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Ganoderic acid C2


  • Brand : BIOFRON

  • Catalogue Number : BD-P0735

  • Specification : 99.0%(HPLC&TLC)

  • CAS number : 103773-62-2

  • Formula : C30H46O7

  • Molecular Weight : 518.68

  • PUBCHEM ID : 57396771

  • Volume : 25mg

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Botanical Source

Ganoderma lucidum (reishi)

Structure Type






(2R,6R)-2-methyl-4-oxo-6-[(3S,5R,7S,10S,13R,14R,15S,17R)-3,7,15-trihydroxy-4,4,10,13,14-pentamethyl-11-oxo-1,2,3,5,6,7,12,15,16,17-decahydrocyclopenta[a]phenanthren-17-yl]heptanoic acid


(2R,6R)-2-methyl-4-oxo-6-[(3S,5R,7S,10S,13R,14R,15S,17R)-3,7,15-trihydroxy-4,4,10,13,14-pentamethyl-11-oxo-1,2,3,5,6,7,12,15,16,17-decahydrocyclopenta[a]phenanthren-17-yl]heptanoic acid


Network pharmacology analysis of the anti-cancer pharmacological mechanisms of Ganoderma lucidum extract with experimental support using Hepal-6-bearing C57 BL/6 mice PUMID/DOI:DOI: 10.1016/j.jep.2017.08.041 J Ethnopharmacol. 2018 Jan 10;210:287-295 Ethnopharmacological relevance: Ganoderma lucidum (GL) is an oriental medical fungus, which was used to prevent and treat many diseases. Previously, the effective compounds of Ganoderma lucidum extract (GLE) were extracted from two kinds of GL, [Ganoderma lucidum (Leyss. Ex Fr.) Karst.] and [Ganoderma sinense Zhao, Xu et Zhang], which have been used for adjuvant anti-cancer clinical therapy for more than 20 years. However, its concrete active compounds and its regulation mechanisms on tumor are unclear. Aim of the study: In this study, we aimed to identify the main active compounds from GLE and to investigate its anticancer mechanisms via drug-target biological network construction and prediction. Materials and methods: The main active compounds of GLE were identified by HPLC, EI-MS and NMR, and the compounds related targets were predicted using docking program. To investigate the functions of GL holistically, the active compounds of GL and related targets were predicted based on four public databases. Subsequently, the Identified Compound-Target network and Predicted-Compound-Target network were constructed respectively, and they were overlapped to detect the hub potential targets in both networks. Furthermore, the qRT-PCR and western-blot assays were used to validate the expression levels of target genes in GLE treated Hepa1-6-bearing C57 BL/6 mice. Results: In our work, 12 active compounds of GLE were identified, including Ganoderic acid A, Ganoderenic acid A, Ganoderic acid B, Ganoderic acid H, Ganoderic acid C2, Ganoderenic acid D, Ganoderic acid D, Ganoderenic acid G, Ganoderic acid Y, Kaemferol, Genistein and Ergosterol. Using the docking program, 20 targets were mapped to 12 compounds of GLE. Furthermore, 122 effective active compounds of GL and 116 targets were holistically predicted using public databases. Compare with the Identified-Compound-Target network and Predicted-Compound-Target network, 6 hub targets were screened, including AR, CHRM2, ESR1, NR3C1, NR3C2 and PGR, which was considered as potential markers and might play important roles in the process of GLE treatment GLE effectively inhibited tumor growth in Hepa1-6-bearing C57 BL/6 mice. Finally, consistent with the results of qRT-PCR data, the results of western-blot assay demonstrated the expression levels of PGR and ESR1 were up-regulated, as well as the expression levels of NR3C2 and AR were down-regulated, while the change of NR3C1 and CHRM2 had no statistical significance. Conclusions: The results indicated that these 4 hub target genes, including NR3C2, AR, ESR1 and PGR, might act as potential markers to evaluate the curative effect of GLE treatment in tumor. And, the combined data provide preliminary study of the pharmacological mechanisms of GLE, which may be a promising potential therapeutic and chemopreventative candidate for anti-cancer. Hepatoprotective Effects and Mechanisms of Action of Triterpenoids from Lingzhi or Reishi Medicinal Mushroom Ganoderma lucidum (Agaricomycetes) on alpha-Amanitin-Induced Liver Injury in Mice PUMID/DOI:DOI: 10.1615/IntJMedMushrooms.v18.i9.80 Int J Med Mushrooms. 2016;18(9):841-850. Most fatal mushroom poisonings are caused by species of the genus Amanita; the amatoxins arc responsible for acute liver failure and death in humans. Ganoderma lucidum is a well-known traditional medicinal mushroom that has been shown to have obvious hepatoprotective effects. This study evaluated the hepatoprotective effects of triterpenoids from G. lucidum on liver injury induced by a-amanitin (alpha-AMA) in mice and the mechanisms of action of these triterpenoids, including radical scavenging and antiapoptosis activities. Mice were treated with a-AMA, followed by G. lucidum total triterpenoids or individual triterpenoids, and their hepatoprotective effects were compared with those of the reference drug silibinin (SIL). Treatment with SIL, G. lucidum total triteipenoids, and each of the 5 individual triterpenoids significantly reduced serum alanine aminotransaminase and aspartate aminotransaminase concentrations and reduced mortality rates 20 L.10%. Moreover, triterpenoids and SIL significantly enhanced superoxide dismutase and catalase activity and reduced malondialdehyde content in livers. Treatment with ganoderic acid C2 significantly inhibited DNA fragmentation and decreased caspase-3, -8, and -9 activities. The results demonstrated that triterpenoids have hepatoprotective effects on alpha-AMA-induced liver injury and that their hepatoprotective mechanisms may be the result of their antioxidative and radical scavenging activities and their inhibition of apoptosis. Activating mitochondrial regulator PGC-1 alpha expression by astrocytic NGF is a therapeutic strategy for Huntington's disease PUMID/DOI:DOI: 10.1016/j.neuropharm.2012.05.019 Neuropharmacology. 