Chrysophanol

Chrysophanol at a Glance

Chrysophanol is a 1,8-dihydroxy-3-methyl anthraquinone found across the anthraquinone laxative herbs — rhubarb, yellow dock and cascara.

Unlike its relatives sennoside and emodin, it is a weak laxative; its preclinical literature instead spans neuroprotection, anti-inflammatory, anticancer and metabolic activity.

That mismatch — a laxative-herb constituent studied mostly for everything except laxation — is the thing to hold when reading claims about it.

Chrysophanol vs. Chrysarobin

Chrysophanol’s other name is chrysophanic acid, and under that name it has a medical history it did not actually earn. In the 1870s and 1880s “chrysophanic acid” was one of the standard treatments for psoriasis, prescribed and argued over in the Lancet and the BMJ. The substance being used was Goa powder, from the Brazilian tree Andira araroba, and its active principle turned out not to be chrysophanol but chrysarobin — which the chemistry of the period could not cleanly separate from it ^{17Reference 17Farber EM · 1992ReviewHistory of the treatment of psoriasis — reviewView study →}.

The two are one oxidation step apart. Chrysophanol is 1,8-dihydroxy-3-methyl-9,10-anthraquinone; chrysarobin is 1,8-dihydroxy-3-methyl-9-anthrone — the same skeleton in its reduced, anthrone form. That single difference is the whole story, and the pharmacology follows it rather than the name:

• Chrysarobin is biologically aggressive. In mouse skin it induces epidermal ornithine decarboxylase and acts as a tumour promoter, and the anthrone series it belongs to produced the licensed psoriasis drug anthralin (dithranol), which is 1,8-dihydroxy-9-anthrone — the same molecule without the methyl group ^{16,17Reference 16DiGiovanni J et al. · 1988AnimalStructure-activity relationships for epidermal ornithine decarboxylase induction and skin tumor promotion by anthrones — mouse modelView study →Reference 17Farber EM · 1992ReviewHistory of the treatment of psoriasis — reviewView study →}.
• Chrysophanol is not. In the same experiment, chrysophanic acid was inactive as a tumour promoter at the doses tested ^{16Reference 16DiGiovanni J et al. · 1988AnimalStructure-activity relationships for epidermal ornithine decarboxylase induction and skin tumor promotion by anthrones — mouse modelView study →}.

The same logic runs through the whole anthraquinone-laxative story: the anthrones are the active forms and the anthraquinones are the oxidised, quiet ones. It is why gut bacteria have to reduce sennosides to rhein-anthrone before anything happens, and why chrysophanol is a weak laxative in a family of strong ones.

So two things should not be read onto chrysophanol: the Victorian antipsoriatic record, which belongs to chrysarobin and its descendant anthralin, and the tumour-promoting activity that goes with it.

What It's Used For

Chrysophanol (chrysophanic acid; 1,8-dihydroxy-3-methylanthraquinone) is one of the simplest hydroxyanthraquinones — the same anthraquinone-laxative family as emodin, rhein and physcion — and it turns up across rhubarb, yellow dock, cascara sagrada and, as a minor non-characteristic marker, dagga ^{1,2Reference 1Xie L et al. · 2019ReviewChrysophanol: a review of its pharmacology, toxicity and pharmacokinetics — reviewView study →Reference 2Prateeksha et al. · 2019ReviewChrysophanol: A Natural Anthraquinone with Multifaceted Biotherapeutic Potential — reviewView study →}.

In those plants it is usually a smaller share of the anthraquinone pool than emodin or rhein — roughly 1.5% of a representative rhubarb free-anthraquinone extract, versus ~27% emodin and ~43% rhein ^{15Reference 15Li P et al. · 2017AnimalPharmacokinetics and pharmacodynamics of rhubarb anthraquinones extract in normal and disease rats — rat pharmacokinetic animal modelView study →}.

