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  • Brand : BIOFRON

  • Catalogue Number : BF-P3013

  • Specification : 98%

  • CAS number : 60-82-2

  • Formula : C15H14O5

  • Molecular Weight : 274.27

  • PUBCHEM ID : 4788

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



Off-white crystalline powder

Botanical Source

Malus pumila

Structure Type



Standards;Natural Pytochemical;API




QR CQ EQ BV2R DQ/1-Propanone, 3-(4-hydroxyphenyl)-1-(2,4,6-trihydroxyphenyl)-/Dihydronaringenin/2',4',6',4-tetrahydroxydihydrochalcone/3-(4-Hydroxyphenyl)-1-(2,4,6-trihydroxyphenyl)-1-propanone/1887240/β-(p-Hydroxyphenyl)phloropropiophenone/phloretol/4,2',4',6'-tetrahydroxydihydrochalcone/b-(p-Hydroxyphenyl)phloropropiophenone/3-(4-Hydroxyphenyl)-1-(2,4,6-trihydroxyphenyl)propan-1-one/Phloretin




1.4±0.1 g/cm3



Flash Point

291.1±20.8 °C

Boiling Point

534.4±29.0 °C at 760 mmHg

Melting Point

~260 °C


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#:60-82-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Toll-like receptor 2 (TLR2) responses are involved in various inflammatory immune disorders. Phloretin is a naturally occurring dietary flavonoid that is abundant in fruit. Here, we investigated whether the anti-inflammatory activity of phloretin is mediated through TLR2 pathways, and whether phloretin acts as an inhibitor of TLR2/1 heterodimerization using the TLR2/1 agonist Pam₃CSK₄. We tested the effects of phloretin on tumor necrosis factor (TNF)-α production induced by various TLRs using known TLR-specific agonists. Phloretin significantly inhibited Pam₃CSK₄-induced TRL2/1 signaling in Raw264.7 cells compared to TLR signaling induced by the other agonists tested. Therefore, we further tested the effects of phloretin in human embryonic kidney (HEK) 293-hTLR2 cells induced by Pam₃CSK₄, and confirmed that phloretin has comparable inhibition of TLR2/1 heterodimerization to that induced by the known TLR2 inhibitor CU-CPT22. Moreover, phloretin reduced the secretion of the inflammatory cytokines TNF-α and interleukin (IL)-8 in Pam₃CSK₄-induced HEK293-hTLR2 cells, whereas it did not significantly reduce these cytokines under Pam₂CSK₄-induced activation. Western blot results showed that phloretin significantly suppressed Pam₃CSK₄-induced TLR2 and NF-κB p65 expression. The molecular interactions between phloretin and TLR2 were investigated using bio-layer interferometry and in silico docking. Phloretin bound to TLR2 with micromolar binding affinity, and we proposed a binding model of phloretin at the TLR2⁻TLR1 interface. Overall, we confirmed that phloretin inhibits the heterodimerization of TLR2/1, highlighting TLR2 signaling as a therapeutic target for treating TLR2-mediated inflammatory immune diseases.


TLR1; TLR2; dietary flavonoid; inflammation; inhibitor; phloretin


Phloretin as a Potent Natural TLR2/1 Inhibitor Suppresses TLR2-Induced Inflammation.


Kim J1, Durai P2, Jeon D3, Jung ID4, Lee SJ5, Park YM6, Kim Y7.

Publish date

2018 Jul 5




Reactive oxygen species generated as a by-product in metabolism play a central role in the development of obesity and obesity-related metabolic complications. The objective of the current study is to explore the possibility to block obesity and improve metabolic homeostasis via phloretin, a natural antioxidant product from apple tree leaves and Manchurian apricot. Both preventive and therapeutic activities of phloretin were assessed using a high-fat diet-induced obesity mouse model. Phloretin was injected intraperitoneally twice weekly into regular and obese mice fed a high-fat diet. The effects of phloretin treatment on body weight and composition, fat content in the liver, glucose and lipid metabolism, and insulin resistance were monitored and compared to the control animals. Phloretin treatment significantly blocks high-fat diet-induced weight gain but did not induce weight loss in obese animals. Phloretin improved glucose homeostasis and insulin sensitivity and alleviated hepatic lipid accumulation. RT-PCR analysis showed that phloretin treatment suppresses expression of macrophage markers (F4/80 and Cd68) and pro-inflammatory genes (Mcp-1 and Ccr2) and enhances adiponectin gene expression in white adipose tissue. In addition, phloretin treatment elevated the expression of fatty acid oxidation genes such as carnitine palmitoyltransferase 1a and 1b (Cpt1a and Cpt1b) and reduced expression of monocyte chemoattractant protein-1 (Mcp-1), de novo lipogenesis transcriptional factor peroxisome proliferator-activated receptor-γ 2 (Pparγ2), and its target monoacylglycerol O-acyltransferase (Mgat-1) genes. These results provide direct evidence to support a possible use of phloretin for mitigation of obesity and maintenance of metabolic homeostasis.


