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  • Brand : BIOFRON

  • Catalogue Number : BF-T2019

  • Specification : 98%

  • CAS number : 4192-90-9

  • Formula : C21H24O10

  • Molecular Weight : 436.413

  • PUBCHEM ID : 6451798

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

herbs of Lithocarpus pachyphyllus

Structure Type



Standards;Natural Pytochemical;API




1-Propanone, 1-[4-(β-D-glucopyranosyloxy)-2,6-dihydroxyphenyl]-3-(4-hydroxyphenyl)-/3,5-Dihydroxy-4-[3-(4-hydroxyphenyl)propanoyl]phenyl β-D-glucopyranoside/p-Phloridzin/phloretin-4-D-glucoside/T6OTJ BOR CQ EQ DV2R DQ&& CQ DQ EQ F1Q &&β-D-Gluco Form/p-Phlorizin/1-Propanone, 1-(4-(β-D-glucopyranosyloxy)-2,6-dihydroxyphenyl)-3-(4-hydroxyphenyl)-/Trilobatin/1-(4-(β-D-Glucopyranosyloxy)-2,6-dihydroxyphenyl)-3-(4-hydroxyphenyl)-1-propanone




1.6±0.1 g/cm3


Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

277.1±26.4 °C

Boiling Point

787.9±60.0 °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#:4192-90-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




The study determined the comparative antioxidant capacities of five similar dihydrochalcones: phloretin, phloridzin, trilobatin, neohesperidin dihydrochalcone, and naringin dihydrochalcone. In the ferric-reducing antioxidant power (FRAP) assay, the antioxidant activities of pairs of dihydrochalcones had the following relationship: phloretin > phloridzin, phloretin > trilobatin, trilobatin > phloridzin, trilobatin > naringin dihydrochalcone, and neohesperidin dihydrochalcone > naringin dihydrochalcone. Similar relative antioxidant levels were also obtained from 1,1-diphenyl-2-picryl-hydrazl radical (DPPH•)-scavenging, 2,2′-azino-bis(3-ethylbenzo-thiazoline-6-sulfonic acid) (ABTS•+)-scavenging, and superoxide radical (•O2−)-scavenging assays. Using ultra-performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight tandem mass spectrometry (UPLC−ESI−Q−TOF−MS/MS) analysis for the reaction products with DPPH•, phloretin, phloridzin, and trilobatin were found to yield both dihydrochalcone-DPPH adduct and dihydrochalcone-dihydrochalcone dimer, whereas naringin dihydrochalcone gave a naringin dihydrochalcone-DPPH adduct, and neohesperidin dihydrochalcone gave a dimer. In conclusion, the five dihydrochalcones may undergo redox-based reactions (especially electron transfer (ET) and hydrogen atom transfer (HAT)), as well as radical adduct formation, to exert their antioxidant action. Methoxylation at the ortho-OH enhances the ET and HAT potential possibly via p-π conjugation, whereas the glycosylation of the -OH group not only reduces the ET and HAT potential but also hinders the ability of radical adduct formation. The 2′,6′-di-OH moiety in dihydrochalcone possesses higher ET and HAT activities than the 2′,4′-di-OH moiety because of its resonance with the adjacent keto group.


antioxidant, dihydrochalcone, naringin dihydrochalcone, neohesperidin dihydrochalcone, phloretin, phloridzin, trilobatin


Antioxidant Structure-Activity Relationship Analysis of Five Dihydrochalcones


Xican Li,1,2,* Ban Chen,1,2 Hong Xie,1,2 Yuhua He,1 Dewei Zhong,1 and Dongfeng Chen3,4,*

