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Product name: Theaflavin-3-gallate
Synonym name:
Catalogue No.: BP1387
Cas No.: 30462-34-1
Formula: C36H28O16
Mol Weight: 716.604
Botanical Source: Black Tea
Physical Description:
Type of Compound: Polyphenols
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Storage: Store in a well closed container, protected from air and light. Put into refrigerate or freeze for long term storage.
Whenever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20℃. Generally, these will be useable for up to two weeks.
The product could be supplied from milligrams to grams
Inquire for bulk scale.
Description:
Theaflavin-3-gallate has anticancer and apoptotic effects in non-small cell lung carcinoma, it acts as prooxidants and induce oxidative stress, with carcinoma cells more sensitive than normal fibroblasts. Theaflavin-3-gallate can play a role in decreased intestinal cholesterol absorption via inhibition of micelle formation.
References:
Basic Clin Pharmacol Toxicol. 2008 Jul;103(1):66-74.
Theaflavin-3-gallate and theaflavin-3'-gallate, polyphenols in black tea with prooxidant properties.
This study compared the in vitro responses of human gingival fibroblasts and of carcinoma cells derived from the tongue to Theaflavin-3-gallate (TF-2A) and theaflavin-3'-gallate (TF-2B), polyphenols in black tea.
METHODS AND RESULTS:
The antiproliferative and cytotoxic effects of the theaflavin monomers were more pronounced to the carcinoma, than to the normal, cells. In phosphate buffer at pH 7.4, the theaflavins generated hydrogen peroxide and the superoxide anion, suggesting that their mode of toxicity may be due, in part, to the induction of oxidative stress. In a cell-free assay, Theaflavin-3-gallate and TF-2B reacted directly with reduced glutathione (GSH), in a time- and concentration-dependent manner. Intracellular storages of GSH were depleted on treatment of the cells with the theaflavin monomers. Depletion of intracellular GSH was more extensive with Theaflavin-3-gallate than with TF-2B and was more pronounced in the carcinoma, than in the normal, cells. The toxicities of the theaflavins were potentiated when the cells were cotreated with the GSH depleter, d,l-buthionine-[S,R]-sulfoximine. In the presence of catalase, pyruvate and divalent cobalt, all scavengers of reactive oxygen species, the cytotoxicities of the theaflavins were lessened. Theaflavin-3-gallate and TF-2B induced lipid peroxidation in the carcinoma cells, whereas in the fibroblasts, peroxidation was evident upon exposure to Theaflavin-3-gallate, but not to TF-2B.
CONCLUSIONS:
These studies demonstrated that the black tea theaflavin monomers, Theaflavin-3-gallate and TF-2B, act as prooxidants and induce oxidative stress, with carcinoma cells more sensitive than normal fibroblasts.
Bangl. J. Pharmacol., 2015, 10(4):3047-53.
Anticancer and apoptotic effects of theaflavin-3-gallate in non-small cell lung carcinoma.
The objective was to determine the antiproliferative and apoptotic effects of Theaflavin-3-gallate in human non-small cell lung cancer cells (A-549) along with determining the effect on cell cycle phase distribution, cell migration and invasion.
METHODS AND RESULTS:
Cell viability was determined by MTT assay while as phase contrast and fluorescence microscopies were involved to study apoptotic morphologi-cal features in these cells. Flow cytometry investigated the effect of Theaflavin-3-gallate on cell cycle phase distribution. Theaflavin-3-gallate treatment led to a substantial cytotoxic effect in A-549 cancer cells with IC50 values of 42.1 μM and 27.9 μM at 24 and 48 hours respectively. Further, 80 and 160 μM dose of Theaflavin-3-gallate induced apoptotic features including chromatin margina-tion and micronuclei presence. The population of cells in G2/M phase increased from 2.7% (control) to 6.8%, 17.2% and finally to 46.5% after treatment with 20, 80 and 160 μM concentration of Theaflavin-3-gallate respectively indicating G2/M phase cell cycle arrest.
