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Theaflavin 3,3′-digallate


  • Brand : BIOFRON

  • Catalogue Number : BD-P0630

  • Specification : 98.0%(HPLC)

  • CAS number : 30462-35-2

  • Formula : C43H32O20

  • Molecular Weight : 868.7

  • PUBCHEM ID : 135403795

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



Brown-yellow powder

Botanical Source

Structure Type



Standards;Natural Pytochemical;API




8-Gingerol/(3,4,5-Trihydroxy-6-oxo-6H-benzo[7]annulene-1,8-diyl)bis[(2R,3R)-5,7-dihydroxy-3,4-dihydro-2H-chromene-2,3-diyl] bis(3,4,5-trihydroxybenzoate)/theaflavin 3,3'-O-digallate/Theaflavin-3,3'-digallate/theaflavin-3,3'-di-O-gallate/theaflavin 3,3'-gallate/Benzoic acid, 3,4,5-trihydroxy-, (3,4,5-trihydroxy-6-oxo-6H-benzocycloheptene-1,8-diyl)bis[(2R,3R)-3,4-dihydro-5,7-dihydroxy-2H-1-benzopyran-2,3-diyl] ester/Theaflavin digallate/TF-3/Theaflavin 3,3'-digallate


[(2R,3R)-2-[1-[(2R,3R)-5,7-dihydroxy-3-(3,4,5-trihydroxybenzoyl)oxy-3,4-dihydro-2H-chromen-2-yl]-3,4,6-trihydroxy-5-oxobenzo[7]annulen-8-yl]-5,7-dihydroxy-3,4-dihydro-2H-chromen-3-yl] 3,4,5-trihydroxybenzoate


2.0±0.1 g/cm3



Flash Point

402.9±27.8 °C

Boiling Point

1324.7±65.0 °C at 760 mmHg

Melting Point



InChl Key


WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:30462-35-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




Recent evidence indicates that ovarian cancer stem cells (CSCs) are responsible for ovarian cancer recurrence and drug resistance, resulting in the low long-term survival rate of patients with advanced ovarian cancer. We aimed to study the inhibitory effect of theaflavin-3, 3′-digallate (TF3), a black tea polyphenol on ovarian CSCs. Here, we showed that TF3 inhibited the proliferation of A2780/CP70 and OVCAR3 tumorshpere cells by suppressing their cell viability and colony formation capacity. TF3 inhibited the tumorsphere formation capacity of A2780/CP70 and OVCAR3 CSCs in serum-free and non-adherent conditions. TF3 inhibited A2780/CP70 and OVCAR3 CSCs isolated from tumorspheres by decreasing their cell viability and upregulating the protein expression of caspase-3 and -7 in the cells. We also revealed that TF3 inhibited ovarian CSCs through Wnt/β-catenin signaling pathway. Our results suggested that TF3 could inhibit ovarian CSCs and might be a potential agent for eradicating ovarian cancer.


3’-digallate; ALDH; anti-proliferation; ovarian cancer stem cell; theaflavin-3; β-Catenin.


Theaflavin-3, 3'-digallate Inhibits Ovarian Cancer Stem Cells via Suppressing Wnt/β-Catenin Signaling Pathway


Haibo Pan # 1 2 , Eunhye Kim # 1 , Gary O Rankin 3 , Yon Rojanasakul 4 , Youying Tu 1 , Yi Charlie Chen 2

