Emodin

Emodin at a Glance

Emodin is a trihydroxy-methyl anthraquinone found throughout the anthraquinone laxative herbs — rhubarb, cascara, senna and yellow dock — and also in Japanese knotweed.

It has an enormous preclinical literature, one of the largest for any plant anthraquinone, spanning anticancer, anti-inflammatory, antiviral and metabolic activity.

Essentially none of it has been tested in humans as the isolated molecule, and poor oral bioavailability is the limit on any systemic claim — which is a recurring pattern for compounds whose laboratory record vastly outruns their clinical one.

An Enormous Literature and a 3–5% Bioavailability

Emodin has one of the largest preclinical literatures of any plant molecule — thousands of papers, targets in every disease area, mechanisms resolved down to named kinases. It also has an oral bioavailability of roughly 3–5% in rats ^{3Reference 3Liu Z et al. · 2012Coupling of UGTs and MRPs is responsible for the intestinal disposition and poor bioavailability of emodinView study →}. Holding both facts at once is the whole reading problem for this molecule.

The reason for the gap is specific rather than vague. Emodin is heavily glucuronidated in the intestine and liver, and the conjugates are pumped straight back out by multidrug-resistance-associated protein efflux — a coupled UGT/MRP system that clears the parent before it can accumulate ^{3Reference 3Liu Z et al. · 2012Coupling of UGTs and MRPs is responsible for the intestinal disposition and poor bioavailability of emodinView study →}. Free emodin is largely undetectable in plasma; the glucuronide dominates systemic exposure. It then undergoes enterohepatic recycling — biliary excretion, colonic deconjugation, reabsorption — which produces secondary plasma peaks but never a high free-drug concentration ^{2Reference 2Dong X et al. · 2016ReviewEmodin: a review of its pharmacology, toxicity and pharmacokineticsView study →}.

So the in-vitro concentrations at which emodin inhibits CK2, blocks HER-2/neu signalling or interferes with the SARS-CoV spike–ACE2 interface are, with few exceptions, concentrations an oral dose does not produce ^{6,7,8Reference 6Zhang L et al. · 1998Tyrosine kinase inhibitors: emodin and its derivative repress HER-2/neu-induced cellular transformationView study →Reference 7Janeczko M et al. · 2017Emodin, a natural inhibitor of protein kinase CK2, suppresses growth, hyphal development and biofilm formation of Candida albicansView study →Reference 8Ho TY et al. · 2007Emodin blocks the SARS coronavirus spike protein and angiotensin-converting-enzyme-2 interactionView study →}. That does not make the mechanisms wrong; it makes them mechanisms in search of a delivery route.

Two corollaries are worth stating plainly. A large literature is not the same as strong evidence — volume here reflects how easy emodin is to buy and assay, not how well it works. And the tissue that does see high emodin concentrations is the gut, which is where the class’s real effects, and its real problems, are found.

The Hydroxyanthracene Class Story

Emodin belongs to a family — with chrysophanol, rhein, physcion and aloe-emodin — that has been argued over by regulators for decades. The class questions are written up here, once, and the sibling pages carry only their own numbers.

How the laxative herbs actually work. Rhubarb, senna, cascara and yellow dock deliver anthraquinone glycosides — sennosides, cascarosides, anthraquinone-O-glucosides — which are not absorbed in the small intestine and reach the colon intact. There, bacterial enzymes cleave and reduce them to anthrones, and the anthrones are what alter water and electrolyte transport and stimulate motility. Free emodin, absorbed upstream in the oxidised form, is a minor contributor to laxation ^{14Reference 14Demarque DP et al. · 2018Cytotoxicity of structurally diverse anthranoids and correlation with mechanism of action and side effectsView study →}. The oxidation state is the whole mechanism: reduced anthrones are active, oxidised anthraquinones are comparatively quiet — the same rule that makes chrysarobin a skin-active tumour promoter while chrysophanol is inert ^{24Reference 24DiGiovanni J et al. · 1988AnimalStructure-activity relationships for epidermal ornithine decarboxylase induction and skin tumor promotion by anthrones — mouse modelView study →}.

