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  • Brand : BIOFRON

  • Catalogue Number : BF-P3001

  • Specification : 98%

  • CAS number : 60-81-1

  • Formula : C21H24O10

  • Molecular Weight : 436.4

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Malus toringoides

Structure Type








1.6±0.1 g/cm3


DMSO : ≥ 50 mg/mL (114.57 mM)
H2O : 1 mg/mL (2.29 mM; Need ultrasonic)
*"≥" means soluble, but saturation unknown.

Flash Point

270.7±26.4 °C

Boiling Point

770.0±60.0 °C at 760 mmHg

Melting Point

113-114 °C(lit.)



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#:60-81-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




The objective of this work was the development of an on-line extraction/fractionation method based on the coupling of pressurized liquid extraction and solid-phase extraction for the separation of phenolic compounds from apple pomace. Several variables of the process were evaluated, including the amount of water of the first stage (0-120 mL), temperature (60-80 °C), solid-phase extraction adsorbent (Sepra, Isolute, Strata X and Oasis) and activation/elution solvent (methanol and ethanol). The best results were observed with the adsorbent Sepra. The temperature had a small effect on recovery, but significant differences were observed for phlorizin and a quercetin derivative. Results indicate that ethanol can be used to replace methanol as an activation, extraction/elution solvent. While using mostly green solvents (water, ethanol, and a small amount of methanol that could be reused), the developed method produced higher or similar yields of acids (2.85 ± 0.19 mg/g) and flavonoids (0.97 ± 0.11 mg/g) than conventional methods.


Apple pomace; Chlorogenic acid (PubChem CID: 1794427); Epicatechin (PubChem CID: 72276); Flavonoids; Gallic acid (PubChem CID: 370); Hyperoside (PubChem CID: 5281643); Phenolics; Phloretin xylosil glucoside; Phlorizin (PubChem CID: 6072); Pressurized liquid extraction; Quercetin rhamnoside (PubChem CID: 5353915); Rutin (PubChem CID: 5280805); Solid-phase extraction.


Simultaneous extraction and separation of bioactive compounds from apple pomace using pressurized liquids coupled on-line with solid-phase extraction


Laise C da Silva 1, Mariana C Souza 1, Beatriz R Sumere 1, Luiz G S Silva 1, Diogo T da Cunha 2, Gerardo F Barbero 3, Rosangela M N Bezerra 4, Mauricio A Rostagno 5

Publish date

2020 Jul 15




Astrocytes generate robust cytoplasmic calcium signals in response to reductions in extracellular glucose. This calcium signal, in turn, drives purinergic gliotransmission, which controls the activity of catecholaminergic (CA) neurons in the hindbrain. These CA neurons are critical to triggering glucose counter-regulatory responses (CRRs) that, ultimately, restore glucose homeostasis via endocrine and behavioral means. Although the astrocyte low-glucose sensor involvement in CRR has been accepted, it is not clear how astrocytes produce an increase in intracellular calcium in response to a decrease in glucose. Our ex vivo calcium imaging studies of hindbrain astrocytes show that the glucose type 2 transporter (GLUT2) is an essential feature of the astrocyte glucosensor mechanism. Coimmunoprecipitation assays reveal that the recombinant GLUT2 binds directly with the recombinant Gq protein subunit that activates phospholipase C (PLC). Additional calcium imaging studies suggest that GLUT2 may be connected to a PLC-endoplasmic reticular-calcium release mechanism, which is amplified by calcium-induced calcium release (CICR). Collectively, these data help outline a potential mechanism used by astrocytes to convert information regarding low-glucose levels into intracellular changes that ultimately regulate the CRR.


counter-regulation; ex vivo brain slice; live cell calcium imaging; low-glucose sensing; solitary nucleus.


Evidence that hindbrain astrocytes in the rat detect low glucose with a glucose transporter 2-phospholipase C-calcium release mechanism


Richard C Rogers 1, Susan J Burke 2, J Jason Collier 3, Sue Ritter 4, Gerlinda E Hermann 1

Publish date

2020 Jan 1;




Respiratory infection can be exacerbated by the high glucose concentration in the airway surface liquid (ASL). We investigated the effects of salbutamol and phlorizin on the pulmonary function, oxidative stress levels and SGLT1 activity in lung, pulmonary histopathological damages and survival rates of rats with sepsis. Sepsis was induced by cecal ligation and puncture surgery (CLP). Twenty-four hours after surgery, CLP rats were intranasally treated with saline, salbutamol or phlorizin. After 2 hours, animals were anesthetized and sacrificed. Sepsis promoted atelectasis and bronchial inflammation, and led to increased expression of SGLT1 on cytoplasm of pneumocytes. Salbutamol treatment reduced bronchial inflammation and promoted hyperinsuflation in CLP rats. The interferon-ɤ and Interleucin-1β concentrations in bronchoalveolar lavage (BAL) were closely related to the bronchial inflammation regulation. Salbutamol stimulated SGLT1 in plasma membrane; whereas, phlorizin promoted the increase of SGLT1 in cytoplasm. Phlorizin reduced catalase activity and induced a significant decrease in the survival rate of CLP rats. Taken together, sepsis promoted atelectasis and lung inflammation, which can be associated with SGLT1 inhibition. The loss of function of SGLT1 by phlorizin are related to the augmented disease severity, increased atelectasis, bronchial inflammation and a significant reduction of survival rate of CLP rats. Alternatively salbutamol reduced BAL inflammatory cytokines, bronchial inflammation, atelectasis, and airway damage in sepsis. These data suggest that this selective β2-adrenergic agonist may protect lung of septic acute effects.


Effects of salbutamol and phlorizin on acute pulmonary inflammation and disease severity in experimental sepsis


Leia Cardoso-Sousa 1, Emilia Maria Gomes Aguiar 1, Douglas Carvalho Caixeta 2, Danielle Diniz Vilela 2, Danilo Pereira da Costa 1, Tamires Lopes Silva 3, Thúlio Marquez Cunha 4, Paulo Rogerio Faria 5, Foued Salmen Espindola 2, Ana Carolina Jardim 6, Alexandre Antônio Vieira 1, Tales Lyra Oliveira 7, Luiz Ricardo Goulart 2 8, Robinson Sabino-Silva 1

Publish date

2019 Sep 19;

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