Two framing points carry through every claim. First, oral bioavailability is poor: chrysophanol is lipophilic and poorly water-soluble, absorbed and conjugated so extensively that most of the applied literature reaches for liposomes, nanoparticles or drug combinations to raise exposure, and its movement across the blood–brain barrier is limited ^{1,2Reference 1Xie L et al. · 2019ReviewChrysophanol: a review of its pharmacology, toxicity and pharmacokinetics — reviewView study →Reference 2Prateeksha et al. · 2019ReviewChrysophanol: A Natural Anthraquinone with Multifaceted Biotherapeutic Potential — reviewView study →}.

Second, all of it is preclinical — there is no human efficacy trial of the isolated molecule, and the whole-herb use of its source plants is a multi-constituent, laxative-dominated exposure, not a chrysophanol result. Against that backdrop it has a broad in-vitro/in-vivo signal (neuroprotective, anti-inflammatory, anticancer, metabolic) ^{1,2Reference 1Xie L et al. · 2019ReviewChrysophanol: a review of its pharmacology, toxicity and pharmacokinetics — reviewView study →Reference 2Prateeksha et al. · 2019ReviewChrysophanol: A Natural Anthraquinone with Multifaceted Biotherapeutic Potential — reviewView study →} and a materially heavier safety profile than most dietary constituents (see Toxicity).

Evidence by IndicationStrength of support · Beta

01NeuroprotectionShaky38%Isolated chrysophanol; cerebral ischemia–reperfusion rodent models; poor BBB penetration ^{1,3Reference 1Xie L et al. · 2019ReviewChrysophanol: a review of its pharmacology, toxicity and pharmacokinetics — reviewView study →Reference 3Cui WH et al. · 2022AnimalEffects of chrysophanol on hippocampal damage and mitochondrial autophagy in mice with cerebral ischemia reperfusion — mouse modelView study →}

02Anti-inflammatoryShaky32%Isolated chrysophanol; sepsis-AKI cell + mouse model, plus whole-root fraction data ^{4,5Reference 4Gou X et al. · 2025In vitroChrysophanol promotes M2 polarization and inhibits M1 polarization through the NF-κB signaling pathway to attenuate sepsis-associated acute kidney injury — in vitro and mouse modelView study →Reference 5Eom T et al. · 2020In vitroIn Vitro Antioxidant, Antiinflammation, and Anticancer Activities and Anthraquinone Content from Rumex crispus Root Extract and Fractions — in vitroView study →}

03Metabolic / antidiabeticShaky26%Isolated chrysophanol; in-vitro PTP1B/GLUT4, obese-mouse SIRT6/AMPK, α-glucosidase assay ^{8,9,10Reference 8Lee MS · 2008In vitroAnti-diabetic properties of chrysophanol and its glucoside from rhubarb rhizome — in vitroView study →Reference 9Liu X et al. · 2020In vitroChrysophanol Alleviates Metabolic Syndrome by Activating the SIRT6/AMPK Signaling Pathway in Brown Adipocytes — in vitro and animal modelView study →Reference 10Nguyen TK et al. · 2023In vitroNepetifoliol — a new glutinane-triterpenoid from Leonotis nepetifolia — in vitroView study →}

04AnticancerShaky24%Isolated chrysophanol; in-vitro cell lines; less cytotoxic than emodin/aloe-emodin ^{6,7Reference 6Ni CH et al. · 2014In vitroChrysophanol-induced cell death (necrosis) in human lung cancer A549 cells is mediated through increasing reactive oxygen species and decreasing the level of mitochondrial membrane potential — in vitroView study →Reference 7Demarque DP et al. · 2018In vitroCytotoxicity of Structurally Diverse Anthranoids and Correlation with Mechanism of Action and Side Effects — in vitroView study →}

05Laxative (class effect)Shaky8%Anthraquinone class; chrysophanol a weak/minor contributor vs the glycosides ^{7,14Reference 7Demarque DP et al. · 2018In vitroCytotoxicity of Structurally Diverse Anthranoids and Correlation with Mechanism of Action and Side Effects — in vitroView study →Reference 14EFSA Panel on Food Additives et al. · 2018ReviewSafety of hydroxyanthracene derivatives for use in food — reviewView study →}

