60-82-2

Basic information

• Product Name: Phloretin
• Synonyms: Phloretin Synonyms 2',4',6'-Trihydroxy-3-(4-hydroxyphenyl)propiophenone;1-Propanone, 3-(4-hydroxyphenyl)-1-(2,4,6-trihydroxyphenyl)-;Phloretin 2',4',6'-Trihydroxy-3-(4-hydroxyphenyl)propiophenone;METHYL-4-4-(4-HYDROXYDIPHENYL METHYL)-PIPERIDINE-1-OXOBUTYL-2,2-DIMETHYLPHENYL ACETIC ACID.FEXOFENADINE INTERMEDIATE;PHLORETIN;PHLORETIN (NATURAL);4,2',4',6'-TETRAHYDROXYDIHYDROCHALCONE;3-[4-HYDROXYPHENYL]-1-[2,4,6-TRIHYDROXYPHENYL]-1-PROPANONE
• CAS NO: 60-82-2
• Molecular Formula: C₁₅H₁₄O₅
• Molecular Weight: 274.27
• EINECS: 200-488-7
• Product Categories: standardized herbal extract;Chalcones;All Inhibitors;Inhibitors;Protein Kinase Inhibitors and Activators;Aromatics;Intermediates & Fine Chemicals;Pharmaceuticals;chemical reagent;pharmaceutical intermediate;phytochemical;reference standards from Chinese medicinal herbs (TCM).
• Mol File: 60-82-2.mol
• Article Data: 22

Chemical Properties

• Melting Point: ~260 °C
• Boiling Point: 337.26°C (rough estimate)
• Flash Point: 291.1 °C
• Appearance: White to beige/Powder
• Density: 1.1827 (rough estimate)
• Vapor Pressure: 1.4E-05mmHg at 25°C
• Refractive Index: 1.573-1.575
• Storage Temp.: 2-8°C
• Solubility: Acetonitrile (Slightly), Methanol (Slightly)
• PKA: 7.16±0.40(Predicted)
• Water Solubility: soluble
• Merck: 14,7326
• BRN: 1887240
• CAS DataBase Reference: Phloretin(CAS DataBase Reference)
• NIST Chemistry Reference: Phloretin(60-82-2)
• EPA Substance Registry System: Phloretin(60-82-2)

Safety Data

• Hazard Codes: Xi
• Statements: 36/37/38
• Safety Statements: 37/39-26-36
• WGK Germany: 3
• F: 3-10
• HazardClass: IRRITANT
• Hazardous Substances Data: 60-82-2(Hazardous Substances Data)

Usage

Chemical Properties

Different sources of media describe the Chemical Properties of 60-82-2 differently. You can refer to the following data:
1. Crystalline Solid
2. White to pale yellow solid.

Uses

Different sources of media describe the Uses of 60-82-2 differently. You can refer to the following data:
1. Phloretin has been used:to study its effect on the 2-[N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-d-glucose (2-NBDG) and 2-[N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-l-glucose (2-NBDLG) uptaketo incubate microvesicles in order to inhibit GLUT1 (glucose transporter 1)-mediated transport in radioactive ligand up-take assayas a component of KRH buffer to stop glucose uptake by trophoblast cells in vitro
2. As glucose transport inhibitor, Phloretin can inhibits protein kinase C and has been shown to inhibit the entry of five enveloped viruses into human fibroblasts.

Definition

ChEBI: Phloretin is a member of the class of dihydrochalcones that is dihydrochalcone substituted by hydroxy groups at positions 4, 2', 4' and 6'. It has a role as a plant metabolite and an antineoplastic agent. It is functionally related to a dihydrochalcone.

General Description

Phloretin is a dihydrochalcone flavonoid with antioxidant activity usually found in apples and apple-derived products. It is extensively used for peroxynitrite scavenging and the inhibition of lipid peroxidation. It has been found to inhibit the growth of several cancer cells and induce apoptosis of B16 melanoma and HL60 human leukemia cells.

