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Emodin

Common Name(s): 1,3,8-trihydroxy-6-methyl-anthraquinone, 1,3,8-trihydroxy-6-methylemodin, 3',4',5',7-tetrahydroxyflavone, Emodin

Medically reviewed by Drugs.com. Last updated on Jul 21, 2022.

Clinical Overview

Use

Clinical studies of emodin were not identified for this review. Data from animal and experimental studies demonstrate strong anti-inflammatory and antioxidant effects that may prove useful in cancer, osteoporosis, and cardiovascular, CNS, liver, metabolic, and respiratory conditions. Antimicrobial and laxative activity has also been noted. No clinical data exist to support any of these uses.

Dosing

Clinical data are lacking to provide dosing recommendations.

Contraindications

Data are lacking regarding contraindications to emodin. As with other laxatives, use in patients with fecal compaction, intestinal obstruction, and undiagnosed abdominal pain is contraindicated.

Pregnancy/Lactation

Anthranoid metabolites may be excreted in breast milk. Emodin has been shown to impair embryonic development in mouse blastocysts, and in vitro studies have demonstrated a dose-dependent inhibitory effect on sperm motility but not sperm viability.

Interactions

None well documented.

Adverse Reactions

Concentration- and time-dependent toxicity of emodin has been observed in liver and kidney cell lines.

Toxicology

Overdose of anthraquinone laxatives results in intestinal pain and severe diarrhea with consequent electrolyte imbalance and dehydration. The carcinogenicity of emodin has been studied with equivocal results.

Source

Emodin is a polyphenol found in the roots, leaves, and bark of several plants, including aloe vera (Aloe barbadensis), cascara (Rhamnus pushiana), rhubarb (Rheum officinale), senna (Cassia angustifolia), Polygonum multiflorum, Polygonum cuspidatum, Psychotria camponutans, Radix et Rhizoma Rhei, Rheum palmatum, Stephania dinklagei, and Ventilago madraspatana.Di 2015, Han 2015, Jia 2014, Lee 2011, Lin 2015, Nemmar 2015, Sharma 2017, Xue 2015

History

Due to its laxative effect, emodin has been used in traditional Chinese medicine for obesity-related diseases. More recently, animal and experimental studies have supported emodin's use in cancerCha 2015, Di 2015, Jia 2014, Srinivas 2007 and conditions related to imbalances in inflammatory and oxidative processes, including cardiovascular disease, nonalcoholic fatty liver disease, liver transplant, and osteoporosis.Alisi 2012, Kim 2014, Lee 2012, Tong 2011, Yang 2014 Clinical application has been limited because of emodin's extremely low bioavailability.Di 2015

Chemistry

A variety of extraction methods have been examined for cascara; boiling water prevents the losses and changes to the compounds that occur in cold water extraction. Techniques for the production of emodin derivatives have been published.Alaerts 2007, Bisset 1994, Coskun 1989, Duke 1985, Evans 1989, FDA 2002, Koyama 2008, Leung 1980, Lu 2006, Tan 2006, Wei 1992 The content of free anthraquinones, including emodin, changes during the processing of P. multiflorum, with emodin content increasing after prolonged processing times. In traditional Chinese medicine, anthraquinones have been used as indicator constituents to determine the quality of P. multiflorum, which should have a minimum content of 0.1%, based on emodin and physcion.Lin 2015

Hydroxyanthraquinones, such as emodin, are phytoestrogens with an affinity for human estrogen receptors.Yang 2014 Antioxidant and anti-inflammatory effects of emodin are supported by experimental and animal studies that have led to identification of hepatoprotective and anticancer activity, as well as protective effects for cardiovascular, neurological, metabolic, respiratory, and bone disease.Alisi 2012, Cha 2015, Chen 2009, Jia 2014, Kim 2014, Kitano 2007, Lee 2012, Lin 2015, Liu 2009, Liu 2014, Nemmar 2015, Srinivas 2007, Tang 2015, Tong 2011, Xue 2015

Acetylcholinesterase inhibitory activity by emodin-8-O-beta-D-glucopyranoside, an active constituent of P. multiflorum, as well as antihyperlipidemic effects via the inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and diacylglycerol acyltransferase I, have been demonstrated by emodin.Lin 2015 Inhibition of protein tyrosine kinases has been documented, resulting in reduced phosphorylation of tyrosine in numerous protein substrates important in cellular functions.Luo 2015