Mechanisms

Pharmacokinetics

Bioavailability is the load-bearing caveat for the whole chrysophanol literature. It is highly lipophilic and poorly water-soluble, and although its absorption rate is reported as higher than some other anthraquinones, systemic exposure is constrained by extensive conjugation and it distributes unevenly (kidney > liver > heart > brain), with poor blood–brain-barrier penetration despite the neuroprotective signals ^{1,2Reference 1Xie L et al. · 2019ReviewChrysophanol: a review of its pharmacology, toxicity and pharmacokinetics — reviewView study →Reference 2Prateeksha et al. · 2019ReviewChrysophanol: A Natural Anthraquinone with Multifaceted Biotherapeutic Potential — reviewView study →}. Metabolically it is a substrate for cytochrome-P450 oxidation — CYP1A2 converts chrysophanol to aloe-emodin (a hydroxymethyl anthraquinone that is itself more genotoxic than the parent), so a fraction of an oral dose is bioactivated rather than simply cleared ^{12Reference 12Mueller SO et al. · 1998In vitroBiotransformation of the anthraquinones emodin and chrysophanol by cytochrome P450 enzymesView study →}. This is why the applied literature leans heavily on liposomes, gold nanoparticles and drug combinations to raise exposure and blunt toxicity ^{1Reference 1Xie L et al. · 2019ReviewChrysophanol: a review of its pharmacology, toxicity and pharmacokinetics — reviewView study →}. The practical upshot mirrors emodin’s: potent in-vitro concentrations are not trivially reachable from an oral dose, which tempers every downstream claim.

Clinical Trials

There are no human efficacy trials of isolated chrysophanol. The only human exposure is incidental, via anthraquinone-containing herbs (rhubarb, cascara, yellow dock) used as laxatives — multi-constituent, glycoside-driven preparations whose effect cannot be attributed to this molecule. The chrysophanol evidence base is entirely preclinical.

Last checked: September 2026.

Isolate vs. Plant Studies

Almost every pharmacology result here used purified chrysophanol — the neuroprotection, macrophage-polarisation, PTP1B, SIRT6/AMPK and cytotoxicity work all dosed the isolate at stated concentrations ^{3,4,6,8,9Reference 3Cui WH et al. · 2022AnimalEffects of chrysophanol on hippocampal damage and mitochondrial autophagy in mice with cerebral ischemia reperfusion — mouse modelView study →Reference 4Gou X et al. · 2025In vitroChrysophanol promotes M2 polarization and inhibits M1 polarization through the NF-κB signaling pathway to attenuate sepsis-associated acute kidney injury — in vitro and mouse modelView study →Reference 6Ni CH et al. · 2014In vitroChrysophanol-induced cell death (necrosis) in human lung cancer A549 cells is mediated through increasing reactive oxygen species and decreasing the level of mitochondrial membrane potential — in vitroView study →Reference 8Lee MS · 2008In vitroAnti-diabetic properties of chrysophanol and its glucoside from rhubarb rhizome — in vitroView study →Reference 9Liu X et al. · 2020In vitroChrysophanol Alleviates Metabolic Syndrome by Activating the SIRT6/AMPK Signaling Pathway in Brown Adipocytes — in vitro and animal modelView study →}. That is clean attribution, and it is also the problem: the plants that supply chrysophanol are used for something the isolate barely does.

The source herbs are laxatives, and chrysophanol is not the laxative. Rhubarb, cascara and yellow dock work through anthraquinone glycosides that survive to the colon, where flora reduce them to active anthrones; free chrysophanol is a weak laxative and a minor share of the pool — roughly 1.5% of a representative rhubarb free-anthraquinone extract against ~27% emodin and ~43% rhein ^{15Reference 15Li P et al. · 2017AnimalPharmacokinetics and pharmacodynamics of rhubarb anthraquinones extract in normal and disease rats — rat pharmacokinetic animal modelView study →}. So the whole-herb human exposure is not a chrysophanol exposure in any useful sense, and no herbal result transfers to this molecule.

Where extract and isolate were run side by side, the extract result belongs to the extract: the antioxidant, anti-inflammatory and anticancer activities of Rumex crispus root fractions were measured on fractions, with anthraquinone content reported alongside ^{5Reference 5Eom T et al. · 2020In vitroIn Vitro Antioxidant, Antiinflammation, and Anticancer Activities and Anthraquinone Content from Rumex crispus Root Extract and Fractions — in vitroView study →}. And the α-glucosidase figure comes from a Leonotis nepetifolia isolation paper where chrysophanol was one of several compounds tested ^{10Reference 10Nguyen TK et al. · 2023In vitroNepetifoliol — a new glutinane-triterpenoid from Leonotis nepetifolia — in vitroView study →}.

