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Gamabufotalin

$225

  • Brand : BIOFRON

  • Catalogue Number : BF-G4001

  • Specification : 98%(HPLC)

  • CAS number : 465-11-2

  • Formula : C24H34O5

  • Molecular Weight : 402.52

  • PUBCHEM ID : 259803

  • Volume : 10mg

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Quantity
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Catalogue Number

BF-G4001

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

402.52

Appearance

Powder

Botanical Source

glandular body of Bufo bufo gargarizans Cantor

Structure Type

Others

Category

Standards;Natural Pytochemical;API

SMILES

CC12CCC(CC1CCC3C2C(CC4(C3(CCC4C5=COC(=O)C=C5)O)C)O)O

Synonyms

(3β,5β,11α)-3,11,14-Trihydroxybufa-20,22-dienolide/Gammabufotalin/3b,11a,14-Trihydroxy-5b-bufa-20,22-dienolide/Bufa-20,22-dienolide, 3,11,14-trihydroxy-, (3β,5β,11α)-/Gamabufotalin/(3b,5b,11a)-3,11,14-Trihydroxybufa-20,22-dienolide/Gamabufagin/Gamabufogenin

IUPAC Name

5-[(3S,5R,8R,9S,10S,11R,13R,14S,17R)-3,11,14-trihydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tetradecahydrocyclopenta[a]phenanthren-17-yl]pyran-2-one

Applications

Gamabufotalin (Gamabufagin), a major bufadienolide of Chansu, has been used for cancer therapy due to its desirable metabolic stability and less adverse effect.IC50 value:Target: in vitro: Gamabufotalin (CS-6) strongly suppressed COX-2 expression by inhibiting the phosphorylation of IKKβ via targeting the ATP-binding site, thereby abrogating NF-κB binding and p300 recruitment to COX-2 promoter. In addition, CS-6 induced apoptosis by activating the cytochrome c and caspase-dependent apoptotic pathway [1]. Gamabufotalin significantly potentiated human breast cancer cells with different status of ER-alpha to apoptosis induction of TRAIL, as evidenced by enhanced Annexin V/FITC positive cells (apoptotic cells), cytoplasmic histone-associated-DNA-fragments, membrane permeability transition (MPT), caspases activation and PARP cleavage [2].in vivo: CS-6 markedly down-regulated the protein levels of COX-2 and phosphorylated p65 NF-κB in tumor tissues of the xenograft mice, and inhibited tumor weight and size [1].

Density

1.3±0.1 g/cm3

Solubility

Methanol; Chloroform

Flash Point

203.4±23.6 °C

Boiling Point

595.8±50.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C24H34O5/c1-22-9-7-16(25)11-15(22)4-5-18-21(22)19(26)12-23(2)17(8-10-24(18,23)28)14-3-6-20(27)29-13-14/h3,6,13,15-19,21,25-26,28H,4-5,7-12H2,1-2H3/t15-,16+,17-,18-,19-,21-,22+,23-,24+/m1/s1

InChl Key

FMTLOAVOGWSPEF-KJRPADTMSA-N

WGK Germany

RID/ADR

HS Code Reference

2938900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:465-11-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30637918

Abstract

We analyzed the small RNA transcriptome from 5‐month‐old, 24‐month‐old, and 36‐month‐old mouse liver and found 56 miRNAs that changed their expression profile with age. Among these is a cluster of 18 miRNAs that are upregulated between 50‐ and 1,000‐fold at 24 and 36 months of age. This cluster is located in a 60‐kb region of the X‐chromosome that is devoid of other coding sequences and is part of a lamin‐associated domain. Potential targets of the miRNAs in the cluster suggest they may regulate several pathways altered in aging, including the PI3K‐Akt pathway. Total transcriptome analyses indicate that expression of several potential genes in the PI3K‐Akt pathway that may be targeted by the mir‐465 family (mmu‐mir‐465a, mmu‐mir‐465b, and mmu‐mir‐465c) is downregulated with age. Transfection of the liver cell line AML12 with mir‐465 family members leads to a reduction of three of these potential targets at the mRNA level: a 40% reduction of the growth hormone receptor (GHR), and a 25% reduction in Kitl and PPP2R3C. Further investigation of the GHR 3′UTR revealed that the mir‐465 family directly targets the GHR mRNA. Cells transfected with mir‐465 showed a reduction of JAK2 and STAT5 phosphorylation upon growth hormone (GH) stimulation, resulting in a reduction in insulin‐like growth factor 1 (IGF‐1) and IGF‐1‐binding protein 3 expression. With age, GH signaling falls and there is a reduction in circulating IGF‐1. Our data suggest that an increase in expression of the mir‐465 family with age may contribute to the reduction in the GH signaling

KEYWORDS

aging, growth hormone receptor, growth hormone signaling, liver, miRNAs, mouse

Title

The mir‐465 family is upregulated with age and attenuates growth hormone signaling in mouse liver