Uses and Pharmacology

Reviews of the pharmacology and observed effects of emodin from in vitro and animal studies have been published.(Akkol 2021, Dong 2020)

Antifibrotic effects

Animal and in vitro data

Emodin demonstrated protective activity in animal models of hepatic injury, pancreatitis, renal failure, and pulmonary fibrosis,(Chen 2009, Dang 2008, Gui 2007, Li 2009, Wang 2007, Wang 2007, Wang 2007, Zhang 2005) as well as fibrinolytic activity via activation of plasminogen activator in vitro.(Radha 2008)

Anti-inflammatory/Immune system effects

Animal and experimental data

Experimental models of inflammation, including rat paw edema and ocular surface inflammation, have been used to demonstrate the mechanisms of action of emodin, which involve influence on cytokines and transcription factors.(Chen 2009, Kitano 2007, Liu 2009, Srinivas 2007) Animal studies investigating the effect of emodin on bone remodeling have demonstrated inhibitory effects on the inflammatory and immune signal mediator nuclear factor kappa B (NF-KB).(Kim 2014) Regulation of inflammasone activation and expression of interleukin 1beta (IL-1beta) in a sepsis mouse model confirmed in vitro findings of these processes, which are downstream of NF-KB activation.(Han 2015) A water extract of P. multiflorum that contained emodin effectively protected the liver of rats treated with carbon tetrachloride by diminishing the release of IL-1beta and tumor necrosis factor-alpha (TNF-alpha). No difference was found in TNF-alpha levels between the P. multiflorum water extract and the positive control, silymarin. The water extract was observed to be a stronger inhibitor of TNF-alpha than emodin alone, whereas the effect on IL)-1beta was similar between emodin and the P. multiflorum water extract.(Lee 2012) Other animal and experimental studies have reported similar improvements in TNF-alpha, IL-1beta, and other inflammatory cytokines in plasma as well as various tissues.(Alisi 2012, Lin 2015, Nemmar 2015, Tong 2011, Xue 2015)

Antimicrobial activity

Animal and in vitro data

In vitro studies of cell cultures have shown that emodin possesses antibacterial (Helicobacter pylori, Escherichia coli, Pseudomonas aeruginosa, Bacilius cereus, and some Staphylococcus aureus strains), virucidal (herpes simplex), and antifungal (Candida) activity.(Chen 2009, Hsiang 2008, Liu 2015, Srinivas 2007) The antibacterial efficacy of emodin against methicillin-resistant S. aureus (MRSA) was confirmed by in vitro and in vivo studies. Emodin exhibited dose-dependent effects comparable to linezolid and superior to imipenem and cefepime, with minimum inhibitory concentrations (MICs) between 2 and 8 mcg/mL and minimum bacterial concentrations (MBCs) between 4 and 32 mcg/mL. At 8 and 16 mcg/mL (1 times and 2 times the MBC, respectively), emodin demonstrated reduced viability of MRSA over 16 hours comparable to that with norvancomycin 0.5 mcg/mL (1 times MIC). Resistance did not develop easily with emodin, as no increase in MIC developed after 20 passages of the resistance selection assay, whereas norvancomycin demonstrated 2-fold and 4-fold increases in MIC after 4 and 15 passages, respectively. These data were confirmed using in vivo lethal and sublethal mice models. At 5 and 10 mg/kg, emodin resulted in 50% and 87.5% survival rates, respectively, compared with 12.5% with emodin 2.5 mg/kg and 0% for controls. The mechanism appears to be related to disruption of cell membrane integrity and not the involvement of genes related to cell wall synthesis, lysis, drug accumulation, or beta-lactamase activity. Additionally, bactericidal concentrations did not display cytotoxicity.(Liu 2015)

Antituberculosis activity of emodin extracted from Aloe vera leaf has been reported, with an MIC of 6.25 mcg/mL against Mycobacterium tuberculosis.(Sharma 2017) In vitro, emodin has also been shown to block severe acute respiratory syndrome (SARS) coronavirus spike protein binding to angiotensin-converting enzyme 2, suggesting potential application in treating SARS.(Lin 2015)