The practical position: a well-attributed isolate literature, attached to plants nobody takes for the reasons this molecule is studied.

Its Role in Plants

Anthraquinones like chrysophanol are polyketides — built by a type III polyketide synthase condensing acetate units into a folded chain that cyclises to the three-ring anthracene skeleton, then oxidised and methylated. That is a different biosynthetic origin from the coumarins and flavonoids, and it is why anthraquinones turn up in unrelated places: flowering plants, fungi, lichens and insects all make them by convergent polyketide routes.

They are pigments first. The 1,8-dihydroxyanthraquinones are yellow to orange, and in Rheum and Rumex they colour the root and rhizome; the same chemistry gives lichens their oranges. Colour and defence are not separate functions here — the molecules absorb strongly in the UV and are antimicrobial and antifeedant, so a pigment that deters is doing two jobs at once.

The plant stores them glycosylated, as chrysophanol-8-O-glucoside and as the C-glycosyl anthrones that become cascarosides C and D. Glycosylation keeps the reactive aglycone locked up in the vacuole until something cleaves it — the same storage logic as the coumarin glucosides, and the reason the purgative action of these plants happens in the colon rather than the stomach.

Chrysophanol also appears well outside the laxative herbs — in dagga (Leonotis nepetifolia), where it is a minor non-characteristic constituent ^{10Reference 10Nguyen TK et al. · 2023In vitroNepetifoliol — a new glutinane-triterpenoid from Leonotis nepetifolia — in vitroView study →}, and across ordinary vegetables at trace levels (see below).

Prevalence in Nature

Chrysophanol is far more widespread than the laxative-herb framing suggests, and almost always in trace amounts.

Its concentrated sources are the anthraquinone-laxative plants: rhubarb (Rheum spp.), yellow dock (Rumex crispus) and cascara sagrada (Rhamnus purshiana), where it is present largely as glycosides rather than free aglycone, and where it is consistently a minor share of the anthraquinone pool — about 1.5% of a representative rhubarb free-anthraquinone extract ^{15Reference 15Li P et al. · 2017AnimalPharmacokinetics and pharmacodynamics of rhubarb anthraquinones extract in normal and disease rats — rat pharmacokinetic animal modelView study →}.

Its dilute sources are food. A survey of ordinary vegetables found free emodin, chrysophanol and physcion in cabbage lettuce, beans and peas, with large batch-to-batch variability: total anthraquinone ranged from 0.04 to 3.6 mg/kg fresh weight in peas, up to 5.9 mg/kg in lettuce and up to 36 mg/kg in beans, with physcion predominating. Grape-vine leaves, couch-grass root and plantain herb carried under 1 mg/kg dry weight, and seven of eleven herbal-flavoured liquors contained all three anthraquinones at 0.05–7.6 mg/kg ^{11Reference 11Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →}. The same study concluded that at those intakes, and given the protective effect of the food matrix, these constituents are not a high-priority genotoxic risk in a balanced diet ^{11Reference 11Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →}.

Major Natural Sources

Source	Part	Chrysophanol content	Notes
Rhubarb (Rheum spp.)	Rhizome	~1.5% of the free-anthraquinone fraction 15Reference 15Li P et al. · 2017AnimalPharmacokinetics and pharmacodynamics of rhubarb anthraquinones extract in normal and disease rats — rat pharmacokinetic animal modelView study →	Mostly as chrysophanol-8-O-glucoside; rhein ~43%, emodin ~27% of the same fraction
Yellow dock (Rumex crispus)	Root	Quantified in root fractions 5Reference 5Eom T et al. · 2020In vitroIn Vitro Antioxidant, Antiinflammation, and Anticancer Activities and Anthraquinone Content from Rumex crispus Root Extract and Fractions — in vitroView study →	With emodin, physcion, rhein
Cascara sagrada (Rhamnus purshiana)	Aged bark	Parent aglycone of cascarosides C and D	C-glycosyl anthrones, not free aglycone
Dagga (Leonotis nepetifolia)	Aerial	Present 10Reference 10Nguyen TK et al. · 2023In vitroNepetifoliol — a new glutinane-triterpenoid from Leonotis nepetifolia — in vitroView study →	Minor, non-characteristic
Beans, lettuce, peas	Edible parts	Trace; total anthraquinone 0.04–36 mg/kg fresh wt 11Reference 11Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →	Physcion predominates
Herbal-flavoured liquors	—	0.05–7.6 mg/kg 11Reference 11Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →	Found in 7 of 11 sampled