Melanosis coli. Long-term use of anthraquinone laxatives produces a dark brown-black pigmentation of the colonic mucosa — lipofuscin-laden macrophages in the lamina propria, following apoptosis of epithelial cells. It is the visible marker of chronic anthranoid exposure, its incidence has been rising, and it is the reason gastroenterologists can often tell from a colonoscopy that someone has been using these herbs for years ^{22Reference 22Zhang R et al. · 2023ReviewReview on melanosis coli and anthraquinone-containing traditional Chinese herbs that cause melanosis coli — reviewView study →}. It is generally described as reversible on stopping, and it is not itself a malignancy — but it is evidence of sustained epithelial injury.

Dependence and the chronic-use problem. The stimulant laxatives are for short-term use. Chronic exposure carries potassium loss — which compounds digoxin, diuretic and antiarrhythmic risk — and a pattern in which bowel function becomes difficult to re-establish without them. That, rather than any acute toxicity, is what makes an anthraquinone herb a poor long-term answer to constipation.

The genotoxicity question, and how it splits. This is where the siblings genuinely differ, and the differences are the reason each page carries its own numbers rather than a class label:

• Emodin is genotoxic in multiple in-vitro assays — comet, micronucleus and mouse-lymphoma ^{23,17Reference 23Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →Reference 17Brusick D · 1997Assessment of the genotoxic risk from laxative senna productsView study →}.
• Chrysophanol and physcion were not, in the same assay panel ^{23Reference 23Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →}; chrysophanol’s contribution comes indirectly, through CYP1A2 bioactivation to aloe-emodin.
• Aloe-emodin and danthron carry the heavier direct signals, and danthron was withdrawn as a human laxative on carcinogenicity grounds.
• The whole-plant picture is more forgiving than the isolate picture. Complete vegetable extract showed no effect in the micronucleus test, and a lettuce extract abolished danthron-induced micronuclei entirely — the food matrix is protective, and the same survey concluded that dietary anthraquinone intakes are not a high-priority genotoxic risk in a balanced diet ^{23Reference 23Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →}.

What the regulators concluded. EFSA’s 2018 opinion on hydroxyanthracene derivatives found the class raises a genotoxicity and safety concern in food, which underpins the EU restriction on their use in food and food supplements ^{16Reference 16EFSA ANS Panel · 2018Safety of hydroxyanthracene derivatives for use in foodView study →}. That restriction covers the class, including molecules like chrysophanol whose own direct genotoxicity is weak. Against it sits the senna risk assessment, which concluded the genotoxic risk from laxative senna products at therapeutic use was not established ^{17Reference 17Brusick D · 1997Assessment of the genotoxic risk from laxative senna productsView study →}, and the NTP bioassay result below, which was equivocal rather than positive.

The honest summary is that this is an unresolved regulatory disagreement about a real but modest signal, not a settled finding in either direction — and that the exposure that matters is chronic use, not an occasional dose.

What It's Used For

Emodin is a trihydroxy-methyl anthraquinone (1,3,8-trihydroxy-6-methylanthraquinone) found across the anthraquinone-laxative herbs — rhubarb, yellow dock, cascara, Japanese knotweed and senna ^{20,21Reference 20Eom TJ et al. · 2020In-vitro antioxidant, anti-inflammation and anticancer activities and anthraquinone content from Rumex crispus rootView study →Reference 21Qian H et al. · 2024ReviewRumex crispus L.: a comprehensive review on botany, traditional uses, phytochemistry, pharmacology and safety — reviewView study →}.

Two framing points matter before any claim. First, the purgative action of those herbs is driven by the anthraquinone glycosides (sennosides, cascarosides, anthraquinone-O-glucosides) surviving to the colon where flora liberate active anthrones — not by free emodin, which is absorbed upstream and is only a minor contributor to laxation ^{14Reference 14Demarque DP et al. · 2018Cytotoxicity of structurally diverse anthranoids and correlation with mechanism of action and side effectsView study →}.

Second, emodin has poor oral bioavailability (~3–5% in rats) because it is heavily glucuronidated on absorption, so free parent is largely undetectable in plasma ^{3,2Reference 3Liu Z et al. · 2012Coupling of UGTs and MRPs is responsible for the intestinal disposition and poor bioavailability of emodinView study →Reference 2Dong X et al. · 2016ReviewEmodin: a review of its pharmacology, toxicity and pharmacokineticsView study →}.

Against that, emodin has an enormous preclinical literature — anti-inflammatory (NF-κB/NLRP3), anticancer, metabolic (11β-HSD1) and antiviral — but no human efficacy trial of the isolated molecule, and a materially heavier safety profile than most dietary constituents (see Toxicity).