Antioxidant activity

Animal and in vitro data

Antioxidant activity has been observed in in vitro and in vivo studies(Alisi 2012, Lee 2012, Liu 2014, Nemmar 2015, Xue 2015) that used rat liver cell lines and rats, respectively. Emodin and/or the water extract of P. multiflorum root, with emodin as the main antioxidant, effectively reduced carbon tetrachloride-induced (CCl4) cytotoxicity. CCl4–induced elevations in AST and ALT levels were reduced by emodin and the water extract; recovery of key antioxidant enzymes, including glutathione peroxidase, glutathione reductase, glutathione S-transferase, and superoxide dismutase (SOD), was also observed. Additionally, emodin and the water extract reduced other biomarkers of lipid peroxidation such as malondiadehyde. Preventative effects of hepatotoxicity were also seen at the histological and organ level.(Lee 2012) Similar results occurred in a nonalcoholic fatty liver disease rat model that also demonstrated improved future response to oxidative stress in emodin-treated groups as well as enhanced activity of concomitant antioxidant therapy with emodin and N-acetylcysteine.(Alisi 2012) An adaptogenic effect of emodin has been demonstrated in a rat stroke model, in which rats were exposed to pulmonary diesel exhaust particles (DEP). Compared with the control group, DEP exposure induced both a decrease in the antioxidant SOD (P<0.01) and an increase in the antioxidant glutathione reductase (P<0.001); both processes were significantly reversed by emodin, indicating an ability to provide an adaptive response.(Nemmar 2015)

Cancer

Animal and in vitro data

The potential applications of emodin in the management of cancer have been reviewed.(Srinivas 2007). Cell cycle inhibition of many human cancer lines has been reported in vitro.(Brown 2007, Cai 2008, Cha 2005, Chen 2009, Fu 2007, Guo 2009, Huang 2009, Kaneshiro 2006, Kuo 2009, Lev-Goldman 2006, Lu 2008, Olsen 2007, Wang 2006, Wang 2007, Yan 2008, Yu 2008) A definitive mechanism of action, however, is unclear.(Srinivas 2007) Apoptosis, as well as antitumor action, has been demonstrated, and a role as an adjunct to chemotherapy has been suggested.(Chen 2009, Guo 2009) Antiangiogenic action has also been revealed.(Kaneshiro 2006, Lu 2008) Direct cytotoxicity is not thought to be responsible for apoptosis, with some researchers suggesting the involvement of signaling pathways, inhibition of kinases, and microsomal enzyme activation.(Kaneshiro 2006, Olsen 2007, Yan 2008) Data from more recent in vitro studies demonstrate emodin's ability to inhibit non–small cell lung cancer (NSCLC) cell growth in a dose- and time-dependent manner. Mechanisms involved the signaling pathway of adenosine monophosphate-activated protein kinase (AMPK) with subsequent inhibition of integrin-linked kinase, both of which are highly expressed in several human malignancies, including NSCLC. Additionally, the combination of emodin with metformin, which is also an AMPK inhibitor, enhanced the effects of emodin.(Tang 2015) Few animal experiments have been conducted(Guo 2009) and limited clinical studies have been identified.(Srinivas 2007, Sanders 2018)

In a breast cancer mouse model, intraperitoneal administration of emodin 40 mg/kg/day for 18 days significantly suppressed lung metastases, although no difference was found between the control and treatment groups in size, weight, and growth rate of primary tumors. A novel mechanism via tumor-associated macrophages was suggested based on reduced accumulation of M2 macrophages in the lungs. These data highlight the role of transcriptional control of macrophage activation and differentiation as a mechanism of metastasis and as a potential target for therapy.(Jia 2014) In vitro studies in bladder cancer cell lines further support the ability of emodin to affect gene transcriptional expression and reverse histone-induced epigenetic dysregulation of genes associated with cancer progression, cell survival, and proliferation. Emodin reversed the oncogenic epigenetic modifications, inhibited the binding affinity of RNA polymerase II, and restored healthy cellular epigenetic processes.(Cha 2015) An additional mechanism may be antilysosomal activity. Emodin-treated HeLa cervical cancer cells demonstrated lysosomal degradation, including increased autophagic vacuoles and cathepsin leakage, inducing apoptosis.(Trybus 2017)

Clinical data

A clinical study (N=240) reported that and aloe-emodin compound combined with chemotherapy improved solid tumor regression and 3-year survival time.(Lissoni 2009)

Cardiac and smooth muscle effects

Animal and in vitro data

In animal models of acute myocardial infarction and reperfusion injury, emodin appeared to have a protective role on the cardiac tissue by unclear mechanisms.(Du 2005, Wu 2007) Anti- and pro-oxidant effects have been described for emodin.(Hei 2006, Srinivas 2007, Wang 2007) In smooth muscle tissue, calcium and potassium efflux mechanisms are affected by emodin.(Wu 2008, Wu 2009, Zheyu 2006)

