spec sheet11 rows
Emodin is a bright orange pigment found in rhubarb, Japanese knotweed, senna and buckthorn, and it is one of the chemicals that makes those herbs work as laxatives. In the laboratory it blocks several human enzymes, most convincingly the cortisol-regenerating enzyme 11beta-HSD1 and the signalling kinase CK2, and it has been tested very heavily in cancer cell cultures. Almost none of this has been checked in people; there is no established human dose, absorption from the gut is poor because the body rapidly conjugates and clears it, and the single controlled human trial applied it to the gums as a light-activated gel rather than swallowing it. European food safety regulators concluded emodin is genotoxic and were unable to set any daily intake they considered safe, and a two-year rodent feeding study found kidney changes at every dose tested; the cell-culture literature claiming broad anti-inflammatory and anticancer benefits also contains an unusual number of retracted papers.
- the bright orange pigment behind rhubarb and knotweed
- inhibits 11beta-HSD1, the cortisol regenerating enzyme
- also blocks the signalling kinase CK2 in the lab
- one of the most heavily studied natural anthraquinones
- cell culture work is vast; human data has not caught up yet
- The component most linked to the liver toxicity that can follow high or prolonged use of rhubarb and knotweed preparations
- Can act as a laxative and cause digestive upset, reflecting its anthraquinone nature
- Some genotoxicity has been reported in laboratory tests, so high intake warrants caution
Overview
Emodin is a naturally occurring anthraquinone, chemically 1,3,8-trihydroxy-6-methylanthraquinone, that gives several medicinal plants their biological punch. It is found in the roots and rhizomes of rhubarb (Rheum species), in knotweed (Fallopia multiflora, also known as Polygonum multiflorum), in Cassia and buckthorn, and in certain lichens and fungi [4]. As one of the principal active constituents of rhubarb, it has been part of traditional Chinese medicine for centuries, historically valued for its purgative and anti-inflammatory actions.
Contemporary pharmacology has turned emodin into one of the most heavily investigated natural anthraquinones. Reviews document a wide spectrum of activity that includes anti-inflammatory, anticancer, antimicrobial, antiviral, hepatoprotective, and metabolic effects, and it has been studied in models of cancer, organ fibrosis, obesity, diabetes, and non-alcoholic fatty liver disease [1][2][3]. Much of this interest centers on its ability to influence central signaling pathways that govern inflammation, energy metabolism, and cell survival.
Emodin is not an approved drug; it exists as a purified natural product used in research, as a marker compound for standardizing herbal preparations, and as a constituent of traditional herbal medicines. It is available as a research chemical, typically a powder. Its safety profile is double-edged: while emodin is broadly bioactive, it is also the component most associated with the liver toxicity that can accompany high or prolonged intake of rhubarb-root and knotweed preparations, and its bioavailability is limited, both of which shape how it is studied and used [4].
- Emodin's name comes from Rheum emodi, the Himalayan rhubarb it was characterized from.
- It acts on several of the cell's master control pathways at once, including the energy sensor AMPK and the inflammatory regulator NF-kappa B.
- It is also the anthraquinone most associated with the liver injury that can follow heavy use of rhubarb and knotweed preparations.
Mechanism
The appeal of emodin lies in the breadth of its molecular targets, which lets a single small molecule touch inflammation, metabolism, and cancer biology at once. In metabolic tissues it activates AMP-activated protein kinase (), the cell's master energy sensor, and modulates the peroxisome proliferator-activated receptors (PPARs), a combination that improves lipid and glucose handling and underlies its studied benefits in obesity, hyperlipidemia, diabetes, and fatty liver disease [1]. In inflammation, emodin dampens the NF-kappa B signaling pathway, lowering the output of pro-inflammatory cytokines, which is the common thread running through its anti-inflammatory and anti-fibrotic effects across multiple organs [2].
In cancer models emodin behaves as a multi-target agent. In a rat model of hepatocellular carcinoma it increased survival and reduced the number of liver nodules while shifting a network of biomarkers in a favorable direction: it strengthened antioxidant defenses by raising Nrf2 and heme oxygenase-1, and it suppressed proliferation, tissue destruction, and blood-vessel formation by lowering protein kinase C, ERK5, ADAMTS4, MMP3, and the angiogenesis driver VEGF [3]. Through such mechanisms emodin has shown anti-proliferative, pro-apoptotic, and anti-angiogenic activity in a range of tumor types [2][3].
