IngredientsGallic acid (also known as 3,4,5-trihydroxybenzoic acid) is a trihydroxybenzoic acid with the molecular formula C6H2(OH)3CO2H, classified as a phenolic acid. It belongs to a class of phytochemicals known as phenols or phenolic compounds; phenols are characterized by one or more hydroxyl (-OH) groups attached to an aromatic ring. Salts and esters of gallic acid are termed "gallates." Its name is derived from oak galls, which were historically used to prepare tannic acid; despite the name, gallic acid does not contain the element gallium. The compound carries the CAS registry number 149-91-7.
Pure gallic acid is a colorless, crystalline powder. Besides being soluble in water, it can also be dissolved in alcohol, ether, and glycerol; it is practically insoluble in benzene, chloroform, and ether petroleum. The compound is odorless, usually colorless or slightly yellow. Its melting point is 210 °C, and its decomposition point is 235–240 °C.
Gallic acid is a phytochemical, a biologically active natural compound found in plant-based foods, first identified in 1786 by the scientist Carl Wilhelm Scheele. In 1786, the French chemist Carl Wilhelm Scheele isolated "gallotannic acid," later refined by Henri Braconnot in 1833 to pure gallic acid crystals. By the mid-20th century, research shifted from ink to physiology: the 1940s saw the first papers on antioxidant capacity, and by the 1980s, scientists studied its antimicrobial potential.
Gallic acid is formed in plants in the shikimate pathway, which provides aromatic amino acids that are precursors of numerous secondary metabolites such as coumarins, alkaloids, lignans, or polyphenols, including gallic acid. Gallic acid is formed from 3-dehydroshikimate by the action of the enzyme shikimate dehydrogenase to produce 3,5-didehydroshikimate; this latter compound aromatizes.
Gallic acid is found in many plants of the families Anacardiaceae, Fabaceae, and Myrtaceae, as well as in fungi of the genus Termitomyces, in the form of both free and more complex molecules. Gallic acid is a natural phenolic compound that is widely found in gallnuts, sumac, tea, grapes, lemons, and other plants, and also appears in high concentration in green tea, red wine, coffee, and other beverages.
Gallic acid and its derivatives naturally occur in almost all plant parts, such as bark, wood, leaves, fruits, roots, and seeds. These compounds are found in different amounts in various common foods, including blueberries, blackberries, strawberries, plums, grapes, mangoes, cashew nuts, hazelnuts, walnuts, tea, wine, and more. Gallic acid is a phenolic compound abundantly found in various plants such as tea leaves, oak bark, or the galls of some trees and shrubs, as well as in some foods such as walnuts, apples, strawberries, pineapples, bananas, blackberry, lemons, or grapes.
Gallic acid occurs in nature mainly in the form of hydrolysable tannins; however, their amounts as dietary components are limited. The main sources of this compound in the human diet are non-sugar galloyl esters of gallic acid such as epigallocatechin gallate. Gallate concentrations differ depending on the type of plant species, as well as within a plant species, in response to various environmental elements like UV rays, microbial diseases, insect attacks, and chemical stressors.
Gallic acid is generally obtained in both free and conjugated forms, either as an ester or as derivatives of catechin (catechin gallates). The most common ester derivatives of gallic acid are the alkyl esters — for example, methyl, propyl, octyl, and dodecyl gallate. Gallic acid and its derivatives such as lauryl gallate, propyl gallate, octyl gallate, tetradecyl gallate, and hexadecyl gallate can inhibit the oxidation and rancidity of oils and fats, ascribed to their free radical scavenging and antioxidant nature; they are therefore useful as additives in the food industry.
As a supplement or pharmaceutical preparation, gallic acid appears in several forms:
Gallic acid is present to the extent of 40–60 percent combined as gallotannic acid in tara and in Aleppo and Chinese galls, from which it is obtained commercially by the action of acid.
Gallic acid has been used as a healing agent since ancient times. Its medicinal use dates back centuries, with roots in traditional systems such as Ayurveda and Traditional Chinese Medicine (TCM). Historically, gallic acid-rich extracts were prized for their potent astringent, anti-inflammatory, and antimicrobial properties.
Gallic acid-rich gallnuts have been used in Traditional Chinese Medicine (wu bei zi) and Ayurveda (mayaphal) for over 2,000 years as astringents for diarrhea, dysentery, wounds, and oral ulcers. In traditional Chinese medicine (TCM), herbs rich in gallic acid, such as Phyllanthus emblica (Amla), have been used for their purported benefits in promoting digestion, boosting immunity, and treating various ailments.