Discovery & Synthesis

Chrysophanol was known as chrysophanic acid long before it was understood — the name is from the Greek for “golden”, and it was one of the yellow crystalline substances that nineteenth-century chemistry pulled out of rhubarb root and out of lichens. Its structure was settled in 1903, when H. A. D. Jowett and C. E. Potter established the constitution of chrysophanic acid and of emodin together ^{18Reference 18Jowett HAD · 1903The constitution of chrysophanic acid and of emodinView study →} — the two molecules differ by a single hydroxyl, and were worked out in the same paper.

That work sat inside a much larger project. Anthraquinone chemistry was the most commercially important organic chemistry of the late nineteenth century, because Graebe and Liebermann’s synthesis of alizarin in 1868 — the first synthesis of a natural dye — turned the anthraquinone skeleton into industrial territory. Emodin was isolated from alder-buckthorn bark by Liebermann himself in 1876 ^{19Reference 19Liebermann C · 1876Emodin aus Rhamnus frangula RindeView study →}. The plant anthraquinones were mapped by people whose day job was dyes.

Manufacture today is extraction, from rhubarb or Rumex root, for research use; chrysophanol is a reference standard in the quality control of anthraquinone herbs rather than a product. Total synthesis of simple hydroxyanthraquinones is straightforward but has no commercial point.

Patents: not yet researched.

Toxicity & Safety

Chrysophanol warrants more caution than most dietary constituents, but its case is more equivocal than emodin’s, and the two should not be read as carrying the same risk.

• Direct genotoxicity — weaker than emodin. In the assay panel that flagged emodin as genotoxic (comet, micronucleus, mouse-lymphoma), chrysophanol and physcion showed no genotoxic effect ^{11Reference 11Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →}, and across a structure–activity series chrysophanol is less cytotoxic than emodin or aloe-emodin ^{7Reference 7Demarque DP et al. · 2018In vitroCytotoxicity of Structurally Diverse Anthranoids and Correlation with Mechanism of Action and Side Effects — in vitroView study →}. So the “hydroxyanthraquinone = genotoxic” story is not straightforwardly chrysophanol’s.
• But it is metabolically bioactivated. CYP1A2 oxidizes chrysophanol to aloe-emodin, and aloe-emodin induced significantly higher micronucleus frequencies than chrysophanol — i.e. part of chrysophanol’s genotoxic risk is carried by a downstream metabolite rather than the parent ^{12Reference 12Mueller SO et al. · 1998In vitroBiotransformation of the anthraquinones emodin and chrysophanol by cytochrome P450 enzymesView study →}. This is the pathway that keeps it inside the class concern.
• Hepatotoxicity is documented. The pharmacology reviews describe chrysophanol as having “obvious” hepatotoxicity and nephrotoxicity ^{1Reference 1Xie L et al. · 2019ReviewChrysophanol: a review of its pharmacology, toxicity and pharmacokinetics — reviewView study →}, and its glycoside chrysophanol-8-O-glucoside is strongly hepatotoxic in vitro — inhibiting mitochondrial respiratory-chain complexes, collapsing membrane potential, raising ROS, depleting glutathione and driving hepatocyte apoptosis ^{13Reference 13Lin L et al. · 2019In vitroHepatotoxicity and mechanism study of chrysophanol-8-O-glucoside in vitro — in vitroView study →}.
• Regulatory context. Chrysophanol is a hydroxyanthracene derivative, the class EFSA (2018) concluded raises a genotoxicity/safety concern in food, underpinning the EU/EMA restriction on hydroxyanthracene derivatives in food and supplements ^{14Reference 14EFSA Panel on Food Additives et al. · 2018ReviewSafety of hydroxyanthracene derivatives for use in food — reviewView study →}. It is regulated with the class even where its own direct genotoxicity is weak.
• Interactions / class effect. As an anthraquinone-laxative-class molecule, chronic exposure via the source herbs carries the class’s potassium-loss risk (compounding digoxin, diuretic and antiarrhythmic effects); the reviews note chrysophanol is often combined with other drugs specifically to reduce toxicity and modulate exposure ^{1Reference 1Xie L et al. · 2019ReviewChrysophanol: a review of its pharmacology, toxicity and pharmacokinetics — reviewView study →}. Human interaction data for the isolated molecule are absent.

