01 Identity and provenance
- Accepted binomial
- Chondrodendron tomentosum
- Common names
- Curare Vine
- Family (APG IV)
- Menispermaceae
- Part used
- Stem bark
- Verification tier
- Tier 2 · Verified Clinical columns reviewed and a source is on record.
- Reviewer note (2026 audit)
- Griffith HR & Johnson GE, 1942 (first clinical use of Intocostrin) | Britannica, Chondrodendron tomentosum | 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. | ROUTE
02 Constituent chemistry
| Chemical class | Marker compound | Synthetic analogue in use |
|---|---|---|
| Bisbenzylisoquinoline alkaloids | (+)-Tubocurarine
Stem bark
|
Cisatracurium, rocuronium, vecuronium (modern non-depolarising blockers that replaced it). Tubocurarine is the prototype of the class. |
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.
03 Stated application
- Reported activity
- HISTORICAL ONLY. Source of d-tubocurarine, the first clinically used non-depolarising neuromuscular blocker (Intocostrin, 1942), which made lighter general anaesthesia possible. Now effectively obsolete - safer synthetics with faster onset and shorter duration have replaced it.
- Reported adverse effects
- Flaccid paralysis progressing to respiratory muscles. HISTAMINE RELEASE is the hallmark and the reason it was abandoned: hypotension and bronchospasm, particularly hazardous in asthma or cardiovascular disease. Slow onset (300 s or more) and long duration (60-120 min) made it hard to titrate. CRITICAL: it is a paralytic, NOT an anaesthetic or analgesic - the patient remains conscious and can feel pain, so it must never be given without adequate anaesthesia. ROUTE-DEPENDENT: tubocurarine is poorly absorbed across mucous membranes, which is why hunters could safely eat game killed with curare-tipped arrows - the mirror image of the Conium secondary-exposure route (entry 183).
04 Interaction matrix
Source column, verbatim: CLINICAL: reversed by anticholinesterases (neostigmine, and galantamine - see entry for Galanthus nivalis). Additive with aminoglycosides, magnesium and volatile anaesthetics, which potentiate blockade.
Normalised onto 3 canonical drug classes below.
Curated from the reviewed source
| Drug class | Severity | Mechanism type | Provenance | Expected effect | |
|---|---|---|---|---|---|
|
Cholinesterase inhibitors and cholinergic drugs
Autonomic
|
4Contraindicated | PD-additive | curated A | Cholinergic crisis: bradycardia, bronchorrhoea, bronchospasm, miosis, sei… | why ▾ |
Class mechanism. Physostigmine-, galantamine- and arecoline-type constituents inhibit acetylcholinesterase or agonise muscarinic receptors, adding to donepezil, rivastigmine, neostigmine or pyridostigmine.
| |||||
|
General and local anaesthetics (perioperative)
Perioperative
|
3Major | PD-additive + PK-CYP | curated A | Prolonged emergence, intraoperative haemodynamic instability, excess surg… | why ▾ |
Class mechanism. Botanical CNS depressants prolong anaesthetic recovery, antiplatelet and coumarin constituents raise surgical bleeding, and sympathomimetics destabilise intraoperative haemodynamics. CYP modulation changes opioid and muscle-relaxant handling.
| |||||
|
Nephrotoxic drugs
Organ toxicity
|
3Major | Organ-toxicity additive | curated A | Rising creatinine, tubulointerstitial nephritis, urothelial carcinoma wit… | why ▾ |
Class mechanism. Aristolochic acid, high oxalate loads and anthraquinone-driven volume depletion add to aminoglycoside, NSAID, contrast and calcineurin-inhibitor nephrotoxicity.
| |||||
Predicted from constituent chemistry
| Drug class | Severity | Mechanism type | Provenance | Expected effect | |
|---|---|---|---|---|---|
|
Immunosuppressants (ciclosporin, tacrolimus, mycophenolate)
Transplant
|
4Contraindicated | PK-CYP3A4/P-gp + PD-antagonistic | predicted D | Acute graft rejection with inducers; nephrotoxicity, neurotoxicity and hy… | why ▾ |
Chemistry of this pair. Berberine inhibits CYP3A4 and P-glycoprotein, lowers glucose through AMPK activation, and displaces bilirubin from albumin. 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.
| |||||
|
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. Berberine inhibits CYP3A4 and P-glycoprotein, lowers glucose through AMPK activation, and displaces bilirubin from albumin. 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.
| |||||
|
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. Berberine inhibits CYP3A4 and P-glycoprotein, lowers glucose through AMPK activation, and displaces bilirubin from albumin. 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.
| |||||
|
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.
| |||||
05 Hazard register
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.
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.
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 | Weight | Jaccard |
|---|---|---|---|---|
| Tinospora cordifolia
Giloy |
Menispermaceae | 4 | 0.57 | |
| Chelidonium majus
Greater Celandine |
Papaveraceae | 4 | 0.50 | |
| Berberis vulgaris
Barberry |
Berberidaceae | 4 | 0.57 | |
| Coptis chinensis
Chinese Goldthread |
Ranunculaceae | 4 | 0.57 | |
| Stephania tetrandra
Han Fang Ji |
Menispermaceae | 4 | 0.57 | |
| Corydalis yanhusuo
Yan Hu Suo |
Papaveraceae | 4 | 0.57 |
10 References and notes
Source column: Bowman WC. Br J Pharmacol 2006;147:S277-86 (neuromuscular block, historical review)
147:S277-86 (neuromuscular block, historical review)
Bowman WC. Br J Pharmacol 2006
BibTeX for all 2 records
@article{anon,
title = {147:S277-86 (neuromuscular block, historical review)},
}
@article{BowmanWC2006,
title = {Bowman WC. Br J Pharmacol 2006},
author = {Bowman WC},
year = {2006},
}
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