Because DEPs are a source of particulate air pollution that have been linked to various cardiovascular conditions (ie, angina, myocardial infarction, heart failure), DEP animal models are used to investigate potential therapies and key underlying mechanisms. These mechanisms involve oxidative stress that lead to proinflammatory responses related to atherogenesis. Studies in rats, including a stroke model, have demonstrated that the significant worsening of inflammatory (IL-1-beta, TNF-alpha), oxidative (SOD), and thrombotic (platelet aggregation, aPTT, PT) processes induced by pulmonary DEP exposure were significantly mitigated by administration of emodin 4 mg/kg. DEP exposure induced both pro-oxidant and antioxidant effects such that the antioxidant SOD was decreased significantly with exposure (P<0.01) and the antioxidant glutathione reductase was significantly increased (P<0.001). Emodin significantly reversed both of these processes, indicating an ability to provide an adaptive response.(Nemmar 2015)

Limited by toxicity, clinical studies for effect in cardiovascular disease are lacking.(Li 2020)

CNS effects

Animal and in vitro data

In vitro and animal studies suggest emodin exerts action on receptor signaling mechanisms in models of schizophrenia, and may also possess serotonin or muscarinic activity by protecting against induced amnesia in animals.(Lu 2007, Mizuno 2008) In a rat model of epilepsy, administration of emodin 200 mg/kg intraperitoneally improved epileptic symptoms as well as reduced gene expression of receptors and enzymes that contribute to seizures and multidrug resistance (P-glycoprotein and N-methyl-D-aspartate [NMDA], cyclooxygenase-2, and multidrug resistance gene 1).(Yang 2015) The first evidence of emodin to stimulate neuronal differentiation and neurite outgrowth was demonstrated in mouse neuroblastoma cells. Neurite outgrowth activity was observed to be both concentration- and time-dependent and was superior to that induced by retinoic acid, a known inducer of neuronal differentiation. Enhanced activity was observed with the combination of emodin and retinoic acid. Mechanisms were related to signaling pathways involving phosphatidylinositol 3-kinase, protein kinase B, glycogen synthase kinase-3-beta, and cAMP responsive element binding protein.(Park 2015)

Additionally, neuroprotection from traumatic injury was evidenced in a rat model.(Zeng 2017) Brain edema was reduced and multiple contributing mechanisms were identified, including inhibition of aquaporins and metalloprotein-9.

Clinical data

The emodin-related multi-ingredient preparation known as Qizhitongluo (QZTL) was evaluated for effect in recovery after stroke. At week 12 the participants in the QZTL group (n=309) showed significantly larger improvements compared with the placebo group in the indices measured for lower limb motor impairment.(Yu 2021)

Glucose metabolism

Animal data

A limited systematic review of studies published between 2008 and 2010 identified relevant literature on nutritional supplements used to treat type 2 diabetes. Of those identified, 4 animal studies reported the use of emodin. Body weight, blood glucose, and/or insulin resistance, as well as various lipid parameters, were improved with administration of emodin. These antidiabetic effects were attributed, in part, to the peroxisome proliferator-activated receptor (PPAR)-gamma agonist activity of emodin. Inhibition of 11-beta-hydroxysteroid dehydrogenase type 1 was also confirmed due to emodin's ability to prevent prednisone-induced, but not dexamethasone-induced, insulin resistance.(Lee 2011)

Clinical trials evaluating the effect of emodin in diabetes are lacking, and studies on the related anthraquinone diacerein are limited and report contradicting results.(Martorell 2021)

Hepatoprotection

Animal data

In a nonalcoholic fatty liver disease (NAFLD) rat model in which rats were fed a high transfat and high fructose diet, administration of emodin 40 mg/kg/day for 15 weeks significantly improved metabolic parameters (ie, triglycerides, ALT, glucose, insulin, insulin resistance) and liver weight (P<0.01 for all values) compared with those not receiving emodin. Values in NAFLD rats fed emodin were not different than those achieved with controls fed a standard diet. Histology analysis of NAFLD animal livers revealed that emodin-treated animals lacked the inflammatory cells prevalent in the livers of untreated NAFLD rats. Additionally, a reduction in cytological steatosis and ballooning was evident in the emodin group. An increase in the inflammatory biomarker TNF-alpha, but not IL-6, was induced by the high transfat/high fructose diet compared with the standard diet, an increase that was inhibited by emodin. In vitro, emodin treatment also protected primary hepatocytes extracted from the NAFLD models against redox imbalance, further protecting against oxidative stress. Potential synergy was shown with coadministration of other antioxidants (eg, N-acetylcysteine). These data reflect a potential preventative effect of emodin on the systemic inflammation that occurs in NAFLD.(Alisi 2012) In another study using a liver transplant rat model and an accompanying tissue analysis, emodin significantly improved median survival time (27.3 days vs 10.5 days; P<0.001), decreased acute graft rejection as measured by a marked confinement of inflammatory cell infiltration, and resulted in a reduced rejection grading (from severe to moderate), with significant improvement in the Rejection Activity Index compared with untreated animals (P<0.01). The mechanism of protective action appears to be related to the shift of the T-helper (Th) cell balance from Th-1 to Th-2 (downregulation of inflammatory cytokines TNF-alpha and IL-2, and upregulation of IL-10 in both serum and transplanted liver tissue).(Tong 2011)

