Shipping to United States We Offer Worldwide Shipping
Login Wishlist

Herbacetin

$275

  • Brand : BIOFRON

  • Catalogue Number : BF-H4001

  • Specification : 98%(HPLC)

  • CAS number : 527-95-7

  • Formula : C15H10O7

  • Molecular Weight : 302.237

  • PUBCHEM ID : 5280544

  • Volume : 25mg

In stock

Quantity
Checkout Bulk Order?

Catalogue Number

BF-H4001

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

302.237

Appearance

White crystalline powder

Botanical Source

Rhodiola rosea

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC(=CC=C1C2=C(C(=O)C3=C(O2)C(=C(C=C3O)O)O)O)O

Synonyms

3,5,7,8-Tetrahydroxy-2-(4-hydroxyphenyl)-4H-chromen-4-one/8-Hydroxykaempferol/4H-1-Benzopyran-4-one, 3,5,7,8-tetrahydroxy-2-(4-hydroxyphenyl)-/Herbacetin/3,4',5,7,8-Pentahydroxyflavone/3,4´,5,7,8-pentahydroxyflavone/3,5,7,8,4'-pentahydroxyflavone

IUPAC Name

3,5,7,8-tetrahydroxy-2-(4-hydroxyphenyl)chromen-4-one

Applications

Density

1.799

Solubility

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

Flash Point

239.0±25.0 °C

Boiling Point

618.7±55.0 °C at 760 mmHg

Melting Point

284ºC

InChl

InChI=1S/C15H10O7/c16-7-3-1-6(2-4-7)14-13(21)12(20)10-8(17)5-9(18)11(19)15(10)22-14/h1-5,16-19,21H

InChl Key

ZDOTZEDNGNPOEW-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

2914500000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:527-95-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31504240

Abstract

Neuroinflammation and microglial activation are significant processes in Alzheimer’s disease pathology. Recent genome-wide association studies have highlighted multiple immune-related genes in association with Alzheimer’s disease, and experimental data have demonstrated microglial proliferation as a significant component of the neuropathology. In this study, we tested the efficacy of the selective CSF1R inhibitor JNJ-40346527 (JNJ-527) in the P301S mouse tauopathy model. We first demonstrated the anti-proliferative effects of JNJ-527 on microglia in the ME7 prion model, and its impact on the inflammatory profile, and provided potential CNS biomarkers for clinical investigation with the compound, including pharmacokinetic/pharmacodynamics and efficacy assessment by TSPO autoradiography and CSF proteomics. Then, we showed for the first time that blockade of microglial proliferation and modification of microglial phenotype leads to an attenuation of tau-induced neurodegeneration and results in functional improvement in P301S mice. Overall, this work strongly supports the potential for inhibition of CSF1R as a target for the treatment of Alzheimer’s disease and other tau-mediated neurodegenerative diseases.

KEYWORDS

Alzheimer’s disease, microglia, neuroinflammation, tau, CSF1R

Title

CSF1R inhibitor JNJ-40346527 attenuates microglial proliferation and neurodegeneration in P301S mice

Author

Renzo Mancuso,1 Gemma Fryatt,1 Madeleine Cleal,1 Juliane Obst,1 Elena Pipi,1 Jimena Monzon-Sandoval,2,3 Elena Ribe,2 Laura Winchester,2 Caleb Webber,2,3 Alejo Nevado,2 Tom Jacobs,4 Nigel Austin,4 Clara Theunis,5 Karolien Grauwen,5 Eva Daniela Ruiz,1 Amrit Mudher,1 Marta Vicente-Rodriguez,6 Christine A Parker,7 Camilla Simmons,6 Diana Cash,6 and Jill Richardson8

