Allocryptopine

Allocryptopine at a Glance

Allocryptopine, usually written α-allocryptopine, is a protopine-type isoquinoline alkaloid found in California poppy, greater celandine, plume poppy (Macleaya cordata) and other members of the poppy (Papaveraceae) and fumitory families. It is a close structural relative of protopine — the two are the defining members of the small “protopine-type” subgroup, sharing an unusual ten-membered nitrogen-containing ring — and the two almost always occur together in the same plants.

Its distinctive research signal is cardiac. Isolated allocryptopine blocks several of the ion currents that shape the heartbeat — the hERG (rapid delayed-rectifier) potassium current, the transient outward and slow delayed-rectifier potassium currents, the cardiac sodium current and the L-type calcium current — and in animal models this multi-channel action produces an antiarrhythmic effect ^{1,2,3,4,5Reference 1Li Y et al. · 2008Effect of alpha-allocryptopine on transient outward potassium current in rabbit ventricular myocytesView study →Reference 2Fu YC et al. · 2016Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardiumView study →Reference 3Lin K et al. · 2013Allocryptopine and benzyltetrahydropalmatine block hERG potassium channels expressed in HEK293 cellsView study →Reference 4Xu B et al. · 2015AnimalEffect of α-allocryptopine on delayed afterdepolarizations and triggered activities in mice cardiomyocytes treated with isoproterenolView study →Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →}. That pharmacology is genuine but entirely preclinical: every study to date is in isolated channels, cardiac myocytes or whole-animal hearts, with no human trials.

The other firmly established fact about this molecule is a drug-interaction one: allocryptopine is a potent inhibitor of several drug-metabolising cytochrome-P450 enzymes ^{6Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →}. That, together with its own ion-channel activity, is the reason it carries a moderate safety flag rather than being treated as an inert minor constituent.

Allocryptopine & Cardiac Ion Channels

This is the section only allocryptopine needs, and the reason it has its own research literature. The compound is a broad-spectrum cardiac ion-channel blocker, and the combination of currents it touches is what gives it an antiarrhythmic — but also potentially proarrhythmic — profile.

Potassium currents (repolarisation).

• hERG / IKr — allocryptopine reversibly suppresses the rapid delayed-rectifier current carried by hERG channels in a concentration- and voltage-dependent way, with an IC50 of ~49.7 µmol/L; unusually for a hERG blocker it does not shift the channel’s steady-state inactivation ^{3Reference 3Lin K et al. · 2013Allocryptopine and benzyltetrahydropalmatine block hERG potassium channels expressed in HEK293 cellsView study →}. Blocking IKr is the classic mechanism of Class III antiarrhythmics — and also the mechanism behind drug-induced QT prolongation.
• Ito (transient outward K+) — it blocks Ito in rabbit ventricular myocytes with an IC50 of ~37 µmol/L in a frequency-independent manner, and — importantly — flattens the transmural gradient of Ito across the ventricular wall (reducing dispersion from ~11.2 to ~4.7 pA/pF) ^{1Reference 1Li Y et al. · 2008Effect of alpha-allocryptopine on transient outward potassium current in rabbit ventricular myocytesView study →}. A later study put the Ito IC50 lower still (~18.6 µmol/L) and showed the block reaches all three myocardial layers ^{2Reference 2Fu YC et al. · 2016Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardiumView study →}.
• IKs (slow delayed rectifier K+) — blocked with an IC50 of ~28.8 µmol/L, with slowed channel deactivation ^{2Reference 2Fu YC et al. · 2016Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardiumView study →}.

Depolarising currents (excitation and triggered activity).

• Cardiac sodium current (Nav1.5) — inhibited in HEK-293 cells expressing the channel, a Class I-like action ^{5Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →}.
• L-type calcium current (ICa,L) — blocked with an IC50 of ~16.1 µmol/L; in isoproterenol-stressed mouse myocytes allocryptopine markedly reduced the transient inward current (Iti) and suppressed delayed- and early-afterdepolarisation-related triggered activity ^{4Reference 4Xu B et al. · 2015AnimalEffect of α-allocryptopine on delayed afterdepolarizations and triggered activities in mice cardiomyocytes treated with isoproterenolView study →}.

