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Alisol B 23-acetate


  • Brand : BIOFRON

  • Catalogue Number : BF-A2013

  • Specification : 98%

  • CAS number : 26575-95-1

  • Formula : C32H50O5

  • Molecular Weight : 514.74

  • PUBCHEM ID : 14036811

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Alisma orientale

Structure Type



Standards;Natural Pytochemical;API




8alpha,9beta,14beta-Dammar-13(17)-en-3-one,24,25-epoxy-11beta,23-dihydroxy-,23-acetate,(23S,24R)/Alisol B 23-monoacetate/Alisol B monoacetate/(8α,9β,11β,14β,20R,23S,24R)-11-Hydroxy-3-oxo-24,25-epoxydammar-13(17)-en-23-yl acetate/Alisol B acetate/N1550/Dammar-13(17)-en-3-one, 23-(acetyloxy)-24,25-epoxy-11-hydroxy-, (8α,9β,11β,14β,23S,24R)-/Alisol-B-Monoacetat/Alisol B 23-acetate/Dammar-13(17)-en-3-one, 23-(acetyloxy)-24,25-epoxy-11-hydroxy-, (8α,9β,11β,14β,20R,23S,24R)-/AlisolB-23-acetate/23-O-Acetylalisol B/(8α,9β,11β,14β,23S,24R)-11-Hydroxy-3-oxo-24,25-epoxydammar-13(17)-en-23-yl acetate/Alisol B (23-acetate)


[(1S,3R)-1-[(2R)-3,3-dimethyloxiran-2-yl]-3-[(5R,8S,9S,10S,11S,14R)-11-hydroxy-4,4,8,10,14-pentamethyl-3-oxo-1,2,5,6,7,9,11,12,15,16-decahydrocyclopenta[a]phenanthren-17-yl]butyl] acetate


1.1±0.1 g/cm3


Methanol; DMSO; Acetontrile

Flash Point

179.9±23.6 °C

Boiling Point

590.7±50.0 °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#:26575-95-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Despite efforts to use adeno-associated viral (AAV) vector-mediated gene therapy for treatment of pancreatic ductal adenocarcinoma (PDAC), transduction efficiency remains a limiting factor and thus improvement of AAV delivery would significantly facilitate the treatment of this malignancy. Site-directed mutagenesis of specific tyrosine (Y) residues to phenylalanine (F) on the surface of various AAV serotype capsids has been reported as a method for enhancing gene transfer efficiencies. In the present studies, we determine whether Y-to-F mutations could also enhance AAV8 gene transfer in the pancreas to facilitate gene therapy for PDAC. Three different Y-to-F mutant vectors (a single-mutant, Y733F; a double-mutant, Y447F+Y733F; and a triple-mutant, Y275F+Y447F+Y733F) and wild-type AAV8 (WT-AAV8) were administered by intraperitoneal or tail-vein routes to KrasG12D+/−, KrasG12D+/−/Pten+/−, and wild-type mice. The transduction efficiency of these vectors expressing the mCherry reporter gene was evaluated 2 weeks post administration in pancreas or PDAC and correlated with viral genome copy numbers. Our comparative and quantitative analyses of the transduction profiles demonstrated that the Y-to-F double-mutant exhibited the highest mCherry expression in pancreatic tissues (range 45-70%) compared with WT-AAV8 (7%; p < 0.01). We also detected a 7-fold higher level of vector genome copy numbers in normal pancreas following transduction with the double-mutant AAV8 compared with WT-AAV8 (10,285 vs. 1,500 vector copies/μg DNA respectively, p < 0.05). In addition, we observed that intraperitoneal injection of the double-mutant AAV8 led to a 15-fold enhanced transduction efficiency as compared to WT-AAV8 in mouse PDAC, with a corresponding ∼14-fold increase in vector genome copy numbers (26,575 vs. 2,165 copies/μg DNA respectively, p < 0.05). These findings indicate that the Y447+Y733F-AAV8 leads to a significant enhancement of transduction efficiency in both normal and malignant pancreatic tissues, suggesting the potential use of this vector in targeting pancreatic diseases in general, and PDAC in particular.


gene therapy, pancreatic cancer, adeno-associated virus, AAV8


Efficient Gene Delivery and Expression in Pancreas and Pancreatic Tumors by Capsid-Optimized AAV8 Vectors


Min Chen,1,†,‡ Kyungah Maeng,1,† Akbar Nawab,1 Rony A. Francois,1 Julie K. Bray,1 Mary K. Reinhard,2 Sanford L. Boye,3 William W. Hauswirth,3 Frederic J. Kaye,4 Georgiy Aslanidi,5 Arun Srivastava,5 and Maria Zajac-Kaye1,*

