tomentosa
Common names: Cat's Claw
Family (APG IV): Rubiaceae
Part used: Bark
Verification tier: Tier 2 · Verified Clinical columns reviewed and a source is on record.
Reviewer note (2026 audit): MDPI Appl Sci 2020;10:2668 (review of constituents and interactions) | CAM-Cancer monograph, Cat’s claw | protease inhibitor case report | 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. | INTERACTION

02 Constituent chemistry

Chemical class	Marker compound	Synthetic analogue in use
Oxindole alkaloids	Mitraphylline Bark	No direct analogue. Oxindole alkaloids (mitraphylline, rhynchophylline) and quinovic acid glycosides; immunomodulatory rather than replacement therapy.

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: Traditional Amazonian use for arthritis, inflammation, gastric ulcer and infection. Despite positive preclinical data there are NO clinical trials of cat’s claw as a direct anticancer agent, and evidence for other outcomes is insufficient.
Reported adverse effects: Generally well tolerated at traditional doses. Risk profile is dominated by interactions rather than intrinsic toxicity.

04 Interaction matrix

Source column, verbatim: CLINICAL: a case report describes RAISED BLOOD LEVELS OF HIV PROTEASE INHIBITORS (atazanavir, ritonavir, saquinavir), attributed to CYP3A4 inhibition - a real human signal in a narrow-therapeutic-index setting. CONTRAINDICATED with immunosuppressants (ciclosporin, tacrolimus, azathioprine, mycophenolate, corticosteroids) and after organ transplant, on immunostimulant grounds. Bleeding risk with anticoagulants, antiplatelets and NSAIDs via rhynchophylline inhibition of platelet aggregation - stop before surgery. May lower blood pressure: caution with antihypertensives. DIRECTION OF CYP EFFECT IS DISPUTED: some work shows CYP3A4 INHIBITION, other work suggests PXR-mediated CYP3A4 INDUCTION, and one in-vitro study found only about 40% inhibition at high concentration. Treat as an interaction risk of uncertain direction rather than a settled inhibitor.
Normalised onto 7 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
Antivirals and antiretrovirals Infection	4Contraindicated	PK-CYP3A4/P-gp induction	curated A	Virological breakthrough and selection of resistant virus - a permanent l…	why ▾
Class mechanism. Protease inhibitors, NNRTIs and direct-acting antivirals are CYP3A4 and P-glycoprotein substrates with steep concentration-effect relationships. Botanical induction produces sustained subtherapeutic exposure. Expected Virological breakthrough and selection of resistant virus - a permanent loss of treatment options. Management Absolute contraindication with antiretroviral therapy. Ask about supplements at every viral-load review. Onset delayed Evidence A - human data with a cited source Matched on “protease inhibitors” Find evidence for this pair Map this mechanism
Immunosuppressants (ciclosporin, tacrolimus, mycophenolate) Transplant	4Contraindicated	PK-CYP3A4/P-gp + PD-antagonistic	curated A	Acute graft rejection with inducers; nephrotoxicity, neurotoxicity and hy…	why ▾
Class mechanism. These are narrow-therapeutic-index CYP3A4 and P-glycoprotein substrates. Botanical induction collapses trough levels; inhibition causes toxic accumulation. Immunostimulant botanicals separately oppose the therapeutic goal. Expected Acute graft rejection with inducers; nephrotoxicity, neurotoxicity and hypertension with inhibitors; autoimmune flare with immunostimulants. Management Treat as contraindicated in transplant recipients. Any exposure requires immediate trough level measurement and transplant team notification. Onset unspecified Evidence A - human data with a cited source Matched on “immunosuppressants” 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 “antiplatelets” Find evidence for this pair Map this mechanism
Corticosteroids Endocrine	3Major	PD-additive + PK-CYP3A4	curated A	Pseudohyperaldosteronism: hypertension, hypokalaemia, oedema, myopathy; C…	why ▾
Class mechanism. Glycyrrhizin inhibits 11-beta-hydroxysteroid dehydrogenase type 2 and prolongs cortisol half-life, potentiating mineralocorticoid effect. Anthraquinone laxatives compound steroid-driven potassium loss, and CYP3A4 inhibition raises systemic corticosteroid exposure. Expected Pseudohyperaldosteronism: hypertension, hypokalaemia, oedema, myopathy; Cushingoid features at unchanged steroid dose. Management Restrict licorice-containing products. Check potassium and blood pressure. Reduce steroid dose if features of excess appear. Onset rapid Evidence A - human data with a cited source Matched on “corticosteroids” Find evidence for this pair Map this mechanism
NSAIDs Analgesia	3Major	PD-additive	curated A	Peptic ulceration, upper GI bleeding, acute kidney injury in volume-deple…	why ▾
Class mechanism. Salicylate-, coumarin- and eugenol-bearing botanicals add both antiplatelet activity and direct gastric mucosal irritation to cyclo-oxygenase inhibition; several also reduce renal prostaglandin-dependent perfusion. Expected Peptic ulceration, upper GI bleeding, acute kidney injury in volume-depleted patients. Management Avoid in ulcer history. Add gastroprotection where the combination is unavoidable, and monitor renal function in the elderly. Onset rapid Evidence A - human data with a cited source Matched on “nsaids” 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

direction disputed - CYP3A4 inhibition vs PXR-mediated induction

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
Vinca minor Lesser Periwinkle	Apocynaceae	8	0.67
Hypericum perforatum St. John's Wort	Hypericaceae	6	0.35
Rauvolfia serpentina Sarpagandha	Apocynaceae	6	0.50
Catharanthus roseus Periwinkle	Apocynaceae	6	0.50
Rubia cordifolia Manjistha	Rubiaceae	7	0.44
Alstonia scholaris Saptaparna	Apocynaceae	6	0.50

10 References and notes

Source column: PMC6337116 (in-vitro herb-drug interaction assessment)

PMC6337116 (in-vitro herb-drug interaction assessment)

manual

BibTeX for all 1 records

@article{anon,
  title = {PMC6337116 (in-vitro herb-drug interaction assessment)},
}

Curator notes

No notes yet.

Sign in to add notes and save monographs.