The net effect. Across rabbit and mouse hearts, allocryptopine prolongs the action-potential duration but reduces the transmural dispersion of repolarisation ^{1,2Reference 1Li Y et al. · 2008Effect of alpha-allocryptopine on transient outward potassium current in rabbit ventricular myocytesView study →Reference 2Fu YC et al. · 2016Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardiumView study →} — it lengthens repolarisation while making it more uniform across the ventricular wall, and it damps the calcium-driven afterdepolarisations that trigger ectopic beats ^{4Reference 4Xu B et al. · 2015AnimalEffect of α-allocryptopine on delayed afterdepolarizations and triggered activities in mice cardiomyocytes treated with isoproterenolView study →}. Reduced dispersion is anti-arrhythmic; a review of the compound frames it as a multi-channel agent that lowers repolarisation heterogeneity rather than hitting a single target ^{5Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →}.

The double-edged caveat is intrinsic to the mechanism: potent hERG block and marked APD prolongation are exactly the properties that, in the wrong context, cause torsadogenic arrhythmia. The review is explicit that toxicology, pharmacokinetics and any clinical efficacy in arrhythmia patients remain uncharacterised ^{5Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →}.

Allocryptopine vs. Protopine

Allocryptopine is best understood as one half of a protopine-type pair with protopine, and the pair is a useful frame because the two travel together and behave similarly.

What they share. Both are protopine-type isoquinoline alkaloids built on the same ten-membered-ring skeleton with an N-methyl group and a bridging ketone — a scaffold distinct from the flat protoberberine cation of berberine or the reduced tetrahydroprotoberberine canadine. Both co-occur as the major protopine-type alkaloids of the same plants (California poppy, greater celandine, plume poppy), both are reversible CYP2D6 inhibitors, and both show smooth-muscle and cardiovascular activity in the laboratory ^{4,6Reference 4Xu B et al. · 2015AnimalEffect of α-allocryptopine on delayed afterdepolarizations and triggered activities in mice cardiomyocytes treated with isoproterenolView study →Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →}.

Where they differ. The structural distinction is in the aromatic substituents — protopine carries two methylenedioxy bridges, whereas allocryptopine has one methylenedioxy ring and two separate methoxy groups. Functionally, the cardiac ion-channel work is concentrated on allocryptopine, which is the more-studied antiarrhythmic of the two; and at the drug-metabolising enzymes the two diverge in strength — allocryptopine is a time-dependent (mechanism-based) inhibitor of CYP3A4, CYP2C9 and CYP2C19 as well as a reversible CYP2D6 inhibitor, a broader CYP profile than protopine’s ^{6Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →}.

The practical read: treat them as a closely-related pair with overlapping activity, not interchangeable molecules — the antiarrhythmic evidence base is specifically allocryptopine’s, and so is the wider mechanism-based CYP inhibition.

What It's Used For

Beyond the cardiac work, allocryptopine’s pharmacology is thin and almost entirely in-vitro on the isolated molecule (or, for the antimicrobial data, as one alkaloid in a plant extract). The evidence splits sharply by application.

Evidence by IndicationStrength of support · Beta

Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. Every row here is preclinical, so scores stay modest by design; the antiarrhythmic row leads only because it rests on the most (and most mechanistically detailed) studies.

01Antiarrhythmic and cardiac ion-channel modulationShaky42%Multiple isolate/animal electrophysiology studies + a dedicated review ^{1,2,3,4,5Reference 1Li Y et al. · 2008Effect of alpha-allocryptopine on transient outward potassium current in rabbit ventricular myocytesView study →Reference 2Fu YC et al. · 2016Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardiumView study →Reference 3Lin K et al. · 2013Allocryptopine and benzyltetrahydropalmatine block hERG potassium channels expressed in HEK293 cellsView study →Reference 4Xu B et al. · 2015AnimalEffect of α-allocryptopine on delayed afterdepolarizations and triggered activities in mice cardiomyocytes treated with isoproterenolView study →Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →}

02CYP inhibition and herb-drug interactionShaky34%Defined in-vitro isolate enzyme kinetics (time-dependent CYP3A4/2C9/2C19; reversible 2D6) ^{6Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →}

03Antimicrobial activityShaky24%In-vitro, as one alkaloid of M. cordata / C. majus extracts ^{8,10Reference 8Kosina P et al. · 2010Phytochemical and antimicrobial characterization of Macleaya cordata herbView study →Reference 10Gilca M et al. · 2010ReviewChelidonium majus — an integrative review: traditional knowledge versus modern findingsView study →}

04Cholinesterase inhibitionShaky18%In-vitro isolate; weak, not the most active Papaveraceae alkaloid ^{9Reference 9Siatka T et al. · 2017Cholinesterase and prolyl oligopeptidase inhibitory activities of alkaloids from Argemone platyceras (Papaveraceae)View study →}

Mechanisms

The load-bearing point is that the same multi-channel block that lowers repolarisation dispersion (anti-arrhythmic) is also, in the hERG/APD-prolongation direction, the textbook mechanism of drug-induced arrhythmia — the therapeutic-vs-toxic line depends on exposure, which is unmeasured ^{5Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →}.