These same properties come with real caveats that are part of its mechanism of action. Emodin is the constituent most linked to the liver injury that can follow heavy use of rhubarb and knotweed preparations, an effect tied to disturbances in hepatic metabolism, bile acid balance, and hepatocyte apoptosis, and its usefulness is further limited by poor oral [4]. For the user, emodin represents a genuinely broad-acting plant compound, strong on anti-inflammatory, metabolic, and anticancer mechanisms in preclinical research, yet one whose narrow margin between benefit and hepatic stress means it is best regarded as a research compound rather than a casual supplement [1][3][4].
receptor fingerprint
11-beta-HSD1selective inhibitor
sensitivity / lipidsimproves
Inflammation (TNF-alpha)reduces
11beta-hydroxysteroid dehydrogenase type 1 (HSD11B1)Selective inhibitor; blocks local regeneration of active cortisol from inactive cortisone in liver and fat
Protein kinase CK2 (casein kinase 2, CSNK2A1)ATP-competitive inhibitor; binds the nucleotide pocket between the N- and C-terminal lobes
HER2/neu (ERBB2, p185neu) receptor tyrosine kinaseInhibits receptor tyrosine phosphorylation; reverses HER2-driven chemoresistance
receptor alpha and betaBinds the receptor, displacing 17-beta-estradiol
Aldose reductase (AKR1B1)Uncompetitive inhibitor
Colonic anthranoid / stimulant laxative pathwayActs as the absorbable aglycone released by gut bacteria from plant anthraquinone glycosides, producing the purgative effect of senna, cascara, rhubarb, frangula and buckthorn
NF-kappaB inflammatory signallingReported suppression of NF-kappaB pathway activation in cultured cells
Dosingtypical ranges, not medical advice
interested in protocols and clinical dosages? make an account to see them! ^_^
Safetyrisks and cautions, not medical advice
GENOTOXICITY is the headline concern. EFSA concluded emodin shows evidence of genotoxicity and explicitly could not advise any daily intake free of health concern (PMID 32625659). NTP found emodin mutagenic in Salmonella typhimurium TA100 with S9 activation and clastogenic in cultured CHO cells with and without S9; in vivo micronucleus tests were mostly negative, with a weakly positive result in female mice at 14 weeks (PMID 12563347). CARCINOGENICITY in the NTP 2-year feed study was no evidence in male rats, EQUIVOCAL evidence in female rats (marginal increase in Zymbal's gland carcinoma), EQUIVOCAL evidence in male mice (uncommon renal tubule adenoma and carcinoma), and no evidence in female mice.
ORGAN TOXICITY: the kidney is the consistent target, with renal tubule pigmentation and hyaline droplets at every exposure level in rats and increased nephropathy in mice; reviews additionally report hepatotoxicity, nephrotoxicity and reproductive toxicity at high doses or with long-term use (PMID 27188216). PHOTOSENSITIVITY is intrinsic, not incidental; emodin is used deliberately as a photosensitizer in photodynamic therapy, so light exposure is a plausible skin risk.
CHRONIC LAXATIVE USE of the parent herbs carries the usual anthranoid problems (electrolyte loss, melanosis coli), and EFSA noted epidemiological signal linking general laxative use with colorectal cancer. INTERACTIONS: no verified human drug interaction data was found; emodin is heavily glucuronidated, so UGT-mediated interactions are plausible but unproven, and any specific CYP claim should be treated as unestablished. REGULATORY: EU Commission Regulation 2021/468 (in force April 2021) placed emodin, aloe-emodin, danthron and aloe hydroxyanthracene preparations in Annex III Part A of Regulation 1925/2006, prohibiting them in food.
IMPORTANT UPDATE, the EU General Court annulled that regulation on 13 November 2024 (Case T-189/21 and related) as regards emodin, aloe-emodin and aloe preparations, on the grounds that the Commission overreached by regulating preparations rather than substances and failed the Article 8 "greatly exceed" test; DANTHRON is the only substance whose prohibition survived. So the emodin ban is currently annulled, not in force, though the underlying EFSA genotoxicity assessment stands unchanged. Emodin is not a hormone, stimulant or masking agent and does not appear on the WADA 2026 Prohibited List, nor in any prohibited class; it is not a scheduled controlled substance in the US.