Publish date

2018 May




Studies have indicated that Na+-d-glucose co-transporter (SGLT) inhibitors had anti-proliferative activity by attenuating the uptake of glucose in several tumor cell lines. In this study, the molecular docking showed that, trilobatin, one of the dihydrochalcones from leaves of Lithocarpus polystachyus Rehd., might be a novel inhibitor of SGLT1 and SGLT2, which evidently attenuated the uptake of glucose in vitro and in vivo. To our surprise, we observed that trilobatin did not inhibit, but promoted the proliferation of human hepatoblastoma HepG2 and Huh 7 cells when it was present at high concentrations. At the same time, incubation with high concentrations of trilobatin arrested the cell cycle at S phase in HepG2 cells. We also found that treatment with trilobatin had no significant effect on the expression of hepatitis B x-interacting protein (HBXIP) and hepatocyte nuclear factor (HNF)-4α, the two key regulators of hepatocyte proliferation. Taken together, although trilobatin worked as a novel inhibitor of SGLTs to attenuate the uptake of glucose, it also selectively induced the cell proliferation of HepG2 cells, suggesting that not all the SGLT inhibitors inhibited the proliferation of tumor cells, and further studies are needed to assess the anti-cancer potentials of new glucose-lowering agents.


Anti-tumor; Cell proliferation; Na+-d-glucose co-transporter (SGLT) inhibitors; Trilobatin


Trilobatin, a Novel SGLT1/2 Inhibitor, Selectively Induces the Proliferation of Human Hepatoblastoma Cells.


Wang L1, Liu M2, Yin F3, Wang Y4, Li X5, Wu Y6, Ye C7, Liu J8.

Publish date

2019 Sep 18;




Oxidative stress-induced neuronal cell damage is a crucial factor in the pathogenesis of mitochondria-associated neurological diseases. Therefore, elimination of overproduction of mitochondrial reactive oxygen species (mtROS) may be a potential strategy for prevention and treatment of neurological diseases. In the present study, the neuroprotective effects of trilobatin (TLB), a novel small molecule monomer derived from Lithocarpus polystachyus Rehd, and its underlying mechanisms were investigated in vitro using hydrogen peroxide (H2O2)-induced oxidative stress model in a neuron-like PC12 cell. The findings revealed that pre-treatment with TLB dramatically concentration-dependently suppressed H2O2-induced PC12 cells damage by enhancing cell viability, repressed reduction of mitochondrial membrane potential (MMP) and decreased mtROS overgeneration, thereby deferring cell apoptosis. Further study demonstrated that TLB not only increased the enzymatic activities of glutathione peroxidase (GPx), isocitrate dehydrogenase 2 (IDH2),superoxide dismutase 2 (SOD2) and deacetylation of SOD2, but also activated silent mating-type information regulation 2 homolog 3 (Sirt3) within the mitochondria and thereby upregulating forkheadboxO3a (FoxO3a), which regulated mitochondrial DNA genes, then led to improving complex I activity and adenosine triphosphate (ATP) synthesis. What’s more, TLB up-regulated p-adenosine monophosphate-activated protein kinase (AMPK) level, the expression of peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α), and ERRα. Intriguingly, TLB failed to mitigate H2O2-induced PC12 injury in the presence of the AMPK inhibitor (Compound C), indicating that the beneficial effects of TLB on the regulation of mtROS homeostasis were reliance on AMPK -Sirt3 signaling pathway. Moreover, TLB also facilitated nuclear factor erythroid 2-related factor 2 (Nrf2) and promoted antioxidant gene expression in turn, and knockdown of Nrf2 by siRNA dramatically reduced the neuroprotective effects of TLB. Notably, AMPK inhibitor abolished the activation of Nrf2 and Sirt3, whereas, knockdown of Nrf2 blocked the upregulation of Sirt3, but it did not affect p-AMPK level. In conclusion, our findings demonstrate that TLB protects against oxidative injury in neuronal PC12 cells through regulating mtROS homeostasis in the first time, which is, at least partly, mediated through the AMPK/Nrf2/Sirt3 signaling pathway.


AMPK; Nrf2; PC12 cells; Sirt3; hydrogen peroxide; trilobatin


Trilobatin Protects Against Oxidative Injury in Neuronal PC12 Cells Through Regulating Mitochondrial ROS Homeostasis Mediated by AMPK/Nrf2/Sirt3 Signaling Pathway.


Gao J1,2, Liu S2, Xu F1, Liu Y2, Lv C2, Deng Y2, Shi J2, Gong Q2.

Publish date

2018 Jul 30;

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