2012 Sep;63(4):719-32. Mitochondrial dysfunction plays an important role in Huntington's disease (HD). NGF gene delivery in AD patients showed an increase in brain energy metabolism and NGF has been shown neuroprotective effects against mitochondrial toxins. However, the role of NGF in regulating mitochondrial function is unclear. Here, we found that NGF-stimulated mitochondrial biogenesis in PC12 and primary neuron cells. Our results demonstrated that peroxisome proliferator-activated receptor gamma coactivator 1-a (PGC-1a) is a downstream key target of the NGF signalling pathway. In a 3-nitropropionic acid (3-NP) cell model, NGF treatment rescued the defects in mitochondrial activity and mitochondrial membrane potential. Since NGF cannot freely cross blood-brain barrier, we found an astrocytic NGF inducer, Ganoderma lucidum (GaLu) extract. Its active constituents had potent effects on the induction of NGF in primary astrocytes. Among the identified ingredients, ganoderic acid C2 was most effective. We further found that GaLu-conditioned media can enhance mitochondrial biogenesis in PC12 cells and preventing NGF signalling using NGF antibody or PGC-1a siRNA blocked these effects. Moreover, GaLu and ganoderic acid C2-conditioned media treatment attenuated mitochondrial defects in 3-NP cell model. After 3-NP-induced behavioural impairment and striatal degeneration in mice, GaLu treatment therapeutically restored the behaviour score, sensorimotor ability and neuronal loss. We found that striatal NGF, PGC-1a expression level and succinate dehydrogenase activity were recovered in GaLu-fed mice. These results suggest that the NGF-signalling pathway connected to the mitochondrial regulator, PGC-1a, expression. This signalling triggered by astrocytic NGF with small molecule inducers may offer a therapeutic strategy for HD. Structure-activity relationships of ganoderma acids from Ganoderma lucidum as aldose reductase inhibitors PUMID/DOI:DOI: 10.1016/j.bmcl.2011.10.035 Bioorg Med Chem Lett. 2011 Dec 15;21(24):7295-7. A series of lanostane-type triterpenoids, known as ganoderma acids were isolated from the fruiting body of Ganoderma lucidum. Some of these compounds were identified as active inhibitors of the in vitro human recombinant aldose reductase. To clarify the structural requirement for inhibition, some structure-activity relationships were determined. Our structure-activity studies of ganoderma acids revealed that the OH substituent at C-11 is an important feature and the carboxylic group in the side chain is essential for the recognition of aldose reductase inhibitory act



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

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

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provides coniferyl ferulate(CAS#:103773-62-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

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Health literacy in patients attending a University Hospital. Low level of health literacy is associated with poor communication between patients and clinicians and with increased hospitalization rates, less frequent screening for cancer, poor control of diabetes, and disproportionately high rates of disease and mortality. Despite the importance of health literacy in medicine, there is no information about its prevalence in Latin America. The aim of this study was to assess the prevalence of inadequate health literacy in a random sample of patients, at a University Hospital where a descriptive study was performed during 2007. Health literacy was assessed through the Short Assessment of Health Literacy for Spanish-speaking Adults. Participants were randomly selected from the ambulatory clinic and from the medical inpatient ward during 2007.There were a total of 2345 patients potentially eligible during the time of the study, 234 were approached after random selection and 229 patients were interviewed (98% response); 54.6% of respondents were women and 62% were recruited from the ambulatory clinic. The respondents had a median age of 56 years. The prevalence of inadequate health literacy was 30.1% (69 patients). Patients with ≤ 7 years of formal education had more risk of having inadequate health literacy compared with those with > 12 years of education OR = 45.1 (IC 9.6-211.6). We found a high prevalence of inadequate health literacy, being strongly associated with the level of formal education. It is important that health care providers know the implications of health literacy and its consequences.