Evidence by IndicationStrength of support · Beta

01Anti-inflammatoryShaky40%Rodent mechanism + a whole-rhubarb formula meta-analysis ^{9,10,11Reference 9Hu Q et al. · 2022Emodin attenuates severe acute pancreatitis-associated acute lung injury by suppressing pancreatic-exosome-mediated alveolar-macrophage activationView study →Reference 10Wu C et al. · 2022AnimalRhubarb free anthraquinones improved mice nonalcoholic fatty liver disease by inhibiting the NLRP3 inflammasome — mouse modelView study →Reference 11Zhou Y et al. · 2016Meta-analysisAdd-on effect of crude rhubarb to somatostatin for acute pancreatitis: a meta-analysis of randomized controlled trials — meta-analysisView study →}

02AnticancerShaky30%Broad but redundant in-vitro / xenograft only ^{12,13Reference 12Hsu SC · 2012ReviewAnticancer potential of emodin — reviewView study →Reference 13Xing JY et al. · 2015In vitroAntitumor effects and mechanism of novel emodin rhamnoside derivatives against human cancer cells in vitro — in vitroView study →}

03Metabolic (11β-HSD1)Shaky26%Enzyme assay + rodent models ^{4,5Reference 4Feng Y et al. · 2010AnimalEmodin, a natural product, selectively inhibits 11β-HSD1 and ameliorates metabolic disorder in diet-induced obese miceView study →Reference 5Wang YJ et al. · 2012In vitroEmodin, an 11β-hydroxysteroid dehydrogenase type 1 inhibitor, regulates adipocyte function in vitro and exerts an anti-diabetic effect in ob/ob mice — in vitro and mouse modelView study →}

04Antiviral / antimicrobialShaky20%In-vitro binding/growth assays ^{8,7Reference 8Ho TY et al. · 2007Emodin blocks the SARS coronavirus spike protein and angiotensin-converting-enzyme-2 interactionView study →Reference 7Janeczko M et al. · 2017Emodin, a natural inhibitor of protein kinase CK2, suppresses growth, hyphal development and biofilm formation of Candida albicansView study →}

05Hepatoprotective ↔ hepatotoxicShaky15%Rodent benefit vs documented harm — dose-dependent ^{10,15Reference 10Wu C et al. · 2022AnimalRhubarb free anthraquinones improved mice nonalcoholic fatty liver disease by inhibiting the NLRP3 inflammasome — mouse modelView study →Reference 15Akkol EK et al. · 2021Is emodin with anticancer effects completely innocent? Two sides of the coinView study →}

06Laxative (class effect)Shaky10%Anthranoid class; active species are the glycosides ^{14,16Reference 14Demarque DP et al. · 2018Cytotoxicity of structurally diverse anthranoids and correlation with mechanism of action and side effectsView study →Reference 16EFSA ANS Panel · 2018Safety of hydroxyanthracene derivatives for use in foodView study →}

Mechanisms

Pharmacokinetics

Load-bearing and constraining. Free emodin has poor oral bioavailability (~3–5% in rats) driven by extensive intestinal and hepatic glucuronidation coupled to multidrug-resistance-protein efflux, so parent emodin is rapidly conjugated and largely undetectable in plasma while the glucuronide dominates systemic exposure ^{3,2Reference 3Liu Z et al. · 2012Coupling of UGTs and MRPs is responsible for the intestinal disposition and poor bioavailability of emodinView study →Reference 2Dong X et al. · 2016ReviewEmodin: a review of its pharmacology, toxicity and pharmacokineticsView study →}. It undergoes enterohepatic recycling — biliary excretion of conjugates, colonic deconjugation, reabsorption — producing secondary plasma peaks but sustained low free-drug levels ^{2Reference 2Dong X et al. · 2016ReviewEmodin: a review of its pharmacology, toxicity and pharmacokineticsView study →}. The consequence runs through every application above: the high in-vitro potencies almost certainly overstate the free-plasma concentrations achievable in vivo.

Clinical Trials

There are no human efficacy trials of isolated emodin. The only clinical-grade human evidence in this space is for whole rhubarb or rhubarb-based formulas (e.g. crude rhubarb added to somatostatin for acute pancreatitis) ^{11Reference 11Zhou Y et al. · 2016Meta-analysisAdd-on effect of crude rhubarb to somatostatin for acute pancreatitis: a meta-analysis of randomized controlled trials — meta-analysisView study →} — multi-constituent preparations whose benefit cannot be attributed to the molecule. Treat all human data as herb/formula-level.