In Ayurvedic medicine, Triphala, a combination of three fruits including Amla, which is high in gallic acid, is a popular remedy for detoxification and rejuvenation.
European herbalism has utilized gallic acid since the 1780s, initially for ink production and leather tanning, later extending to folk remedies for sore throats. Traditional cuisines from Persia to medieval Europe prized gallnut extracts for tanning leather and as astringent decoctions in herbal medicine. It was used from the 12th to 19th centuries as a major component of iron gall ink, the standard writing ink in Europe. Gallic acid has a long history of use in the production of inks, dyes, and tanning agents for leather. It is also a precursor to pyrogallol, a developer in early photography.
In ancient remedies, decoctions and infusions containing gallic acid were employed to treat wounds, control bleeding, and alleviate gastrointestinal disorders such as diarrhea and dysentery. Healers also valued it for its ability to soothe skin irritations and promote the healing of ulcers and sores. Gallic acid was frequently used in combination with other herbs to synergize their effects. In Western herbal traditions, it was commonly blended with tannin-rich botanicals to enhance their astringency and effectiveness in managing excessive discharge, bleeding, and infection.
To treat gastrointestinal problems, gallic acid has been commonly found in various herbal preparations, such as infusions and teas made from leaves and fruits rich in gallic acid (e.g., berries), while for the treatment of wounds and skin infections, topical ointments and powders were employed.
In Asian kitchens, tea traditions in China, Japan, and India inadvertently delivered gallic acid daily.
The strong antioxidant activity of gallic acid has been the subject of several studies. Gallic acid provides effective protection against oxidative damage by reactive species such as hydroxyl (HO), superoxide (O2–), and peroxyl (ROO) radicals, as well as hydrogen peroxide (H2O2) and hypochlorous acid (HOCl). Gallic acid displays remarkable antioxidant effects by activating nuclear factor erythroid 2-related factor (Nrf2) and the expression of antioxidant genes.
Gallic acid pretreatment decreases the harmful oxidative consequences of myocardial infarction in the context of its antioxidant potency, either by increasing the activity of antioxidant enzymes such as SOD, CAT, GST, and GPx and/or by elevation of the level of non-enzymatic antioxidant agents such as GSH, vitamin C, and vitamin E. All of these activities can inhibit the detrimental effects of free radicals on the integrity and function of myocytes membranes, and consequently, the concentration of serum cardiac biomarkers including cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB) decreases after infarction.
The anti-inflammatory mechanism of gallic acid is mainly related to the nuclear factor kappa B (NF-κB) signaling pathway and down-regulating inflammation-related factors such as interleukin 1 (IL-1), interleukin 6 (IL-6), transforming growth factor-beta (TGF-β) and tumor necrosis factor alpha (TNF-α). By suppressing the MAPK pathway, gallic acid reduces NF-κB activation, which in turn lowers the expression of pro-inflammatory cytokines and other mediators, thus decreasing inflammation and oxidative stress. Furthermore, gallic acid's activation of Akt and AMPK stimulates Nrf2, enhancing the expression of antioxidant enzymes.
The antimicrobial role of gallic acid is defined primarily through mechanisms such as disruption of microbial cell membranes, inhibition of efflux pumps, and antibiofilm activity. The mechanisms of action of polyphenols with antimicrobial properties are based on different factors at the cellular level, which may be individual or synergistic: (1) the modification of cytoplasmic membrane function; (2) disruption of intracellular functions; and (3) programmed cell death.
In cancer treatment, gallic acid functions as a selective pro-oxidant to induce apoptosis, arrest the cell cycle, inhibit metastasis (via MMPs), and exhibit synergy with tyrosine kinase inhibitors (TKIs) by inhibiting mitochondrial respiration. Gallic acid's role in cancer management has been described via the modulation of signaling pathways.
Gallic acid (3,4,5-trihydroxybenzoic acid) is the end product of hydrolysis of tea tannins, which are believed to be responsible for the lowered iron absorption resulting from excessive tea ingestion. Gallic acid forms a 3:1 complex with iron in the pH range 4–6. Dietary molecules such as gallic acid, caffeic acid, quercetin, ellagic acid, maltol, and many other phytochelators are known to interact with iron and affect iron metabolism and related diseases.
Gallic acid combines with critical proteins or minerals, such as zinc, calcium, and iron to form insoluble complexes that disturb other bioactive substances.
The efficacy of gallic acid in diabetes is largely due to its ability to stimulate insulin secretion from β cells, reduce insulin resistance, and inhibit the intestinal absorption of glucose. Gallic acid acts as a metabolic modulator, regulating PFK-1 in diabetes, the miR-709/Nrf2 axis in diabetic nephropathy, and the LDLR/PCSK9 pathway to enhance LDL cholesterol clearance.