Pharmacokinetics

Allocryptopine’s human pharmacokinetics are not established — a gap the antiarrhythmic review names explicitly ^{5Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →}. It is a lipophilic tertiary-amine alkaloid soluble in ethanol (hence its presence in tinctures rather than aqueous teas ^{6Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →}), which implies reasonable membrane permeability, and its close relative protopine is highly Caco-2 permeable. But no Cmax, oral bioavailability, half-life, metabolism or tissue-distribution data exist for the isolate in humans or animals. This matters directly: the ion-channel IC50 values sit in the 16–50 µmol/L range ^{1,2,3,4Reference 1Li Y et al. · 2008Effect of alpha-allocryptopine on transient outward potassium current in rabbit ventricular myocytesView study →Reference 2Fu YC et al. · 2016Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardiumView study →Reference 3Lin K et al. · 2013Allocryptopine and benzyltetrahydropalmatine block hERG potassium channels expressed in HEK293 cellsView study →Reference 4Xu B et al. · 2015AnimalEffect of α-allocryptopine on delayed afterdepolarizations and triggered activities in mice cardiomyocytes treated with isoproterenolView study →}, and without knowing what plasma or cardiac-tissue concentration a realistic dose produces, it is impossible to say whether those blocking effects are ever reached in vivo — the central unknown of the whole file.

Clinical Trials

There are no clinical trials of isolated allocryptopine for any indication. The entire evidence base is isolated-channel, cell and animal electrophysiology, plus in-vitro enzyme and antimicrobial assays.

Last checked: July 2026.

Isolate vs. Plant Studies

The split is unusually clean for a minor alkaloid. The cardiac pharmacology is all the isolate — the rabbit-myocyte Ito/IKs studies ^{1,2Reference 1Li Y et al. · 2008Effect of alpha-allocryptopine on transient outward potassium current in rabbit ventricular myocytesView study →Reference 2Fu YC et al. · 2016Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardiumView study →}, the HEK-293 hERG and Nav1.5 work ^{3,5Reference 3Lin K et al. · 2013Allocryptopine and benzyltetrahydropalmatine block hERG potassium channels expressed in HEK293 cellsView study →Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →} and the mouse ICa,L/afterdepolarisation study ^{4Reference 4Xu B et al. · 2015AnimalEffect of α-allocryptopine on delayed afterdepolarizations and triggered activities in mice cardiomyocytes treated with isoproterenolView study →} all test purified allocryptopine (much of it sourced from Corydalis decumbens), which is a genuine strength as a mechanism base. The CYP-inhibition data are also the isolate, screened as a defined compound ^{6Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →}. Only the antimicrobial claim is a plant-extract effect, where allocryptopine is one alkaloid among many and the potent activity belongs to the co-occurring benzophenanthridines ^{8,10Reference 8Kosina P et al. · 2010Phytochemical and antimicrobial characterization of Macleaya cordata herbView study →Reference 10Gilca M et al. · 2010ReviewChelidonium majus — an integrative review: traditional knowledge versus modern findingsView study →}. The honest framing: strong isolate mechanism, zero whole-plant-to-human bridge — none of the herbs that contain allocryptopine (California poppy, greater celandine) is used or studied as an antiarrhythmic, so the molecule’s laboratory cardiac profile has never been connected to a botanical outcome in people. It cuts the other way too: California poppy’s own sedative/anxiolytic reputation is attributed to other alkaloids in the fraction — (S)-reticuline’s GABAA modulation, not allocryptopine ^{7Reference 7Fedurco M et al. · 2015Modulatory effects of Eschscholzia californica alkaloids on recombinant GABAA receptorsView study →} — so allocryptopine cannot be credited with the herb’s traditional calming use either.