Last checked: September 2026.

Isolate vs. Plant Studies

The isolate work is clean and the plant work is real, and they are about different things.

The isolate. Purified emodin was used throughout the mechanism literature — 11β-HSD1 selectivity ^{4,5Reference 4Feng Y et al. · 2010AnimalEmodin, a natural product, selectively inhibits 11β-HSD1 and ameliorates metabolic disorder in diet-induced obese miceView study →Reference 5Wang YJ et al. · 2012In vitroEmodin, an 11β-hydroxysteroid dehydrogenase type 1 inhibitor, regulates adipocyte function in vitro and exerts an anti-diabetic effect in ob/ob mice — in vitro and mouse modelView study →}, CK2 inhibition ^{7Reference 7Janeczko M et al. · 2017Emodin, a natural inhibitor of protein kinase CK2, suppresses growth, hyphal development and biofilm formation of Candida albicansView study →}, HER-2/neu repression ^{6Reference 6Zhang L et al. · 1998Tyrosine kinase inhibitors: emodin and its derivative repress HER-2/neu-induced cellular transformationView study →}, the spike–ACE2 binding assay ^{8Reference 8Ho TY et al. · 2007Emodin blocks the SARS coronavirus spike protein and angiotensin-converting-enzyme-2 interactionView study →}, the pancreatitis-associated lung injury model ^{9Reference 9Hu Q et al. · 2022Emodin attenuates severe acute pancreatitis-associated acute lung injury by suppressing pancreatic-exosome-mediated alveolar-macrophage activationView study →}. Attribution is not the problem here; reachable concentration is (see above).

The plant. The only clinical-grade human evidence anywhere near this molecule is for whole rhubarb — crude rhubarb added to somatostatin in acute pancreatitis, meta-analysed across randomised trials ^{11Reference 11Zhou Y et al. · 2016Meta-analysisAdd-on effect of crude rhubarb to somatostatin for acute pancreatitis: a meta-analysis of randomized controlled trials — meta-analysisView study →} — and for rhubarb free-anthraquinone fractions in rodent NAFLD ^{10Reference 10Wu C et al. · 2022AnimalRhubarb free anthraquinones improved mice nonalcoholic fatty liver disease by inhibiting the NLRP3 inflammasome — mouse modelView study →}. Both are multi-constituent preparations. Rhubarb’s free-anthraquinone fraction is roughly 27% emodin, against ~43% rhein and ~1.5% chrysophanol ^{27Reference 27Li P et al. · 2017AnimalPharmacokinetics and pharmacodynamics of rhubarb anthraquinones extract in normal and disease rats — rat pharmacokinetic animal modelView study →}, so emodin is a major component of that fraction — but “major component of an active fraction” is a long way from “the active”.

The direction the transfer actually runs is worth noting, because it is unusual. For most constituents the isolate result is the strong one and the plant result is the muddy one. Here the plant has the human trials and the isolate has none, and the isolate’s own literature is discounted by a pharmacokinetic fact the plant partly circumvents — because a laxative herb delivers glycosides to the colon rather than free aglycone to the portal vein.

Its Role in Plants

Emodin is a polyketide: a type III polyketide synthase condenses acetate units into a chain that folds and cyclises to the anthracene skeleton, which is then oxidised and methylated. That route is independent of the shikimate pathway that makes coumarins and flavonoids, which is why anthraquinones appear in places with no common ancestry — flowering plants, fungi, lichens and scale insects all make them convergently.

They are pigments that also defend. The 1,8-dihydroxyanthraquinones are yellow to orange, absorb strongly in the UV, and are antimicrobial and antifeedant; rhubarb root’s colour and its chemistry of deterrence are the same molecules. Emodin turns up in fungi as well as plants — it is one of the substances that connects Rheum, Rumex, Rhamnus and Reynoutria to moulds and lichens that share none of their botany.

Storage is glycosidic. The plant keeps emodin as emodin-8-O-glucoside and, in Rhamnus, as the frangulins and glucofrangulins; senna stores rhein-anthrone units as sennoside dianthrones. Locking the molecule behind a sugar keeps the reactive anthrone out of the plant’s own cells and — incidentally — is what makes these plants colonic laxatives rather than gastric irritants.

Prevalence in Nature

Emodin is one of the most widely distributed plant anthraquinones, and it occurs at two very different concentrations depending on where you look.