health literacy, education





Publish date

2014 Oct 1.




The oxygen consumption rates (OCRs) in mice and cattle have been reported to change during preimplantation embryogenesis. On the other hand, mitochondrial DNA (mtDNA) copy number has been shown to be unchanged in mice and changed in cattle and pigs. The interactions between mitochondrial functions and mtDNA copy numbers in human embryos during preimplantation development remain obscure.

Sixteen oocytes and 100 embryos were used to assess mtDNA copy numbers and OCR. Three oocytes and 12 embryos were used to determine cytochrome c oxidase activity. All specimens were obtained between July 2004 and November 2014, and donated from couples after they had given informed consent. Mature oocytes and embryos at 2-14-cell, morula, and blastocyst stages were used to assess their OCR in the presence or absence of mitotoxins. The mtDNA copy number was determined using the samples after analysis of OCR. The relationships between developmental stages and OCR, and developmental stages and mtDNA copy number were analyzed. Furthermore, cytochrome c oxidase activity was determined in oocytes and 4-cell to blastocyst stage embryos.

The structure of inner mitochondrial membranes and their respiratory function developed with embryonic growth and the mtDNA copy numbers decreased transiently compared with those of oocytes. The undifferentiated state of inner cell mass cells appears to be associated with a low OCR. On the other hand, the mtDNA copy numbers increased and aerobic metabolism of mitochondria increased in trophectoderm cells.

The mitochondrial respiratory function of human embryos developed along with embryonic growth although the copy numbers of mtDNA decreased transiently before blastulation. OCRs increased toward the morula stage ahead of an increase of mtDNA at the time of blastulation. Data regarding changes in mitochondrial function and mtDNA copy number during preimplantation development of human embryos will be useful for the development of ideal culture media.

Electronic supplementary material
The online version of this article (doi:10.1007/s10815-017-0886-6) contains supplementary material, which is available to authorized users.


Mitochondrial DNA, Mitochondrial function, Oxygen consumption


Quantitative and qualitative changes of mitochondria in human preimplantation embryos


Shu Hashimoto,corresponding author1 Naoharu Morimoto,2 Masaya Yamanaka,1 Hiroshi Matsumoto,1 Takayuki Yamochi,1 Hiroya Goto,1 Masayasu Inoue,1 Yoshiharu Nakaoka,1 Hiroaki Shibahara,2 and Yoshiharu Morimoto3

Publish date

2017 May;




The zinc(II) atom in the title compound, [Zn(C48H31N4)(CF3SO3)](CF3SO3)·1.5CH2Cl2, adopts a distorted five-coordinate square-pyramidal geometry. It is coordinated by one tri­fluoro­methane­sulfonate ligand and four N atoms of the N 2-[(benzo[h]quinolin-2-yl)meth­yl]-N 2′-[(benzo[h]quinolin-2-yl)methyl­idene]-1,1′-binaphthyl-2,2′-di­amine ligand. The complex is present as a single-stranded P-helimer monohelical structure incorporating π-π and/or σ-π inter­actions. One of the imine bonds present in the original ligand framework is reduced, leading to variations in bond lengths and torsion angles for each side of the ligand motif. The imine-bond reduction also affects the bond lengths involving the metal atom with the N-donor atoms located on the imine bond. There are two mol­ecules of the complex in the asymmetric unit. One of the mol­ecules exhibits positional disorder within the coordinating tri­fluoro­methane­sulfonate ion making the mol­ecules symmetric­ally non-equivalent.


crystal structure, five-coordinate zinc(II) complex, chiral ligand, asymmetric catalysis, monohelical structure


Crystal structure of {(R)-N 2-[(benzo[h]quinolin-2-yl)meth­yl]-N 2′-[(benzo[h]quinolin-2-yl)methyl­idene]-1,1′-binaphthyl-2,2′-di­amine-κ4 N,N′,N′′,N′′′}(trifluoromethane­sulfonato-κO)zinc(II)} trifluoromethane­sulfonate di­chloro­methane 1.5-solvate


Shayna R. Skokan,a Monica M. Reeson,a Kayode D. Oshin,a,* Anastasiya I. Vinokur,b John A. Desper,c and Christopher J. Levyc

Publish date

2017 Jul 1