Publish date

2019 Oct;

PMID

25001863

Abstract

Mechanism-based sepsis treatments are unavailable, and their incidence is rising worldwide. Deaths occur during the early acute phase of hyperinflammation or subsequent postacute hypoinflammatory phase with sustained organ failure. The acute sepsis phase shifts rapidly, and multiple attempts to treat early excessive inflammation have uniformly failed. We reported in a sepsis cell model and human sepsis blood leukocytes that nuclear NAD+ sensor SIRT1 deacetylase remodels chromatin at specific gene sets to switch the acute-phase proinflammatory response to hypoinflammatory. Importantly, SIRT1 chromatin reprogramming is reversible, suggesting that inhibition of SIRT1 might reverse postacute-phase hypoinflammation. We tested this concept in septic mice, using the highly specific SIRT1 inhibitor EX-527, a small molecule that closes the NAD+ binding site of SIRT1. Strikingly, when administered 24 h after sepsis, all treated animals survived, whereas only 40% of untreated mice survived. EX-527 treatment reversed the inability of leukocytes to adhere at the small intestine MVI, reversed in vivo endotoxin tolerance, increased leukocyte accumulation in peritoneum, and improved peritoneal bacterial clearance. Mechanistically, the SIRT1 inhibitor restored repressed endothelial E-selectin and ICAM-1 expression and PSGL-1 expression on the neutrophils. Systemic benefits of EX-527 treatment included stabilized blood pressure, improved microvascular blood flow, and a shift toward proimmune macrophages in spleen and bone marrow. Our findings reveal that modifying the SIRT1 NAD+ axis may provide a novel way to treat sepsis in its hypoinflammatory phase.

KEYWORDS

immunosuppression, chromatin remodeling, endotoxin tolerance

Title

SIRT1 inhibition during the hypoinflammatory phenotype of sepsis enhances immunity and improves outcome

Author

Vidula T. Vachharajani,*,1 Tiefu Liu,† Candice M. Brown,† Xianfeng Wang,* Nancy L. Buechler,* Jonathan David Wells,‡ Barbara K. Yoza,†‡ and Charles E. McCall†

Publish date

2014 Nov

PMID

31570394

Abstract

AT-527 is a novel modified guanosine nucleotide prodrug inhibitor of the hepatitis C virus (HCV) NS5B polymerase, with increased in vitro antiviral activity compared to sofosbuvir and a highly differentiated favorable preclinical profile compared to other anti-HCV nucleoside/nucleotide analogs. This was a multiple-part clinical study where multiple ascending doses of AT-527 up to 600 mg (expressed as AT-527 salt form; equivalent to 553 mg free base) once daily for 7 days were evaluated in a randomized, double-blind, placebo-controlled study of treatment-naive, noncirrhotic, genotype 1b, HCV-infected subjects. The highest dose of AT-527 for the same duration was then evaluated in two open-label cohorts of (i) noncirrhotic, genotype 3, HCV-infected subjects and (ii) HCV-infected subjects of any genotype with compensated (Child-Pugh A) cirrhosis. AT-527 was well tolerated for 7 days in all cohorts. At the highest dose tested, mean HCV RNA reductions of up to 2.4 log10 IU/ml occurred within the first 24 h of dosing. Mean maximum reductions observed with 7 days of dosing were 4.4, 4.5, and 4.6 log10 IU/ml in noncirrhotic subjects with HCV genotype 1b, noncirrhotic subjects with HCV genotype 3, and subjects with compensated cirrhosis, respectively. The systemic half-life of AT-273, the nucleoside metabolite considered a surrogate of intracellular phosphates including the active triphosphate, exceeded 20 h, supporting once-daily dosing. In summary, AT-527 demonstrated rapid, potent, dose/exposure-related, and pangenotypic antiviral activity with similar responses between subjects with and without cirrhosis. Exposure-antiviral response analysis identified 550 mg (free base equivalent) as the optimal dose of AT-527. Safety and antiviral activity data from this study warrant continued clinical development of AT-527 dosed once daily. (This study has been registered in the European Union Drug Regulating Authorities Clinical Trials Database [EudraCT] under number 2017-002148-34 and at ClinicalTrials.gov under identifier NCT03219957.)

KEYWORDS

chronic hepatitis C virus infection, pangenotypic, direct-acting antiviral, NS5B, nucleotide, cirrhosis

Title

Safety, Pharmacokinetics, and Antiviral Activity of AT-527, a Novel Purine Nucleotide Prodrug, in Hepatitis C Virus-Infected Subjects with or without Cirrhosis

Author

Elina Berliba,corresponding authora Maxim Bogus,a Frederic Vanhoutte,b Pieter-Jan Berghmans,b Steven S. Good,c Adel Moussa,c Keith Pietropaolo,c Robert L. Murphy,c,d Xiao-Jian Zhou,c and Jean-Pierre Sommadossic

Publish date

2019 Dec