Concentrated, in the anthraquinone herbs. Rhubarb (Rheum spp.), yellow dock (Rumex crispus), cascara sagrada (Rhamnus purshiana), Japanese knotweed (Reynoutria japonica) and senna all carry it, largely bound as glycosides so that free-aglycone content depends on preparation ^{12,20,21Reference 12Hsu SC · 2012ReviewAnticancer potential of emodin — reviewView study →Reference 20Eom TJ et al. · 2020In-vitro antioxidant, anti-inflammation and anticancer activities and anthraquinone content from Rumex crispus rootView study →Reference 21Qian H et al. · 2024ReviewRumex crispus L.: a comprehensive review on botany, traditional uses, phytochemistry, pharmacology and safety — reviewView study →}. Within a rhubarb free-anthraquinone extract, emodin is about 27% — the second-largest share after rhein ^{27Reference 27Li P et al. · 2017AnimalPharmacokinetics and pharmacodynamics of rhubarb anthraquinones extract in normal and disease rats — rat pharmacokinetic animal modelView study →}.

Dilute, in ordinary food. A survey of vegetables found free emodin, chrysophanol and physcion in cabbage lettuce, beans and peas, with large batch-to-batch variation: total anthraquinone ran 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 at 0.05–7.6 mg/kg ^{23Reference 23Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →}. This is the fact that keeps the class debate proportionate: emodin is a normal, low-level dietary constituent as well as a laxative-herb constituent.

Emodin also occurs in fungi and lichens, which is one of the ways the same molecule reaches a diet without any of these plants being involved.

Major Natural Sources

Source	Family	Part	Emodin content	Notes
Rhubarb (Rheum spp.)	Polygonaceae	Rhizome	~27% of the free-anthraquinone fraction 27Reference 27Li P et al. · 2017AnimalPharmacokinetics and pharmacodynamics of rhubarb anthraquinones extract in normal and disease rats — rat pharmacokinetic animal modelView study →	Mostly as emodin-8-O-glucoside
Japanese knotweed (Reynoutria japonica)	Polygonaceae	Root	Quantified in fractions	With resveratrol and polydatin
Yellow dock (Rumex crispus)	Polygonaceae	Root	Quantified in root fractions 20Reference 20Eom TJ et al. · 2020In-vitro antioxidant, anti-inflammation and anticancer activities and anthraquinone content from Rumex crispus rootView study →	With chrysophanol, physcion, rhein
Cascara sagrada (Rhamnus purshiana)	Rhamnaceae	Aged bark	As frangulins and glucofrangulins	Aglycone of the frangulin series
Senna (Senna spp.)	Fabaceae	Leaf, pod	Minor beside the sennosides
Beans, lettuce, peas	—	Edible parts	Trace; total anthraquinone 0.04–36 mg/kg fresh wt 23Reference 23Mueller 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 23Reference 23Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →	Found in 7 of 11 sampled

Discovery & Synthesis

Emodin came out of the most commercially charged organic chemistry of the nineteenth century. In 1868 Graebe and Liebermann synthesised alizarin — the first synthesis of a natural dye — and made the anthraquinone skeleton industrially important; eight years later Carl Liebermann and M. Waldstein isolated emodin from alder-buckthorn bark (Rhamnus frangula), which is why the compound is still sometimes called frangula-emodin ^{25Reference 25Liebermann C · 1876Emodin aus Rhamnus frangula RindeView study →}. The name itself comes from Rheum emodi, Himalayan rhubarb.

Its structure was settled in 1903, when H. A. D. Jowett and C. E. Potter established the constitution of emodin and of chrysophanic acid in a single paper ^{26Reference 26Jowett HAD · 1903The constitution of chrysophanic acid and of emodinView study →} — the two molecules differ by one hydroxyl group and were worked out together, which is a fair summary of how this whole family was mapped.

Manufacture today is extraction, from rhubarb, Rumex or Reynoutria root, for research use and as a reference standard in the quality control of anthraquinone herbs. Total synthesis of hydroxyanthraquinones is well established and industrially routine for dyes, but there is no pharmaceutical demand for synthetic emodin — it is not a licensed drug anywhere, and its poor oral bioavailability is a reason no one has tried to make it one.

Patents: not yet researched.

Toxicity & Safety

Emodin carries a materially heavier safety profile than most plant constituents. The class-level material — laxative dependence, melanosis coli, the genotoxicity dispute and the EU restriction — is set out above; what follows is emodin’s own record.