Author

Amy E. Elias, 1 Bianca Kun, 1 Ian M. C. Sabula, 1 Gail Golomb‐Mello, 1 Andrea Cespedes Zablah, 1 and Jill A. Kreilingcorresponding author 1

Publish date

2019 Apr;

PMID

31263673

Abstract

Temozolomide (TMZ) is the standard of care chemotherapeutic agent used in the treatment of glioblastoma multiforme. Cytotoxic O6-methylguaine lesions formed by TMZ are repaired by O6-methyl-guanine DNA methyltransferase (MGMT), a DNA repair protein that removes alkyl groups located at the O6-position of guanine. Response to TMZ requires low MGMT expression and functional mismatch repair. Resistance to TMZ conferred by MGMT, and tolerance to O6-methylguanine lesions conferred by deficient MMR severely limit TMZ clinical applications. Therefore, development of new TMZ derivatives that can overcome TMZ-resistance is urgent. In this study, we investigated the anti-tumor mechanism of action of two novel TMZ analogs: C8-imidazolyl (377) and C8-methylimidazole (465) tetrazines. We found that analogs 377 and 465 display good anticancer activity against MGMT-overexpressing glioma T98G and MMR deficient colorectal carcinoma HCT116 cell lines with IC50 value of 62.50, 44.23, 33.09, and 25.37 μM, respectively. Analogs induce cell cycle arrest at G2/M, DNA double strand break damage and apoptosis irrespective of MGMT and MMR status. It was established that analog 377, similar to TMZ, is able to ring-open and hydrolyze under physiological conditions, and its intermediate product is more stable than MTIC. Moreover, DNA adducts of 377 with calf thymus DNA were identified: N7-methylguanine, O6-methylguanine, N3-methyladenine, N3-methylthymine, and N3-methylcytidine deoxynucleotides. We conclude that C8 analogs of TMZ share a mechanism of action similar to TMZ and are able to methylate DNA generating O6-methylguanine adducts, but unlike TMZ are able at least in part to thwart MGMT- and MMR-mediated resistance.

KEYWORDS

glioblastoma, colorectal carcinoma, O6-methylguanine-DNA methyltransferase, apoptosis, DNA adducts

Title

C8-Substituted Imidazotetrazine Analogs Overcome Temozolomide Resistance by Inducing DNA Adducts and DNA Damage

Author

Zhikuan Yang,1,† Danping Wei,1,† Xiaoli Dai,1,† Malcolm F. G. Stevens,2 Tracey D. Bradshaw,2 Ying Luo,1 and Jihong Zhang1,*

Publish date

2019

PMID

21489410

Abstract

Background
Post-traumatic stress disorder (PTSD) is associated with increased risk for age-related diseases and early mortality. An accelerated rate of biological aging could contribute to this increased risk. To investigate, we assessed leukocyte telomere length (LTL), an emerging marker of biological age, in men and women with and without PTSD. We also examined childhood trauma, a risk factor for both PTSD and short LTL, as a potential contributor to short LTL in PTSD.

Methods
Participants included 43 adults with chronic PTSD (n=18 with multiple categories of childhood trauma) and 47 controls (none with multiple categories of childhood trauma) (M age = 30.55, SD = 7.44). Exclusion criteria included physical illness, medication use, obesity, alcohol or substance abuse, and pregnancy. Structured clinical interviews were conducted to assess PTSD and other psychiatric disorders and childhood trauma exposure. LTL was measured with quantitative polymerase chain reaction.

Results
As predicted, participants with PTSD had shorter age-adjusted LTL than controls. Exposure to childhood trauma was also associated with short LTL. In fact, childhood trauma appeared to account for the PTSD group difference in LTL; only participants with PTSD and exposure to multiple categories of childhood trauma had significantly shorter LTL than controls.

Conclusions
Childhood trauma is associated with short LTL in individuals with PTSD. Chronic exposure to the psychobiological sequelae of childhood trauma could increase risk for PTSD and short LTL. Thus, the lasting psychological impact of exposure to trauma in childhood may be accompanied by equally enduring changes at the molecular level.

KEYWORDS

anxiety, biological aging, childhood trauma, post-traumatic stress disorder, telomere length

Title

CHILDHOOD TRAUMA ASSOCIATED WITH SHORT LEUKOCYTE TELOMERE LENGTH IN POST-TRAUMATIC STRESS DISORDER

Author

Aoife O’Donovan,1,2,3 Elissa Epel,1 Jue Lin,4 Owen Wolkowitz,1 Beth Cohen,1,2,5 Shira Maguen,1,2,3 Thomas Metzler,3 Maryann Lenoci,3 Elizabeth Blackburn,4 and Thomas C Neylan1,2,3

Publish date

2012 Sep 1.