HPLC of Theaflavin-3-gallate
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
284.3600
2.0844
2.0843
.0395
1.1572
.0941
Low
89.9048
4.8758
No
No
No
No
Yes
No
0.6
Yes
No
Yes
No
Theaflavin-3-gallate (hereinafter referred to as TF3G) is one of the important theaflavin compounds in black tea and is a derivative of theaflavin monomers. As an important component of tea polyphenols, TF3G has attracted widespread attention in the field of natural product pharmacology in recent years due to its unique biological activity and potential medicinal value. Numerous studies have shown that TF3G not only exhibits significant antioxidant, anti-inflammatory, and antitumor activities, but also effectively resists cell damage caused by ultraviolet B (UVB) rays and regulates the processes of apoptosis and necrosis. Additionally, TF3G exhibits antioxidant effects in cancer cells, inducing oxidative stress and thus exerting anti-cancer effects. Its inhibitory effect on xanthine oxidase (XO) (IC50 7.6 μM) further reveals its potential for treating xanthine-related diseases.
This paper will systematically review the chemical structure and physicochemical properties of TF3G, plant origin, and extraction methods, focusing on its pharmacological activity and mechanism of action, exploring its molecular targets and druggability parameters, and finally looking ahead to its clinical application prospects, providing theoretical basis and reference for in-depth research and drug development of this natural product.
Theaflavin-3-gallate is a theaflavin polyphenolic compound with a molecular formula of C37H30O16 and a molecular weight of 716.6040. Its structure consists of the theaflavin core backbone connected by ester groups of gallate esters, containing multiple phenolic hydroxyl and ester groups, which impart its rich chemical activity. TF3G has a LogP value of 2.0844, indicating moderate lipid solubility, which is beneficial for penetrating cell membranes without being overly hydrophobic, making it suitable for distribution in organisms. Its topological polar surface area (TPSA) is 284.36 Ų, indicating high molecular polarity, which may affect its cell membrane permeability and bioavailability.
Low water solubility (0.0395 mg/mL), which may limit oral absorption and in vivo distribution. TF3G has relatively low blood-brain barrier penetration ability, suggesting its limited role in the central nervous system. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. The Ames test result was 0.6, indicating a low genotoxicity risk and a solid safety foundation.
TF3G is mainly found in black tea (Camellia sinensis) and is an important component of theaflavin compounds during tea fermentation. The fermentation process of black tea produces theaflavins and their derivatives through oxidation and condensation of catechins in the tea, with a relatively high TF3G content.
Traditional extraction methods mostly combine water extraction with organic solvent extraction, followed by high-performance liquid chromatography (HPLC) purification to obtain high-purity TF3G. Modern extraction technologies include ultrasound-assisted extraction, microwave-assisted extraction, and solid-phase extraction, which can improve extraction efficiency and purity. The extraction process typically controls pH, temperature, and fermentation time to optimize TF3G yield.
Additionally, biosynthetic pathway studies have shown that TF3G formation depends on the oxidase activity of catechins in tea. Adjusting fermentation conditions can effectively control TF3G content, providing theoretical guidance for industrial production.
TF3G has a significant protective effect against skin cell damage induced by ultraviolet B (UVB). In vitro cell experiments have shown that TF3G can inhibit UVB-induced apoptosis and necrosis, reduce oxidative stress responses, and maintain cell membrane integrity. Its anti-UVB damage mechanism mainly works by scavenging free radicals, inhibiting the release of inflammatory factors, and regulating cellular signaling pathways, providing natural active ingredients for the development of sunscreens and skin protectants.
Numerous studies have confirmed that TF3G exhibits good anti-proliferative and pro-apoptotic effects across various tumor cell lines. It induces oxidative stress within cancer cells, disrupts the internal redox balance, and promotes apoptosis. TF3G can also inhibit cancer cell migration and invasion, blocking the process of tumor metastasis.