Biological Activity

phloretin is a dihydrochalcone, a type of natural phenols which can be found in apple tree leaves and manchurian apricot. phloretin inhibits the active transport of glucose into cells via sodium-glucose linked transporter (sglt) 1 and 2 with ic50 value of 49±12 μm [2].sglts are a family of glucose transporter which is found in the small intestine mucosa (sglt 1) and nephron proximal tubule (sglt 2). they contribute to the renal glucose reabsorption.after treatment of phloretin, differentiated 3t3-l1 cells exhibited significantly enhanced glycerol and the inhibition of adipogenesis-related transcription factor that were regulated by sglts. additionally, phloretin promoted phosphorylation of amp-activated protein kinase and increased activity of adipose triglyceride lipase and hormone-sensitive lipase [1]. when raw 263.7 cells were cultured from differentiated 3t3-l1 cell media, pt suppressed the sglt-associated nuclear transcription factor kappab and mitogen-activated protein kinase pathways [1].in streptozotocin-induced rat model of diabetes type i, oral administration of phloridzin (5/10/20/40 mg/kg/day) resulted in signi?cant reduction of blood glucose levels and improved dyslipidemia. additionally, administration of phloridzin reduced urine volume and water intake in a dose-dependent manner [3].

Biochem/physiol Actions

Reacts with vic-dicarbonyl compounds such as glyoxal and methylglyoxal, preventing cytotoxic conjugation with biological macromolecules.

Purification Methods

Crystallise phloretin from aqueous EtOH. [Zemplen & Bognár Chem Ber 75 1040 1942, Zemplén Chem Ber 76 386 1943, Beilstein 8 IV 3518.]

references

[1] huang w c et al. , phloretin and phlorizin promote lipolysis and inhibit inflammation in mouse 3t3-l1 cells and in macrophage-adipocyte co-cultures. mol nutr food res. 2013, 57: 1807-1817.[2] kasahara t, kasahara m. expression of the rat glut1 glucose transporter in the yeast saccharomyces cerevisiae. biochem j. 1996, 315 ( pt 1):177-182.[3] najafian m, jahromi m z, nowroznejhad m j, phloridzin reduces blood glucose levels and improves lipids metabolism in streptozotocin-induced diabetic rats. mol biol rep. 2012, 39(5): 5299-306.

InChI:InChI=1/C9H10O4/c1-5(10)9-7(11)3-6(13-2)4-8(9)12/h3-4,11-12H,1-2H3

Upstream product

• 108-73-6 3,5-dihydroxyphenol 
• 17362-17-3 3-(p-hydroxyphenyl)propiononitrile 
• 950186-11-5 3-(4-acetoxyphenyl)propanenitrile 
• 25515-46-2 2',4',6',4-tetrahydroxydihydrochalcone 
• 18065-05-9 1-[2,4-bis(benzyloxy)-6-hydroxyphenyl]ethanone 
• 25324-31-6 phloretin-2',4'-di-O-β-D-glucopyranoside 
• 95456-56-7 4-hydroxyphenylpropionyl-CoA 
• 524-14-1 S-(hydrogen malonyl)coenzyme A 
• 67-56-1 methanol 
• 60-81-1 phloridizin 
• 128837-25-2 1-[2,4-bis(ethoxymethoxy)-6-hydroxyphenyl]ethan-1-one 
• 58-98-0 UDP 
• 25515-46-2 naringenin chalcone 
• 501-97-3 4-hydroxyphenylpropionic acid 

Downstream Products

• 42385-89-7 acetic acid 4-[3-oxo-3-(2,4,6-triacetoxy-phenyl)propyl]phenyl ester 
• 160255-00-5 3',5'-dibromophloretin 
• 501-97-3 4-hydroxyphenylpropionic acid 
• 108-73-6 3,5-dihydroxyphenol 
• 76344-03-1 3-(4-acetoxy-phenyl)-1-(2,4-diacetoxy-6-hydroxy-phenyl)-propan-1-one 
• 1133352-99-4 C₂₉H₃₂O₁₄ 
• 123685-24-5 phloretin-2′-O-β-D-glucuronide 
• 58-98-0 UDP 
• 60-81-1 phloridizin 
• 11023-94-2 1-[3-(β-D-glucopyranosyl)-2,4,6-trihydroxyphenyl]-3-(4-hydroxyphenyl)propan-1-one 
• 200878-68-8 C₁₅H₁₃ClO₅ 
• 107585-77-3 5,7-dihydroxy-3-(4′-hydroxybenzyl)chroman-4-one 
• 157405-84-0 3-bromo-phloretin 
• 1005139-34-3 1-(4-hydroxy-2,6-bis-nitrooxy-phenyl)-3-(4-nitrooxy-phenyl)-propan-1-one 