Prevalence in Nature

Allocryptopine occurs across the poppy (Papaveraceae) and fumitory (Fumariaceae) families, almost always alongside its partner protopine. It is a major leaf alkaloid of plume poppy (Macleaya cordata) ^{8Reference 8Kosina P et al. · 2010Phytochemical and antimicrobial characterization of Macleaya cordata herbView study →}, one of the ethanol-soluble alkaloids of California poppy (Eschscholzia californica) ^{6Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →}, a constituent of greater celandine (Chelidonium majus) ^{10Reference 10Gilca M et al. · 2010ReviewChelidonium majus — an integrative review: traditional knowledge versus modern findingsView study →}, and the isolated-material source for most of the cardiac studies is corydalis (Corydalis decumbens) ^{3,5Reference 3Lin K et al. · 2013Allocryptopine and benzyltetrahydropalmatine block hERG potassium channels expressed in HEK293 cellsView study →Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →}. It is further reported from fumitory (Fumaria), prickly poppy (Argemone), horned poppy (Glaucium) ^{11Reference 11Nigdelioglu Dolanbay S et al. · 2025Allocryptopine, tetrahydropalmatine, and tetrahydroberberine N-oxide alkaloids alleviate cellular stress by modulating calcium homeostasis and the MAPK and Akt/GSK-3β/tau signaling pathwaysView study →} and prickly-ash (Zanthoxylum/Fagara, the origin of the old synonym α-fagarine).

Absolute concentrations vary several-fold with species, plant part (roots and latex are richer than aerial parts), chemotype and season, and — for commercial California-poppy products — with preparation type; allocryptopine-specific quantitative figures are sparse, which is logged in this compound’s gaps tracker rather than guessed at here.

Discovery & Synthesis

Allocryptopine is an early-characterised member of the protopine alkaloid group (molecular formula C21H23NO5, CAS 485-91-6). Its tangle of historical synonyms — α-fagarine (from Fagara/Zanthoxylum), β-homochelidonine (from Chelidonium) and thalictrimine (from Thalictrum) — reflects its repeated independent isolation from different plants before the structures were reconciled as one compound; a single first-isolation date is not reliably established here. Biosynthetically it arises, like protopine, from the benzylisoquinoline → protoberberine pathway, where oxidative rearrangement of the protoberberine skeleton opens the characteristic protopine-type ten-membered ring.

Manufacture today is by extraction from alkaloid-rich Papaveraceae (plume poppy, corydalis, greater celandine) rather than by total synthesis — research and reference material is isolated from plant biomass, and there is no commercial synthetic route in routine use for this molecule.

Patents: not yet researched.

Toxicity & Safety

Allocryptopine carries a moderate flag — higher than an inert minor phenolic — for two specific, evidence-based reasons rather than any documented poisoning: it is a cardiac multi-channel blocker and a mechanism-based inhibitor of major CYP enzymes. Neither is a reason for alarm at ordinary herbal exposure, but both are reasons not to treat concentrated or isolated allocryptopine as harmless.

Cardiac / proarrhythmic caution. The very hERG block and action-potential prolongation that make allocryptopine antiarrhythmic in the lab are, in excess, the mechanism of QT prolongation and torsadogenic arrhythmia ^{3,5Reference 3Lin K et al. · 2013Allocryptopine and benzyltetrahydropalmatine block hERG potassium channels expressed in HEK293 cellsView study →Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →}. No safe-exposure ceiling has been defined, so isolated or high-dose allocryptopine should be regarded cautiously, particularly in anyone with QT-prolongation risk or on other QT-affecting drugs.

Herb–drug interactions. As a time-dependent inhibitor of CYP3A4/2C9/2C19 and a reversible CYP2D6 inhibitor ^{6Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →}, allocryptopine can in principle raise levels of drugs cleared by those enzymes. This is the mechanistic basis for the caution around ethanol tinctures of allocryptopine-containing herbs, which extract these alkaloids far more than aqueous teas do ^{6Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →}.

Context of exposure. In practice allocryptopine is encountered as a minor constituent of whole-plant preparations, not on its own; the reproductive, genotoxic and repeat-dose toxicology of the isolated molecule is not characterised, and pregnancy/lactation decisions belong to the herb or product page where intake is decided, not to this molecule page.

Safety at a Glance

⚠️ Moderate toxicity

• Ordinarily a minor whole-plant constituent. Human exposure is small and indirect, as one alkaloid of California poppy, greater celandine or corydalis preparations.
• Cardiac multi-channel blocker. Potent hERG block and action-potential prolongation are anti-arrhythmic in the lab but are also the mechanism of drug-induced QT prolongation — no safe isolated dose is defined ^{3,5Reference 3Lin K et al. · 2013Allocryptopine and benzyltetrahydropalmatine block hERG potassium channels expressed in HEK293 cellsView study →Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →}.
• Mechanism-based CYP inhibitor. Time-dependent inhibition of CYP3A4/2C9/2C19 plus reversible CYP2D6 inhibition — a plausible herb–drug-interaction route, strongest for ethanol tinctures ^{6Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →}.
• Isolate toxicology is uncharacterised. No pharmacokinetic, reproductive or repeat-dose safety data exist for pure allocryptopine ^{5Reference 5Li J et al. · 2019ReviewAllocryptopine: a review of its properties and mechanism of antiarrhythmic effectView study →}.