• Genotoxicity / carcinogenicity signal. Emodin is the member of this family with a direct in-vitro genotoxicity signal — positive in the comet, micronucleus and mouse-lymphoma assays where chrysophanol and physcion were not ^{23,17,14,19Reference 23Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →Reference 17Brusick D · 1997Assessment of the genotoxic risk from laxative senna productsView study →Reference 14Demarque DP et al. · 2018Cytotoxicity of structurally diverse anthranoids and correlation with mechanism of action and side effectsView study →Reference 19Silva Souza K et al. · 2025In vitroPhytotoxicity and cytogenotoxic effects of extracts from the medicinal bark of Rhamnus purshiana DC. (Rhamnaceae) — in vitroView study →}. The US National Toxicology Program 2-year feed bioassay (Technical Report TR-493, 2001) found no evidence of carcinogenicity in male rats, equivocal evidence in female rats (a marginal increase in Zymbal’s-gland carcinoma) and in male mice (uncommon renal-tubule neoplasms), and non-neoplastic renal-tubule changes across sexes and species ^{1Reference 1National Toxicology Program · 2001AnimalToxicology and carcinogenesis studies of emodin (CAS 518-82-1) in F344/N rats and B6C3F1 mice (feed studies)View study →}. The animal finding is therefore “equivocal,” not definitive — but real, and renal/Zymbal’s-gland-directed.
• Regulatory context. EFSA (2018) reviewed hydroxyanthracene derivatives (emodin, aloe-emodin, danthron and the parent extracts) and concluded they raise a genotoxicity/safety concern in food, underpinning the EU/EMA restriction on hydroxyanthracene derivatives in food and supplements ^{16Reference 16EFSA ANS Panel · 2018Safety of hydroxyanthracene derivatives for use in foodView study →}.
• Organ toxicity. Dose- and duration-dependent hepatotoxicity and nephrotoxicity are documented, coexisting with the hepatoprotective signal — net effect dose-dependent ^{2,15Reference 2Dong X et al. · 2016ReviewEmodin: a review of its pharmacology, toxicity and pharmacokineticsView study →Reference 15Akkol EK et al. · 2021Is emodin with anticancer effects completely innocent? Two sides of the coinView study →}.
• Reproductive/developmental. Developmental-toxicity evaluations in rats and mice, plus preclinical reports of testicular, oocyte and sperm-motility effects ^{18,2Reference 18Jahnke GD et al. · 2004AnimalDevelopmental toxicity evaluation of emodin in rats and mice — animal modelView study →Reference 2Dong X et al. · 2016ReviewEmodin: a review of its pharmacology, toxicity and pharmacokineticsView study →}.
• Interactions. As a UGT substrate and modulator, emodin may perturb glucuronidation-dependent drug clearance; the anthraquinone-laxative class can cause potassium loss, compounding digoxin, diuretic and antiarrhythmic risk ^{2Reference 2Dong X et al. · 2016ReviewEmodin: a review of its pharmacology, toxicity and pharmacokineticsView study →}.

Dosage

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

The gap to a human dose is wider here than for most constituents, in both directions. Upward, because oral bioavailability of ~3–5% means free-emodin exposure from an oral dose does not approach the concentrations the in-vitro results were obtained at ^{3Reference 3Liu Z et al. · 2012Coupling of UGTs and MRPs is responsible for the intestinal disposition and poor bioavailability of emodinView study →}. Downward, because the class safety concerns attach to chronic exposure, so a figure that looks small on a single-dose basis is not automatically reassuring over months.

Human intake happens incidentally, through anthraquinone laxative herbs dosed to their hydroxyanthracene-glycoside content rather than to free emodin, and at trace levels through ordinary vegetables ^{23Reference 23Mueller SO et al. · 1999In vitroOccurrence of emodin, chrysophanol and physcion in vegetables, herbs and liquorsView study →}. These are doses studied in research and are not a personal recommendation.