Oxidative stress plays a critical role in alcohol-induced liver damage that includes induction of cytochrome P450 (CYP-450) 2E1. In mice with ethanol-induced liver injury, emodin 50 mg/kg/day prevented the increases in liver enzymes, triglycerides, cholesterol, and steatosis observed in the ethanol without emodin group (P<0.01 each) and produced levels comparable with controls. The mechanism was related to the potent antioxidant activity of emodin, inhibition of the expression of CYP2E1, reduction in the expression of the fibrotic gene, and an increase in the expression of PPAR-gamma mRNA in the liver, which resulted in reduced adipogenic differentiation and glucose homeostasis.(Liu 2014)

Laxative

Animal and in vitro data

Anthraglycosides produce an active secretion of water and electrolytes within the lumen of the small intestine and inhibit their absorption from the large intestine, causing an increase in the bowel content volume and strengthening of intestinal dilatation pressure to stimulate peristalsis.(Cortex 2002, Evans 1989, Leung 1980) The emodin glycoside causes laxative action, first requiring metabolism to the active aglycone by intestinal flora and possibly increasing the excitability of the smooth muscles of the intestinal wall.(Srinivas 2007, Zhang 2005) More recent studies in mice and human intestinal epithelial cells have suggested that emodin increases the production and gene expression of aquaporin 3 water channels in colonocytes, which are the primary channels that mediate water transfer.(Zheng 2014)

Lipids

Animal data

In animal models, administration of emodin has demonstrated hypolipidemic effects (ie, improvements in total cholesterol, triglycerides, and free fatty acids). Possible mechanisms of action involved agonistic effects on PPAR.(Dong 2005, Lee 2011, Zhao 2009)

Osteoporosis/Bone remodeling

Animal data

Osteoporosis in elderly individuals is accompanied by a decrease in osteoblastogenesis resulting from increased bone marrow adipogenesis. Animal studies have shown that the addition of emodin to ovariectomized mice markedly improved the negative bone structure effects induced in the ovariectomy without emodin group. Cancellous bone trabeculae regained near-normal structure with widening of the trabecular bone. Additionally, because bone and fat tissue derive from the same progenitor cells, the effect of emodin on bone marrow adipocytes was evaluated. Emodin improved the negative effects of ovariectomy on bone marrow fat tissue and adipocytes, with emodin producing results no different from controls (sham ovariectomy). The expression of genes related to formation of cellular collagen matrix was also upregulated with the administration of emodin, whereas those related to adipogenesis were downregulated.(Yang 2014) In addition to the promotion of osteoblastogenesis via stimulation of osteoblast formation, the inhibitory action of emodin on osteoclastogenesis has been demonstrated in mice. Administration of emodin inhibited early, but not late, cellular differentiation of osteoclasts as well as the function of mature osteoclasts by inhibiting pit formation. Emodin also provided a protective effect on trabecular bone loss. Mechanisms related to the inhibition of gene expression and signaling reduction of critical pathways that play fundamental roles in osteoclast development (eg, receptor activator of NF-KB ligand-mediated pathways) were elucidated.(Kim 2014)

Respiratory disease

Animal data

The effect of emodin on oxidative stress and the resulting cellular inflammation and tissue damage that occur in lung tissue subsequent to cigarette smoking was investigated in mice. At 20 mg/kg, and especially at 40 mg/kg, pretreatment with emodin protected against cigarette smoke–induced lung inflammation by improving inflammatory cytokines (ie, IL-1-beta, IL-6, TNF-alpha), antioxidant enzymes (ie, SOD, catalase, glutathione peroxidase, heme oxygenase), and the critical antioxidant nuclear transcription factor Nrf-2 that induces the expression of protective antioxidant genes and enzymes.(Xue 2015) Similarly, emodin significantly improved markers of oxidative stress (ie, lipid peroxidase, reactive oxygen species, reduced glutathione), inflammatory cytokines (ie, TNF-alpha, IL-6, IL-1-beta), and pulmonary infiltrates (eg, neutrophils, macrophages), as well as airway resistance (P<0.001) in a mouse model of airway hypersensitivity induced by DEP.(Nemmar 2015)

Dosing

Clinical studies are lacking to provide dosing recommendations.