Important note on evidence quality: Current evidence confirms the pharmacological and therapeutic interventions of gallic acid in multiple health complications; however, available data are largely limited to cellular and animal studies. Future investigations are essential to further define the safety and therapeutic efficacy of gallic acid in humans. Readers should interpret claims about specific health benefits accordingly. Sections below carefully separate in vitro/animal evidence from the limited human clinical data.
Studies show that the most important pharmacological properties of gallic acid are attributed to its antioxidant and anti-inflammatory potentials. The strongest human-level evidence in this area comes from a placebo-controlled pilot study in patients with type 2 diabetes: researchers performed an intervention study (n = 19) with gallic acid and monitored alterations in DNA stability in single cell gel electrophoresis (SCGE) assays in lymphocytes, measuring a panel of health-related biomarkers before and after consumption of gallic acid at 15 mg per person per day for 7 days. The study concluded that a small amount of gallic acid (in the range of daily consumption in Central Europe) prevents oxidative DNA damage and reduces markers that reflect inflammation and increased risks of cancer and CVD. This is a small-scale, short-duration pilot study; results require replication in larger trials.
Metabolic diseases such as diabetes mellitus and obesity reduce antioxidant capacity by decreasing the level of antioxidant enzymes, leading to progressive cellular dysfunction. With its antioxidant and free radical scavenging abilities, gallic acid may reverse metabolism toward normal condition and may function as an effective agent in the treatment of metabolic diseases.
In a clinical trial, it was found that gallic acid could maintain the stability of genetic materials, protect LDL against oxidative damage, and reduce the levels of C-reactive protein in diabetic patients. The mechanistic basis for antidiabetic effects has been characterized in preclinical settings: gallic acid, recognized for its hypoglycemic properties, plays a beneficial role in both the prevention and treatment of diabetes; its efficacy is largely due to its ability to stimulate insulin secretion from β cells, reduce insulin resistance, and inhibit the intestinal absorption of glucose.
A more recent clinical data point: a 2025 double-blind, randomized, placebo-controlled trial treated patients with type 2 diabetes with a gallic acid-rich phenolic fraction from Anisopus mannii (PhAM, 500 mg/day for 12 weeks). The treatment resulted in a significant decrease in HbA1c and fasting blood glucose levels compared to placebo. It should be noted that this studied a gallic acid-rich fraction, not isolated gallic acid, limiting attribution of effects to gallic acid alone.
Gallic acid and its related edible plants have been specifically credited for reducing systemic inflammation and oxidative stress-associated metabolic complications including diabetes mellitus and related complications in humans. However, the evidence base at the isolated gallic acid level in human trials remains sparse.
Scientific reports on gallic acid and its ester derivatives emphasize cardioprotective effects, among other properties. The body of evidence here is predominantly preclinical. In animal models, studies have demonstrated that gallic acid exerts anti-inflammatory and antioxidant effects, inhibits ferroptosis, and maintains mitochondrial homeostasis; previous experiments in rats showed that gallic acid could ameliorate endothelial dysfunction and hypotension in diabetes mellitus by upregulating plasma miR-24 and miR-126 levels. Additionally, gallic acid has been reported to attenuate cardiac hypertrophy and left ventricular dysfunction following cardiac ischemia-reperfusion injury in diabetic rats.
Gallic acid has been shown to have antihyperglycemic and lipid homeostasis actions in preclinical studies. Mechanistically, gallic acid modulates the LDLR/PCSK9 pathway to enhance LDL cholesterol clearance. No large-scale, prospectively designed human cardiovascular outcomes trials for isolated gallic acid were identified in the literature reviewed.
Numerous studies have reported the antibacterial potential of gallic acid, although in some of them, the exact mechanism of antimicrobial action is not known or not fully explained. The evidence is largely from in vitro studies. Gallic acid's antimicrobial role is defined primarily through mechanisms such as disruption of microbial cell membranes, inhibition of efflux pumps, and antibiofilm activity. Due to its antiseptic properties, gallic acid has been useful for cleaning, disinfecting, and healing wounds, thereby reducing infections — historically used in topical ointments and powders. Human clinical trial data specifically evaluating gallic acid as an antimicrobial therapeutic is lacking.