Publish date

2017 Feb 1;




Primary sequence motifs, with millimolar affinities for binding partners, are abundant in disordered protein regions. In multivalent interactions, such weak linear motifs can cooperate to recruit binding partners via avidity effects. If linear motifs recruit modifying enzymes, optimal placement of weak motifs may regulate access to modification sites. Weak motifs may thus exert stronger physiological relevance than suggested by their affinities, but molecular mechanisms of their function are still poorly understood. Herein, we use the N-terminal disordered region of the Hedgehog transcriptional regulator Gli3 (Gli31-90) to determine the role of weak motifs encoded in its primary sequence for the recruitment of its ubiquitin ligase CRL3SPOP and the subsequent effect on ubiquitination efficiency. The substrate adaptor SPOP binds linear motifs through its MATH domain and forms higher-order oligomers through its oligomerization domains, rendering SPOP multivalent for its substrates. Gli3 has multiple weak SPOP binding motifs. We map three such motifs in Gli31-90, the weakest of which has a millimolar dissociation constant. Multivalency of ligase and substrate for each other facilitates enhanced ligase recruitment and stimulates Gli31-90 ubiquitination in in vitro ubiquitination assays. We speculate that the weak motifs enable processivity through avidity effects and by providing steric access to lysine residues that are otherwise not prioritized for polyubiquitination. Weak motifs may generally be employed in multivalent systems to act as gatekeepers in posttranslational modification.


multivalency, cancer, degron, Speckle-type POZ protein, NMR spectroscopy


Multiple weak linear motifs enhance recruitment and processivity in SPOP-mediated substrate ubiquitination


Wendy K. Pierce,a,1 Christy R. Grace,a Jihun Lee,a Amanda Nourse,b Melissa R. Marzahn,a Edmond R. Watson,a,c Anthony A. High,a Junmin Peng,a Brenda A. Schulman,a,d and Tanja Mittaga,*

Publish date

2017 Mar 27.




Recent genome-wide association studies in stroke have enabled the generation of genomic risk scores (GRS) but their predictive power has been modest compared to established stroke risk factors. Here, using a meta-scoring approach, we develop a metaGRS for ischaemic stroke (IS) and analyse this score in the UK Biobank (n = 395,393; 3075 IS events by age 75). The metaGRS hazard ratio for IS (1.26, 95% CI 1.22-1.31 per metaGRS standard deviation) doubles that of a previous GRS, identifying a subset of individuals at monogenic levels of risk: the top 0.25% of metaGRS have three-fold risk of IS. The metaGRS is similarly or more predictive compared to several risk factors, such as family history, blood pressure, body mass index, and smoking. We estimate the reductions needed in modifiable risk factors for individuals with different levels of genomic risk and suggest that, for individuals with high metaGRS, achieving risk factor levels recommended by current guidelines may be insufficient to mitigate risk.

Subject terms: Genome-wide association studies, Personalized medicine, Stroke, Risk factors


Genomic risk score offers predictive performance comparable to clinical risk factors for ischaemic stroke


Gad Abraham,corresponding author1,2,3 Rainer Malik,4 Ekaterina Yonova-Doing,5 Agus Salim,6,7 Tingting Wang,1 John Danesh,5,8,9,10,11,12 Adam S. Butterworth,5,8,9,10,11,12 Joanna M. M. Howson,5,11 Michael Inouye,corresponding author#1,2,3,5,11,13 and Martin Dichganscorresponding author#4,14,15

Publish date


Description :

Alisol B 23-acetate, a natural triterpenoid, produces protective effects against EE-induced cholestasis, due to FXR-mediated gene regulation.IC50 Value:Target: Anti-hepatotoxic natural product. In vitro: Alisol-B 23-acetate has an effect on FXR activation in a dose-dependent manner using luciferase reporter assay in HepG2 cells [3].In vivo: In alisol B 23-acetate-treated mice, the changes in transporters and enzymes, as well as ameliorative liver histology were abrogated by FXR antagonist guggulsterone [1]. Alisol B 23-acetate treatment in a dose-dependent manner resulted in protection against hepatotoxicity induced by CCl4via FXR activation. Through FXR activation, alisol B 23-acetate promoted hepatocyte proliferation via an induction in hepatic levels of FoxM1b, Cyclin D1 and Cyclin B1. Alisol B 23-acetate also reduced hepatic bile acids through a decrease in hepatic uptake transporter Ntcp, bile acid synthetic enzymes Cyp7a1, Cyp8b1, and an increase in efflux transporter Bsep, Mrp2 expression. In addition, alisol B 23-acetate induced the expression of STAT3 phosphorylation, and STAT3 target genes Bcl-xl and SOCS3, resulting in decreased hepatocyte apoptosis [2].