antioxidant; inflammation; insulin resistance; obesity; phloretin


Phloretin Prevents High-Fat Diet-Induced Obesity and Improves Metabolic Homeostasis.


Alsanea S1, Gao M1, Liu D2.

Publish date

2017 May




Phloretin (Phl) is a dihydrochalcone flavonoid with significant cytoprotective properties; e.g., free radical trapping, electrophile scavenging. Based on this, it has been suggested that Phl might be useful in the treatment of pathogenic processes and prevention of drug toxicities. Therefore, we determined the ability of Phl to provide route- and dose-dependent hepatoprotection in a mouse model of acetaminophen (APAP) overdose. Intraperitoneal (i.p.) administration of Phl produced a bimodal effect; i.e., the highest dose (2.40 mmol/kg) did not prevent APAP-induced lethality, whereas lower doses (0.2-0.4 mmol/kg) afforded modest hepatoprotection. When given alone, the highest i.p. Phl dose was lethal within 24 h, whereas the lower doses were not toxic. Oral Phl (0.40-2.40 mmol/kg) did not prevent APAP-induced hepatotoxicity. The highest oral dose given alone (2.4 mmol/kg) produced 64% lethality, whereas lower doses were not lethal. This toxicity profile was reflected in a study using APAP-exposed isolated mouse hepatocytes, which showed that the Phl pharmacophores, 1,3,5-trihydroxyacetophenone (PG) and 2′,4′,6′-trihydroxyacetophenone (THA) where protective. Corroborative cell free studies showed that polyphenol protectants prevented glutathione loss mediated by the APAP metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Thus, in spite of possessing cytoprotective attributes, Phl was generally toxic in our APAP models. These and earlier findings suggest that Phl is not a candidate for drug design. In contrast, we have found that the enol-forming pharmacophores, THA and PG, are potential platforms for pharmacotherapeutic development.

Copyright © 2018. Published by Elsevier B.V.


Acetaminophen overdose; Drug-induced toxicity; Enol-based cytoprotectants; Hepatoprotection; Phytopolyphenol


Phloretin cytoprotection and toxicity.


Geohagen BC1, Korsharskyy B1, Vydyanatha A1, Nordstroem L2, LoPachin RM3.

Publish date

2018 Dec 25

Description :

Phloretin(NSC 407292; RJC 02792) is a dihydrochalcone, a type of natural phenols. Phloretin inhibits the active transport of glucose into cells by SGLT1 and SGLT2.IC50 Value: 49 +/- 12 microM [4]Target: SGLT1/2in vitro: Phlorizin blocks glucose transport across the renal tubule at concentrations in renal blood and tissue in the range of 10-5 to 10-7 M [1]. PT significantly enhanced glycerol release and inhibited the adipogenesis-related transcription factors. PT also promoted phosphorylation of AMP-activated protein kinase and increased activity of adipose triglyceride lipase and hormone-sensitive lipase in 3T3-L1 cells [2]. Phloretin induced obvious cytotoxicity against BEL-7402 cells with IC50 of 89.23 microg/mL. The growth curve demonstrated decreased growth of the cells as phloretin concentration increased [3]. D-glucose-transport activity was observed with a Km for D-glucose of 3.4 +/- 0.2 mM (mean +/- S.E.M.) and was inhibited by cytochalasin B (IC50= 0.44 +/- 0.03 microM), HgCl2 (IC50)= 3.5 +/- 0.5 microM), phloretin (IC50= 49 +/- 12 microM) and phloridzin (IC50= 355 +/- 67 microM) [4].in vivo: The effect of phloridzin orally doses 5, 10, 20 and 40 mg/kg body weight on diabetes was tested in a streptozotocin-induced rat model of diabetes type 1. From beneficial effect of this compound is significant reduction of blood glucose levels and improve dyslipidemia in diabetic rats [5].