Gallic acid was identified as the main antioxidant component responsible for the antiradical and anticancer activities of various plant extracts. While numerous studies highlight the anticancer properties of gallic acid in various human cells, rat models, and nanoparticle delivery systems, direct clinical (human interventional) trial evidence is limited. Gallic acid is one of the promising natural anticancer agents that has considerable preclinical evidence to support its therapeutic benefits, but human trials are not yet established.
In preclinical oncology models, gallic acid functions as a selective pro-oxidant to induce apoptosis, arrest the cell cycle, and inhibit metastasis. Despite wide-ranging research demonstrating anticancer, neuroprotective, and cardioprotective properties of gallic acid, numerous critical knowledge gaps remain. The 2019 oxidative DNA damage pilot study in diabetic patients — noting that gallic acid at 15 mg/day reduced biomarkers reflecting cancer risk — is the closest approximation of human cancer-relevant data, but it studied a surrogate biomarker, not cancer incidence or mortality.
It has been reported that gallic acid is effective against nervous system disorders including Alzheimer's disease, Parkinson's disease, ischemia and reperfusion, depression, and anxiety. The findings of a neurobiological review suggest that gallic acid can be used to manage several neurological diseases and disorders such as Alzheimer's disease, Parkinson's disease, strokes, sedation, depression, psychosis, neuropathic pain, anxiety, and memory loss, as well as neuroinflammation.
The mechanisms proposed include: the primary effects of gallic acid responsible for its neuroprotection potential involve decreased accumulation and density of the beta-amyloid peptide (relevant to Alzheimer's disease). Gallic acid mitigates the impairment of the mitochondrial membrane potential and decreases intracellular ROS levels and apoptosis triggered by 6-OHDA in SH-SY5Y cells, as observed in in vitro experiments (relevant to Parkinson's disease). Gallic acid demonstrates advanced neuroprotective effects by mitigating ferroptosis (via rescuing GPX4 activity) and inhibiting tau aggregation (specifically liquid-liquid phase separation, LLPS).
However, according to database reports and current literature, gallic acid may be considered a potential lead compound to treat neurological diseases and disorders, but more preclinical and clinical studies are required to establish it as a neuroprotective drug. Its neurological use is limited due to inadequate pharmacokinetic characteristics, including poor absorption, poor distribution, poor ability to cross the blood–brain barrier, low bioavailability, and rapid elimination.
Research findings indicate that gallic acid can effectively reduce non-alcoholic liver injury, alcoholic liver disease, hepatic fibrosis, drug-induced liver injury, and liver cancer. In vivo models have provided convincing evidence that gallic acid ameliorated liver toxicity induced by CCl4, antineoplastic drugs, NSAIDs, alcohols, biotoxins, antidepressants, anti-tuberculosis drugs, and other environmental toxins. These findings are primarily from animal and cellular research. Given the extensive evidence and expert recommendations for the use of gallic acid and its derivatives in treating liver diseases, it is imperative to further investigate their pharmacological effects, mechanisms, and potential significance in the management of these conditions.
In traditional medicine, gallic acid has been used to treat diseases such as diarrhea, dysentery, and internal bleeding, as well as to reduce inflammation and other gastrointestinal diseases. This compound has been reported to have therapeutic activities in gastrointestinal disorders in preclinical research, including antiulcer activity in animal models. Clinical human data specifically for gastrointestinal conditions using isolated gallic acid were not identified in the reviewed literature.
Reviews highlight gallic acid's role as an anti-arthritis agent among its multifaceted health benefits. With prominent anti-inflammatory and antioxidant properties, gallic acid effectively mitigates inflammation and oxidative stress and plays a significant role in modulating various cellular processes and biological activities, ultimately inhibiting the progression of pathogenesis. Evidence in this area remains at the preclinical stage.
Several beneficial effects are reported for gallic acid, including antioxidant, anti-inflammatory, and antineoplastic properties; this compound has been reported to have therapeutic activities in gastrointestinal, neuropsychological, metabolic, and cardiovascular disorders. Reviews explore the multifaceted health benefits of gallic acid, highlighting its role as antidiabetic, anti-obesity, anti-arthritic, hepatoprotective, cardioprotective, and neuroprotective — and additionally discuss its impact on the respiratory, digestive, and reproductive systems.
For gastrointestinal problems, gallic acid has been commonly found in various herbal preparations such as infusions and teas made from leaves and fruits rich in gallic acid; for the treatment of wounds and skin infections, topical ointments and powders have been used.
The following dosages are those reported in specific studies:
The clinical application of gallic acid is limited by a shortage of human trials, low bioavailability, and an inadequate understanding of its mechanisms of action and optimal dosage. No universal recommended human supplemental dose has been established by regulatory authorities.