References

1. National Toxicology Program (2001). Toxicology and carcinogenesis studies of emodin (CAS 518-82-1) in F344/N rats and B6C3F1 mice (feed studies). NTP Technical Report Series (TR-493). https://pubmed.ncbi.nlm.nih.gov/12563347/
2. Dong X, et al. (2016). Emodin: a review of its pharmacology, toxicity and pharmacokinetics. Phytotherapy Research. https://pubmed.ncbi.nlm.nih.gov/27188216/
3. Liu Z, et al. (2012). Coupling of UGTs and MRPs is responsible for the intestinal disposition and poor bioavailability of emodin. Toxicology and Applied Pharmacology. https://pubmed.ncbi.nlm.nih.gov/22982073/
4. Feng Y, et al. (2010). Emodin, a natural product, selectively inhibits 11β-HSD1 and ameliorates metabolic disorder in diet-induced obese mice. British Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/20718744/
5. Wang YJ, Huang SL, Feng Y, et al. (2012). Emodin, an 11β-hydroxysteroid dehydrogenase type 1 inhibitor, regulates adipocyte function in vitro and exerts an anti-diabetic effect in ob/ob mice — in vitro and mouse model. Acta Pharmacologica Sinica. https://pubmed.ncbi.nlm.nih.gov/22922341/
6. Zhang L, et al. (1998). Tyrosine kinase inhibitors: emodin and its derivative repress HER-2/neu-induced cellular transformation. Oncogene. https://pubmed.ncbi.nlm.nih.gov/9671406/
7. Janeczko M, et al. (2017). Emodin, a natural inhibitor of protein kinase CK2, suppresses growth, hyphal development and biofilm formation of Candida albicans. Yeast. https://pubmed.ncbi.nlm.nih.gov/28181315/
8. Ho TY, et al. (2007). Emodin blocks the SARS coronavirus spike protein and angiotensin-converting-enzyme-2 interaction. Antiviral Research. https://pubmed.ncbi.nlm.nih.gov/16730806/
9. Hu Q, Yao J, Wu X, et al. (2022). Emodin attenuates severe acute pancreatitis-associated acute lung injury by suppressing pancreatic-exosome-mediated alveolar-macrophage activation. Acta Pharmaceutica Sinica B. https://pubmed.ncbi.nlm.nih.gov/36213542/
10. Wu C, Bian Y, Lu B, et al. (2022). Rhubarb free anthraquinones improved mice nonalcoholic fatty liver disease by inhibiting the NLRP3 inflammasome — mouse model. Journal of Translational Medicine. https://pubmed.ncbi.nlm.nih.gov/35765026/
11. Zhou Y, Wang L, Huang X, et al. (2016). Add-on effect of crude rhubarb to somatostatin for acute pancreatitis: a meta-analysis of randomized controlled trials — meta-analysis. Journal of Ethnopharmacology. https://pubmed.ncbi.nlm.nih.gov/27693773/
12. Hsu SC, Chung JG (2012). Anticancer potential of emodin — review. Biomedicine (Taipei). https://pubmed.ncbi.nlm.nih.gov/32289000/
13. Xing JY, Song GP, Deng JP, et al. (2015). Antitumor effects and mechanism of novel emodin rhamnoside derivatives against human cancer cells in vitro — in vitro. PLoS One. https://pubmed.ncbi.nlm.nih.gov/26682731/
14. Demarque DP, et al. (2018). Cytotoxicity of structurally diverse anthranoids and correlation with mechanism of action and side effects. Journal of Pharmacy & Pharmaceutical Sciences. https://pubmed.ncbi.nlm.nih.gov/30321134/
15. Akkol EK, et al. (2021). Is emodin with anticancer effects completely innocent? Two sides of the coin. Cancers (Basel). https://pubmed.ncbi.nlm.nih.gov/34073059/
16. EFSA ANS Panel (2018). Safety of hydroxyanthracene derivatives for use in food. EFSA Journal. https://pubmed.ncbi.nlm.nih.gov/32625659/
17. Brusick D, Mengs U (1997). Assessment of the genotoxic risk from laxative senna products. Environmental and Molecular Mutagenesis. https://pubmed.ncbi.nlm.nih.gov/9020301/
18. Jahnke GD, Price CJ, Marr MC, et al. (2004). Developmental toxicity evaluation of emodin in rats and mice — animal model. Birth Defects Research Part B. https://pubmed.ncbi.nlm.nih.gov/15098202/
19. Silva Souza K, da Cunha Neto AR, Chagas-Paula DA, et al. (2025). Phytotoxicity and cytogenotoxic effects of extracts from the medicinal bark of Rhamnus purshiana DC. (Rhamnaceae) — in vitro. Journal of Toxicology and Environmental Health, Part A. https://pubmed.ncbi.nlm.nih.gov/39964315/
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