Dosage

There is no established or recommended human dose for isolated allocryptopine — it has never been used as a stand-alone medicine. The figures in the research are laboratory concentrations, not doses: the cardiac ion-channel effects appear at ~16–50 µmol/L in isolated channels and myocytes ^{1,2,3,4Reference 1Li Y et al. · 2008Effect of alpha-allocryptopine on transient outward potassium current in rabbit ventricular myocytesView study →Reference 2Fu YC et al. · 2016Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardiumView study →Reference 3Lin K et al. · 2013Allocryptopine and benzyltetrahydropalmatine block hERG potassium channels expressed in HEK293 cellsView study →Reference 4Xu B et al. · 2015AnimalEffect of α-allocryptopine on delayed afterdepolarizations and triggered activities in mice cardiomyocytes treated with isoproterenolView study →}, and the CYP and cholinesterase effects are likewise in-vitro ^{6,9Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →Reference 9Siatka T et al. · 2017Cholinesterase and prolyl oligopeptidase inhibitory activities of alkaloids from Argemone platyceras (Papaveraceae)View study →}. Human exposure is indirect and small, as a minor alkaloid within California poppy or greater celandine tinctures, capsules or teas — with the ethanol tincture carrying proportionally more of these alkaloids than the tea ^{6Reference 6Manda VK et al. · 2016Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloidsView study →}. These are research figures and are not a personal recommendation.

References

1. Li Y, Wang S, Liu Y, et al. (2008). Effect of alpha-allocryptopine on transient outward potassium current in rabbit ventricular myocytes. Cardiology. https://pubmed.ncbi.nlm.nih.gov/18434730/
2. Fu YC, Zhang Y, Tian LY, et al. (2016). Effects of allocryptopine on outward potassium current and slow delayed rectifier potassium current in rabbit myocardium. Journal of Geriatric Cardiology. https://pubmed.ncbi.nlm.nih.gov/27403141/
3. Lin K, Liu YQ, Xu B, et al. (2013). Allocryptopine and benzyltetrahydropalmatine block hERG potassium channels expressed in HEK293 cells. Acta Pharmacologica Sinica. https://pubmed.ncbi.nlm.nih.gov/23524574/
4. Xu B, Fu Y, Liu L, et al. (2015). Effect of α-allocryptopine on delayed afterdepolarizations and triggered activities in mice cardiomyocytes treated with isoproterenol. Evidence-Based Complementary and Alternative Medicine. https://pubmed.ncbi.nlm.nih.gov/26557861/
5. Li J, Li B, Huang H, et al. (2019). Allocryptopine: a review of its properties and mechanism of antiarrhythmic effect. Current Protein & Peptide Science. https://pubmed.ncbi.nlm.nih.gov/31389311/
6. Manda VK, Ibrahim MA, Dale OR, et al. (2016). Modulation of CYPs, P-gp, and PXR by Eschscholzia californica (California poppy) and its alkaloids. Planta Medica. https://pubmed.ncbi.nlm.nih.gov/27054913/
7. Fedurco M, Gregorová J, Šebrlová K, et al. (2015). Modulatory effects of Eschscholzia californica alkaloids on recombinant GABAA receptors. Biochemistry Research International. https://pubmed.ncbi.nlm.nih.gov/26509084/
8. Kosina P, Gregorová J, Gruz J, et al. (2010). Phytochemical and antimicrobial characterization of Macleaya cordata herb. Fitoterapia. https://pubmed.ncbi.nlm.nih.gov/20600683/
9. Siatka T, Adamcová M, Opletal L, et al. (2017). Cholinesterase and prolyl oligopeptidase inhibitory activities of alkaloids from Argemone platyceras (Papaveraceae). Molecules. https://pubmed.ncbi.nlm.nih.gov/28708094/
10. Gilca M, Gaman L, Panait E, et al. (2010). Chelidonium majus — an integrative review: traditional knowledge versus modern findings. Forschende Komplementärmedizin. https://pubmed.ncbi.nlm.nih.gov/20980763/
11. Nigdelioglu Dolanbay S, et al. (2025). Allocryptopine, tetrahydropalmatine, and tetrahydroberberine N-oxide alkaloids alleviate cellular stress by modulating calcium homeostasis and the MAPK and Akt/GSK-3β/tau signaling pathways. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/41378220/

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