Animal studies have demonstrated that emodin undergoes extensive glucuronidation after oral dosing that results in extremely low bioavailability (less than 3%). However, coadministration of emodin with piperine has been shown to clinically improve emodin pharmacokinetics, with a 221% increase in area under the curve (AUC), a 258% increase in maximum concentration (Cmax), and a 230% decrease in clearance due to inhibition of glucuronidation.(Di 2015) After oral administration in rats, bioavailability of emodin and other constituents of processed P. multiflorum products were lower compared to the raw product.(Lin 2015)

Pregnancy / Lactation

In mouse blastocysts, emodin has been shown to impair embryonic development via the intrinsic apoptotic signaling processes resulting in embryonic toxicity at doses of 25, 50, and 75 mcM.Lin 2015

In human male sperm cells, in vitro studies have demonstrated a dose-dependent inhibitory effect of emodin on sperm motility but not sperm viability. Additionally, via progesterone signaling pathways, emodin reduced the ability of sperm to penetrate viscous media reflective of the female reproductive tract. Mechanisms appear to be related to reduced capacitation and acrosome reaction that resulted from a decrease in both intracellular calcium levels in sperm heads and the phosphorylation of protein tyrosine processes necessary for motility.Luo 2015

Interactions

Interference with the absorption of other drugs is possible with anthranoid-containing plants, including senna and cascara.Cortex 2002, Fugh-Berman 2000

Adverse Reactions

In liver and kidney cell lines in vitro, concentration- and time-dependent toxicity of emodin has been demonstrated by induction of apoptosis.(Lin 2015) A systematic review of adverse effects of aloe-emodin anthraquinone, cautioning against its use without robust clinical evidence.(Jangra 2022) Similarly, a review including studies to September 2020 has been published for Radix polygoni multiflori.(Li 2020)

Toxicology

In vitro, mutagenicity of emodin was demonstrated at concentrations of 80 and 120 mcg/mL via thymidine kinase gene mutation analysis.Lin 2015

Overdose of anthraquinone laxatives results in intestinal pain and severe diarrhea with consequent electrolyte imbalance and dehydration. Treatment should be symptomatic, with special attention given to potassium and other electrolyte levels, especially in elderly patients and children.Cortex 2002

The carcinogenicity of emodin has been studied with equivocal results.Srinivas 2007 Emodin paradoxically exhibits an antioxidant action as well as pro-oxidant activityCai 2008 and has shown protective and toxic effects in rat glioma cells.Kuo 2009 No consensus on the mutagenicity of emodin has been achieved; a 2-year study conducted by the National Cancer Institute found equivocal evidence of carcinogenicity in rats.NTP 2001

References

Disclaimer

This information relates to an herbal, vitamin, mineral or other dietary supplement. This product has not been reviewed by the FDA to determine whether it is safe or effective and is not subject to the quality standards and safety information collection standards that are applicable to most prescription drugs. This information should not be used to decide whether or not to take this product. This information does not endorse this product as safe, effective, or approved for treating any patient or health condition. This is only a brief summary of general information about this product. It does NOT include all information about the possible uses, directions, warnings, precautions, interactions, adverse effects, or risks that may apply to this product. This information is not specific medical advice and does not replace information you receive from your health care provider. You should talk with your health care provider for complete information about the risks and benefits of using this product.

This product may adversely interact with certain health and medical conditions, other prescription and over-the-counter drugs, foods, or other dietary supplements. This product may be unsafe when used before surgery or other medical procedures. It is important to fully inform your doctor about the herbal, vitamins, mineral or any other supplements you are taking before any kind of surgery or medical procedure. With the exception of certain products that are generally recognized as safe in normal quantities, including use of folic acid and prenatal vitamins during pregnancy, this product has not been sufficiently studied to determine whether it is safe to use during pregnancy or nursing or by persons younger than 2 years of age.

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