History
Emodin is a naturally occurring anthraquinone that has been isolated from a range of traditional medicinal plants, most notably rhubarb of the genus Rheum and knotweeds of the genus Polygonum, whose roots and rhizomes have been used in East Asian and other herbal traditions for centuries. Its common name derives from Rheum emodi, the Himalayan rhubarb from which it was characterized. Rather than emerging from a single company or laboratory, emodin entered modern science gradually as chemists cataloged the pigments and active constituents of these long-used plants.
Over the past several decades it has become one of the most extensively studied anthraquinones in the pharmacological literature, with published investigations spanning anti-inflammatory, anticancer, metabolic, and antimicrobial activity. It is important to note that emodin has never been developed into an approved medicine; it remains a research compound and a constituent of botanical preparations rather than a licensed drug.
Reputation
Emodin enjoys a strong reputation among researchers of plant-derived molecules for the sheer breadth of its documented activity, touching inflammation, metabolism, and cancer biology through action on master regulatory pathways such as AMPK, the PPARs, and NF-kappa B. This mechanistic richness, backed by a large body of preclinical literature, makes it one of the better-characterized natural anthraquinones and a favorite subject for studies of multi-target small molecules.
At the same time, an honest account must foreground its limitations. Emodin is the constituent most closely linked to the liver injury that can follow heavy use of rhubarb and knotweed preparations, and its poor oral bioavailability constrains how much reaches the bloodstream. For these reasons it is best understood as a compound of real scientific interest and genuine mechanistic depth, but one that belongs to research settings rather than casual supplementation.
Subjective profileweighing the evidence above
Interesting pharmacology, wrong side of the ledger. This is the component most closely tied to the liver toxicity seen with high or prolonged use of rhubarb and knotweed, it has shown genotoxicity in laboratory tests, and it acts as a laxative. Not worth taking as an isolated supplement.
Where to buy
Suppliers
Vendors carrying Emodin, with live product details and codes. Links are affiliate links that support the wiki at no cost to you.
Kimera Chems
Emodin
Research
- 1996first citedSensitization of HER-2/neu-overexpressing non-small cell lung cancer cells to chemotherapeutic…
- 2024most recentNano-emodin mediated photodynamic therapy for wound healing of donor site after free gingival g…
- 1.Advances in the pharmacological effects and molecular mechanisms of emodin in the treatment of metabolic diseases
- 2.A comprehensive review of emodin in fibrosis treatment
- 3.Evaluating anticancer activity of emodin by enhancing antioxidant activities and affecting PKC/ADAMTS4 pathway in thioacetamide-induced hepatocellular carcinoma in rats
- 4.Overview of Pharmacokinetics and Liver Toxicities of Radix Polygoni Multiflori
- 5.Emodin, a natural product, selectively inhibits 11beta-hydroxysteroid dehydrogenase type 1 and ameliorates metabolic disorder in diet-induced obese mice
- 6.Advances in the mechanism of emodin-induced hepatotoxicity
- 7.NTP Toxicology and Carcinogenesis Studies of EMODIN (CAS NO. 518-82-1) Feed Studies in F344/N Rats and B6C3F1 Mice.
- 8.Safety of hydroxyanthracene derivatives for use in food.
- 9.Emodin, an 11β-hydroxysteroid dehydrogenase type 1 inhibitor, regulates adipocyte function in vitro and exerts anti-diabetic effect in ob/ob mice.
- 10.The replacement of ATP by the competitive inhibitor emodin induces conformational modifications in the catalytic site of protein kinase CK2.
- 11.Toward the rational design of protein kinase casein kinase-2 inhibitors.
- 12.Sensitization of HER-2/neu-overexpressing non-small cell lung cancer cells to chemotherapeutic drugs by tyrosine kinase inhibitor emodin.
15 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Where does emodin come from?
It is a plant anthraquinone found in rhubarb, knotweed, and related plants.
What is it studied for?
Research has looked at its anti-inflammatory and metabolic effects, including mild 11-beta-HSD1 inhibition linked to fat loss.
Can it affect digestion?
Anthraquinones like emodin can have laxative effects and may cause GI upset.
Is it a proven fat-loss aid?
Human evidence is limited, so its fat-loss benefits are not firmly established.
Adverse effects
- The component most linked to the liver toxicity that can follow high or prolonged use of rhubarb and knotweed preparations
- Can act as a laxative and cause digestive upset, reflecting its anthraquinone nature
- Some genotoxicity has been reported in laboratory tests, so high intake warrants caution
Notes and cautions
- Poor oral absorption limits how much reaches the bloodstream