The class story is on the emodin page. The laxative-dependence, melanosis coli, genotoxicity and EU hydroxyanthracene-derivative material applies to the whole family and is written up once, on emodin. What is chrysophanol’s own is the set of numbers above: no direct genotoxicity in the panel that flagged emodin ^{11Reference 11Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →}, lower cytotoxicity than emodin or aloe-emodin ^{7Reference 7Demarque DP et al. · 2018In vitroCytotoxicity of Structurally Diverse Anthranoids and Correlation with Mechanism of Action and Side Effects — in vitroView study →}, no tumour-promoting activity where its anthrone chrysarobin has plenty ^{16Reference 16DiGiovanni J et al. · 1988AnimalStructure-activity relationships for epidermal ornithine decarboxylase induction and skin tumor promotion by anthrones — mouse modelView study →} — and, against all that, CYP1A2 bioactivation to aloe-emodin ^{12Reference 12Mueller SO et al. · 1998In vitroBiotransformation of the anthraquinones emodin and chrysophanol by cytochrome P450 enzymesView study →} and a strongly hepatotoxic glucoside ^{13Reference 13Lin L et al. · 2019In vitroHepatotoxicity and mechanism study of chrysophanol-8-O-glucoside in vitro — in vitroView study →}.

Dosage

There is no established or safe human dose for isolated chrysophanol, and nothing here is a recommendation. The figures below are the exposures used in the research described above.

Two things widen the gap to a human dose more than usual. The rodent figures are inflated to compensate for poor absorption, and chrysophanol distributes unevenly with poor blood-brain-barrier penetration ^{1,2Reference 1Xie L et al. · 2019ReviewChrysophanol: a review of its pharmacology, toxicity and pharmacokinetics — reviewView study →Reference 2Prateeksha et al. · 2019ReviewChrysophanol: A Natural Anthraquinone with Multifaceted Biotherapeutic Potential — reviewView study →}, so the neuroprotective results in particular rest on brain concentrations an oral dose is unlikely to reach. Human intake happens only incidentally through anthraquinone laxative herbs, which are dosed to their hydroxyanthracene-glycoside content, not to free chrysophanol. These are doses studied in research and are not a personal recommendation.