Relevant articles and documents

Neuroprotective Effects of Trilobatin, a Novel Naturally Occurring Sirt3 Agonist from Lithocarpus polystachyus Rehd., Mitigate Cerebral Ischemia/Reperfusion Injury: Involvement of TLR4/NF-κB and Nrf2/Keap-1 Signaling

Aims: Neuroinflammation and oxidative stress are deemed the prime causes of brain injury after cerebral ischemia/reperfusion (I/R). Since the silent mating-type information regulation 2 homologue 3 (Sirt3) pathway plays an imperative role in protecting against neuroinflammation and oxidative stress, it has been verified as a target to treat ischemia stroke. Therefore, we attempted to seek novel Sirt3 agonist and explore its underlying mechanism for stroke treatment both in vivo and in vitro. Results: Trilobatin (TLB) not only dramatically suppressed neuroinflammation and oxidative stress injury after middle cerebral artery occlusion in rats, but also effectively mitigated oxygen and glucose deprivation/reoxygenation injury in primary cultured astrocytes. These beneficial effects, along with the reduced proinflammatory cytokines via suppressing Toll-like receptor 4 (TLR4) signaling pathway, lessened oxidative injury via activating nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways, in keeping with the findings in vivo. Intriguingly, the TLB-mediated neuroprotection on cerebral I/R injury was modulated by reciprocity between TLR4-mediated neuroinflammatory responses and Nrf2 antioxidant responses as evidenced by molecular docking and silencing TLR4 and Nrf2, respectively. Most importantly, TLB not only directly bonded to Sirt3 but also increased Sirt3 expression and activity, indicating that Sirt3 might be a promising therapeutic target of TLB. Innovation: TLB is a naturally occurring Sirt3 agonist with potent neuroprotective effects via regulation of TLR4/nuclear factor-kappa B and Nrf2/Kelch-like ECH-associated protein 1 (Keap-1) signaling pathways both in vivo and in vitro. Conclusion: Our findings indicate that TLB protects against cerebral I/R-induced neuroinflammation and oxidative injury through the regulation of neuroinflammatory and oxidative responses via TLR4, Nrf2, and Sirt3, suggesting that TLB might be a promising Sirt3 agonist against ischemic stroke.

Catalytic hydrogenation reaction of naringin-chalcone. Study of the electrochemical reaction

The electrocatalytic hydrogenation reaction of naringin derivated chalcone is studied. The reaction is carried out with different catalysts in order to compare with the classic catalytic hydrogenation.

METHODS FOR TREATING CHRONIC FATIGUE SYNDROME AND MYALGIC ENCEPHALOMYELITIS

In one aspect the invention relates to a method of treatment selected from the group consisting of: (a) treating a symptom such as pain in a subject identified or diagnosed as having Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS); (b) treating a symptom such as pain in a subject having dysfunctional TRPM3 ion channel activity; (c) restoring NK cell function in a subject having dysfunctional TRPM3 ion channel activity; and (d) restoring calcium homeostasis in a subject having dysfunctional TRPM3 ion channel activity. The method comprises the step of administering to the subject a therapeutically effective amount of at least one therapeutic compound selected from the group consisting of: (i) an opioid receptor antagonist; (ii) an opioid antagonist; and (iii) a therapeutic compound that restores TRPM3 ion channel activity. In some embodiments the therapeutic compound is naltrexone hydrochloride.

Novel compound from plasma-treated phloridzin and anti-obesity composition comprising the same as effective component

The present invention relates to a novel compound derived from plasma-treated phloridzin and an anti-obesity composition comprising the same as an effective component and, more specifically, to a diameric compound derived from phloridzin, which is newly formed by plasma-treating phloridzin (methylene-bis-phloridzin, diglucosyl-methylene-bis-phloridzin, and methylene-bis-phloretin), and to an anti-obesity composition comprising the same as an effective component. In particular, the compound derived from phloridzin, comapred to phloridzin, inhibits the activity of pancreatic lipase and enhances the effect of suppressing fat accumulation during differentiation of fat cells. In particular, the methylene-bis-phloretin of the present invention, a diameric body formed by phloretin using a methyl group, a form of which sugars are removed from phloridzin, has excellent inhibitory effect on fat accumlation as compared to phloretin, and thus may be beneficially used as a material for anti-obesity therapeutic agents or anti-obesity functional health foods.COPYRIGHT KIPO 2019