In vivo tumor models, TF3G has demonstrated potential to inhibit tumor growth with relatively low side effects. Its antitumor activity involves multiple signaling pathways and key molecular targets, demonstrating the synergistic effect of multiple targets.
TF3G has typical polyphenolic antioxidant properties, scavenging free radicals and protecting normal cells from oxidative damage. However, in the cancer cell environment, TF3G exhibits pro-oxidant properties, inducing excessive intracellular reactive oxygen species (ROS) and triggering apoptosis. This selective regulation of redox status is a key foundation for its antitumor effects.
Xanthine oxidase (XO) is a key enzyme in purine metabolism and is involved in uric acid production. TF3G's inhibitory effect on XO (IC50 7.6 μM) suggests its potential therapeutic value in diseases such as hyperuricemia and gout. By inhibiting XO activity, TF3G can reduce uric acid production and alleviate related inflammatory responses.
The pharmacological effects of TF3G involve multiple molecular targets and signaling pathways, forming a complex regulatory network.
TF3G activates the caspase family by modulating endogenous apoptosis signaling pathways, promoting programmed cell death. At the same time, TF3G inhibits necrotizing cell death, reduces inflammatory responses, and protects tissue function.
TF3G exerts antioxidant effects in normal cells, protecting them from ROS damage; In cancer cells, it induces excessive accumulation of ROS, triggering oxidative stress-mediated cell death. This dual regulatory mechanism provides the molecular basis for its selective antitumor activity.
TF3G has a relatively large molecular weight (716.6 Da), which exceeds the ideal range of traditional oral drugs (typically < 500 Da), potentially affecting its oral absorption. A high TPSA value (284.36 Ų) indicates strong polarity, further limiting membrane penetration and oral bioavailability.
The LogP value was 2.0844, indicating moderate lipid solubility, which is beneficial for distribution in the body. Low water solubility (0.0395 mg/mL) may limit its solubility and absorption rate, so bioavailability needs to be improved through formulation improvements.
The low penetration ability of the blood-brain barrier suggests that TF3G is difficult to enter the central nervous system, reducing the risk of central toxicity but limiting its application in neurological diseases.
The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. Ames trial results showed that it carries a low genotoxicity risk and is relatively safe.
Currently, there is limited research on the systemic pharmacokinetics of TF3G. Previous studies have shown that theaflavin compounds have poor stability in the intestines after oral administration, are easily degraded by metabolic enzymes, and have limited bioavailability. TF3G may be rapidly metabolized through first-pass effects in the liver, affecting plasma concentration and in vivo half-life.
Future research on in vivo pharmacokinetics and metabolic kinetics is needed to clarify their absorption, distribution, metabolism, and excretion (ADME) characteristics, providing a basis for clinical translation.
TF3G, due to its multi-target and multi-mechanism pharmacological activity, shows broad application potential, especially in anti-tumor and UVB damage fields. Its inhibitory effect on xanthine oxidase also provides new approaches for the treatment of gout and related metabolic diseases.
However, TF3G's druggability limits its direct use as an oral drug, requiring modern drug delivery technologies such as nanocarriers, liposomal encapsulation, and structural modification to enhance its bioavailability and targeting.
Future research should focus on the following areas:
Additionally, as a natural product, TF3G has broad potential for food and health product development, serving as an active ingredient in functional beverages and skincare products to meet market demand for natural health products.
Theaflavin-3-gallate, an important member of the black tea theaflavin class, demonstrates significant pharmacological effects such as anti-UVB damage, anti-tumor, and xanthine oxidase inhibition due to its unique chemical structure and diverse biological activities. Its multi-target and multi-mechanism mode of action provides a rich example for pharmacological research of natural products.
Despite challenges in druggability and pharmacokinetics, with the development of modern drug delivery technologies and structural optimization strategies, TF3G is expected to overcome these limitations and become a novel natural drug or adjunct therapy. Future systematic mechanism research and clinical translation work will further promote the application of TF3G in disease prevention and treatment, contributing the wisdom and power of natural products to human health.
Shenshuai
Wenjing
Hedandan