Publish date

2018 Nov




Peri-implant osteolysis (PIO) and the following aseptic loosening is the leading cause of implant failure. Emerging evidence suggests that receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclast formation and osteoclastic bone resorption are responsible for particle-stimulated PIO. Here, we explored the effect of theaflavin-3,3′-digallate (TF3) on titanium particle-induced osteolysis in vivo and in vitro. Twenty-eight male C57BL/6 mice were randomly separated into four groups: sham control (sham), titanium particles only (titanium), titanium particles with low TF3 concentration (low-TF3, 1mg/kg TF3), and titanium particles with high TF3 concentration (high-TF3, 10mg/kg TF3). Two weeks later, micro-computed tomography and histological analysis were performed. Bone-marrow-derived macrophages and RAW264.7 murine macrophages were applied to examine osteoclast formation and differentiation. TF3 significantly inhibited titanium particle-induced osteolysis and prevented bone destruction compared with titanium group. Interestingly, the number of mature osteoclasts reduced after treatment with TF3 in vivo, suggesting osteoclast formation might be inhibited by TF3. In vitro, TF3 suppressed osteoclast formation, polarization and osteoclastic bone resorption by specifically targeting the RANKL-induced ERK signal pathway. Collectively, these results suggest that TF3, a natural active compound derived from black tea, is a promising candidate for the treatment of osteoclast-related osteolytic diseases, such as wear debris-induced PIO.
Statement of significance: Total joint arthroplasty is widely accepted for the treatment of end-stage joint diseases. However, it is reported that aseptic loosening, initiated by peri-implant osteolysis, is the major reason for prosthesis failure. Although the pathophysiology of PIO remains unclear, increasing evidence indicates that osteoclasts are excessively activated at the implant site by wear debris from materials. Here, we demonstrated that theaflavin-3,3′-digallate, a natural active compound derived from black tea, inhibited osteoclast formation and osteoclastic bone resorption mainly via suppressing the ERK pathway. Moreover, the findings of this study have confirmed for the first time that theaflavin-3,3′-digallate has a protective effect on particle-induced osteolysis in a mouse calvarial model, thus preventing bone loss. These results indicate that theaflavin-3,3′-digallate may be a suitable therapeutic agent to treat wear debris-induced peri-implant osteolysis.


3’-digallate; ALDH; anti-proliferation; ovarian cancer stem cell; theaflavin-3; β-Catenin.


Theaflavin-3,3'-digallate Represses Osteoclastogenesis and Prevents Wear Debris-Induced Osteolysis via Suppression of ERK Pathway


Xuanyang Hu 1 , Zichuan Ping 1 , Minfeng Gan 1 , Yunxia Tao 1 , Liangliang Wang 1 , Jiawei Shi 1 , Xiexing Wu 1 , Wen Zhang 2 , Huilin Yang 1 , Yaozeng Xu 3 , Zhirong Wang 4 , Dechun Geng 5

Publish date

2017 Jan 15




Inflammation is a defensive response against various harmful stimuli and stress conditions, such as tissue injury and one of the most common pathological processes occurring in human diseases. Theaflavin-3,3′-digallate, one of the theaflavins present in black tea, exhibits several bioactive properties, including the ability to lower the incidence of coronary heart disease, a positive effect on the bone mineral density, and the ability to prevent cancer. The aim of this study was to evaluate whether theaflavin-3,3′-digallate could reduce the production of pro-inflammatory cytokines in vivo and in vitro and ameliorate acute lung injury (ALI) in a mouse model. In this study, we demonstrated that theaflavin-3,3′-digallate suppressed the lipopolysaccharide (LPS)-induced phosphorylation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase in RAW 264.7 macrophages. In addition, we also showed that theaflavin-3,3′-digallate inhibited the expression of tumor necrosis factor alpha, interleukin -1 beta, and interleukin 6 in phorbol myristate acetate -primed U937 and RAW 264.7 cells. Furthermore, theaflavin-3,3′-digallate treatment attenuated the severity of LPS-induced ALI in mice. These results suggested that theaflavin-3,3′-digallate might be a potential therapeutic candidate for the treatment of inflammation and inflammatory diseases.


Acute lung injury; Inflammation; Theaflavin-3,3′-digallate Lipopolysaccharide; Theaflavins.


In Vitro and in Vivo Anti-Inflammatory Effects of theaflavin-3,3'-digallate on Lipopolysaccharide-Induced Inflammation


Yanting Wu 1 , Fujun Jin 1 , Yiliang Wang 2 , Feng Li 2 , Lu Wang 1 , Qiaoli Wang 1 , Zhe Ren 1 , Yifei Wang 3

Publish date

2017 Jan 5

Description :

Theaflavin 3,3'-digallate (TF3), the typical pigment in black tea, is a good antitumor agent. Theaflavin 3,3'-digallate is generally regarded as the effective component for the inhibitory effects against carcinogenesis without adverse side effects by affecting multiple signal transduction pathways, such as upregulating p53 and p21, inhibiting phosphorylation of the cell survival protein Akt and MAPK pathway, downregulation of NF-κB, shifting the ratio between pro-/antiapoptotic proteins. Theaflavin 3,3'-digallate causes a rapid and sustained decrease in phospho-ERK1/2 and -MEK1/2 protein expression. Theaflavin 3,3'-digallate inhibits HCT116 cell growth with an IC50 of 17.26 μM[1].