References

1. Xie L, Tang H, Song J, et al. (2019). Chrysophanol: a review of its pharmacology, toxicity and pharmacokinetics — review. Journal of Pharmacy and Pharmacology. https://pubmed.ncbi.nlm.nih.gov/31373015/
2. Prateeksha, Yusuf MA, Singh BN, et al. (2019). Chrysophanol: A Natural Anthraquinone with Multifaceted Biotherapeutic Potential — review. Biomolecules. https://pubmed.ncbi.nlm.nih.gov/30781696/
3. Cui WH, Zhang HH, Qu ZM, et al. (2022). Effects of chrysophanol on hippocampal damage and mitochondrial autophagy in mice with cerebral ischemia reperfusion — mouse model. International Journal of Neuroscience. https://pubmed.ncbi.nlm.nih.gov/33032501/
4. Gou X, Zhang W, Wang L, et al. (2025). Chrysophanol promotes M2 polarization and inhibits M1 polarization through the NF-κB signaling pathway to attenuate sepsis-associated acute kidney injury — in vitro and mouse model. Frontiers in Pharmacology. https://pubmed.ncbi.nlm.nih.gov/40808684/
5. Eom T, Kim E, Kim JS (2020). In Vitro Antioxidant, Antiinflammation, and Anticancer Activities and Anthraquinone Content from Rumex crispus Root Extract and Fractions — in vitro. Antioxidants. https://pubmed.ncbi.nlm.nih.gov/32784977/
6. Ni CH, Yu CS, Lu HF, et al. (2014). Chrysophanol-induced cell death (necrosis) in human lung cancer A549 cells is mediated through increasing reactive oxygen species and decreasing the level of mitochondrial membrane potential — in vitro. Environmental Toxicology. https://pubmed.ncbi.nlm.nih.gov/22848001/
7. Demarque DP, Silva RMP, Santos LF, et al. (2018). Cytotoxicity of Structurally Diverse Anthranoids and Correlation with Mechanism of Action and Side Effects — in vitro. Journal of Pharmacy & Pharmaceutical Sciences. https://pubmed.ncbi.nlm.nih.gov/30321134/
8. Lee MS, Sohn CB (2008). Anti-diabetic properties of chrysophanol and its glucoside from rhubarb rhizome — in vitro. Biological & Pharmaceutical Bulletin. https://pubmed.ncbi.nlm.nih.gov/18981591/
9. Liu X, Yang Z, Li H, et al. (2020). Chrysophanol Alleviates Metabolic Syndrome by Activating the SIRT6/AMPK Signaling Pathway in Brown Adipocytes — in vitro and animal model. Oxidative Medicine and Cellular Longevity. https://pubmed.ncbi.nlm.nih.gov/33274005/
10. Nguyen TK, Ton TQ, Ngo TT, et al. (2023). Nepetifoliol — a new glutinane-triterpenoid from Leonotis nepetifolia — in vitro. Natural Product Research. https://pubmed.ncbi.nlm.nih.gov/34365866/
11. Mueller SO, Schmitt M, Dekant W, et al. (1999). Occurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquors. Genotoxicity and anti-genotoxicity of the anthraquinones and of the whole plants — in vitro. Food and Chemical Toxicology. https://pubmed.ncbi.nlm.nih.gov/10456676/
12. Mueller SO, Stopper H, Dekant W (1998). Biotransformation of the anthraquinones emodin and chrysophanol by cytochrome P450 enzymes. Bioactivation to genotoxic metabolites — in vitro. Drug Metabolism and Disposition. https://pubmed.ncbi.nlm.nih.gov/9616189/
13. Lin L, Yuan F, Liu Y, et al. (2019). Hepatotoxicity and mechanism study of chrysophanol-8-O-glucoside in vitro — in vitro. Biomedicine & Pharmacotherapy. https://pubmed.ncbi.nlm.nih.gov/31648163/
14. EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS), Younes M, Aggett P, et al. (2018). Safety of hydroxyanthracene derivatives for use in food — review. EFSA Journal. https://pubmed.ncbi.nlm.nih.gov/32625659/
15. Li P, Lu Q, Jiang W, et al. (2017). Pharmacokinetics and pharmacodynamics of rhubarb anthraquinones extract in normal and disease rats — rat pharmacokinetic animal model. Biomedicine & Pharmacotherapy. https://pubmed.ncbi.nlm.nih.gov/28475921/
16. DiGiovanni J, Kruszewski FH, Coombs MM, et al. (1988). Structure-activity relationships for epidermal ornithine decarboxylase induction and skin tumor promotion by anthrones — mouse model. Carcinogenesis. https://pubmed.ncbi.nlm.nih.gov/3402040/
17. Farber EM (1992). History of the treatment of psoriasis — review. Journal of the American Academy of Dermatology. https://pubmed.ncbi.nlm.nih.gov/1401327/
18. Jowett HAD, Potter CE (1903). The constitution of chrysophanic acid and of emodin. Journal of the Chemical Society, Transactions. https://doi.org/10.1039/ct9038301327
19. Liebermann C, Waldstein M (1876). Emodin aus Rhamnus frangula Rinde. Berichte der deutschen chemischen Gesellschaft. https://doi.org/10.1002/cber.187600902220

View all 19 references▾