According to pharmacokinetic studies, the absorption and elimination of gallic acid after oral administration are fast, while structural optimization or dosage form adjustment of gallic acid is beneficial to increase its bioavailability. Pharmacokinetic studies have shown that gallic acid is quickly absorbed and eliminated when taken orally, which restricts its use in development. However, the bioavailability of gallic acid can be increased by optimizing its structure or changing its form of administration.
Gallic acid is safe and efficient, but its pharmacokinetic features — for instance, low absorption, poor bioavailability, and rapid elimination — limit its use. To overcome these limitations, well-designed clinical trials, in vivo studies, and advanced nanoformulation approaches are required to enhance bioavailability, elucidate mechanisms of action, and increase knowledge of safety and long-term toxicity.
Researchers have explored nanoformulation approaches to address these limitations. The synergistic effects of gallic acid when used in combination with other drugs/compounds and nanoformulation approaches that improve its therapeutic efficacy are active areas of investigation.
According to toxicology studies conducted on a range of animals and clinical trials, gallic acid rarely exhibits toxicity or side effects. The oral LD50 value is 5,000 mg/kg in rabbits and greater than 2,000 mg/kg in mice. Limited information is available regarding the long-term toxicity of gallic acid; hematological studies showed no discrepancies in serum biomarkers such as ALT, AST, GGT, and ACP. A high dose of 900 mg/kg gallic acid administered orally to Swiss albino mice daily for 28 days showed no significant morphological and behavioral alterations, and histopathological findings proved the safety of gallic acid.
Fischer rats orally administered 0%–5% gallic acid for 13 weeks showed toxic effects following 5% in females and 0.6% in males, including anemia (reduction of red blood cell counts, hematocrit, and hemoglobin concentration, and an increase in reticulocytes) and liver cell hypertrophy. Gallic acid exhibits anti-tumor properties by inducing apoptosis in cancerous cell lines; however, it can also be harmful to normal cells by causing chemical changes in the gallic acid molecule at high concentrations.
Gallic acid, as the end product of hydrolysis of tea tannins, is believed to be responsible for the lowered iron absorption resulting from excessive tea ingestion. Gallic acid forms a 3:1 complex with iron in the pH range 4–6. Gallic acid combines with minerals such as zinc, calcium, and iron to form insoluble complexes that disturb other bioactive substances. This interaction is practically relevant: consuming gallic acid-rich foods or supplements alongside iron-rich foods or iron supplements may reduce the absorption of dietary iron. The same chelation property may, in some contexts, be therapeutically beneficial in cases of iron overload.
Gallic acid functions as a selective pro-oxidant in cancer cell lines to induce apoptosis. This pro-oxidant switch at elevated concentrations is a double-edged property: while exploited for anticancer mechanisms in vitro, high doses could theoretically cause oxidative stress in normal tissues. This has been noted in the anticancer literature but has not been characterized as a clinical adverse event in human supplemental use at typical dietary doses.
High supplemental doses of gallic acid have been noted to potentially cause GI distress, as referenced in the context of food-first approaches being safest.
Gallic acid's neurological application is limited by its poor ability to cross the blood–brain barrier, in addition to poor absorption, poor distribution, low bioavailability, and rapid elimination.
Available data are limited to few studies assessing the treatment effects of gallic acid in human subjects to confirm its therapeutic outcomes. Clinical trials are urgently needed to investigate the safety and efficacy of gallic acid treatment in human beings. The clinical application of gallic acid is limited by a shortage of human trials, low bioavailability, and an inadequate understanding of its mechanisms of action and optimal dosage.
Health conditions that Gallic acid may help support.
Gallic acid (GA) is a trihydroxybenzoic acid polyphenol with well-characterized antioxidant properties, acting through direct free-radical scavenging, inhibition of lipid peroxidation, and activation of the Nrf2/ARE pathway to upregulate endogenous antioxidant enzymes (SOD, CAT, GPx) and glutathione. A placebo-controlled pilot study in type 2 diabetes patients (15 mg/day for 7 days) demonstrated significant reductions in oxidized DNA bases, oxidized LDL, and C-reactive protein. The bulk of mechanistic evidence remains preclinical, and large-scale human trials are lacking.
Gallic acid is a phenolic acid found in multiple plants used for periodontal disease including Triphala, pomegranate, and green tea. It demonstrates antimicrobial activity against periodontal pathogens and anticandidal properties relevant to oral biofilm control. Gallic acid is identified as the primary anticandidal component in Triphala, which has clinical evidence for gingival and periodontal conditions.
Body systems that Gallic acid may help support.
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