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Apicidin

$896

  • Brand : BIOFRON

  • Catalogue Number : BN-O1794

  • Specification : 98%(HPLC)

  • CAS number : 183506-66-3

  • Formula : C34H49N5O6

  • Molecular Weight : 609.76

  • PUBCHEM ID : 44593387

  • Volume : 10mg

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Catalogue Number

BN-O1794

Analysis Method

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

609.76

Appearance

Powder

Botanical Source

Structure Type

Category

SMILES

CCC(C)C1C(=O)N2CCCCC2C(=O)NC(C(=O)NC(C(=O)N1)CC3=CN(C4=CC=CC=C43)OC)CCCCCC(=O)CC

Synonyms

Acipidin/(3S,6S,9S,15aR)-9-[(2S)-Butan-2-yl]-6-[(1-methoxy-1H-indol-3-yl)methyl]-3-(6-oxooctyl)octahydro-2H-pyrido[1,2-a][1,4,7,10]tetraazacyclododecine-1,4,7,10(3H,12H)-tetrone/2H-Pyrido[1,2-a][1,4,7,10]tetraazacyclododecine-1,4,7,10(3H,12H)-tetrone, octahydro-6-[(1-methoxy-1H-indol-3-yl)methyl]-9-[(1S)-1-methylpropyl]-3-(6-oxooctyl)-, (3S,6S,9S,15aR)-/OSI-2040/(3S,6S,9S,15aR)-9-(butan-2-yl)-6-[(1-methoxy-1H-indol-3-yl)methyl]-3-(6-oxooctyl)octahydro-2H-pyrido[1,2-a][1,4,7,10]tetraazacyclododecine-1,4,7,10(3H,12H)-tetrone/(3S,6S,9S,15aR)-9-[(2S)-2-Butanyl]-6-[(1-methoxy-1H-indol-3-yl)methyl]-3-(6-oxooctyl)octahydro-2H-pyrido[1,2-a][1,4,7,10]tetraazacyclododecine-1,4,7,10(3H,12H)-tetrone/Apicidin

IUPAC Name

Density

1.27g/cm3

Solubility

Soluble to 2 mM in DMSO and to 2 mM in ethanol

Flash Point

Boiling Point

Melting Point

InChl

InChl Key

JWOGUUIOCYMBPV-VWIQTCEGSA-N

WGK Germany

RID/ADR

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#:183506-66-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

28425856

Abstract

BACKGROUND:
Apicidin, as an inhibitor of histone deacetylase, showed a wide range of antiproliferative activity against various cancer cell lines. Apicidin has also been reported to induce apotosis via Fas/Fas ligand. Yet few studies have been focused on mitochondrial pathway for its anti-tumor activity.

OBJECTIVE:
In this study, we evaluated its involved mitochondrial mechanism against non-small cell lung cancer GLC-82 cells.

METHOD:
Apicidin was isolated from the mangrove endophtic fungi Fusarium sp. by solvent extraction and column chromatography. Its structure was elucidated by MS and NMR spectroscopic data, and comparison of those data with published data. Furthermore, anti-tumor activity and mitochondrial pathway of apicidin against GLC-82 cells were studied.

RESULTS:
Apicidin was obtained from secondary metabolites of Fusarium sp., and it showed potent inhibitory activity against GLC-82 cells with the IC50 value of 6.94 ± 0.27 µM. Furthermore, apicidin suppressed proliferation and invasion, and induced apoptosis via mitochondrial pathway in GLC-82 cells, including loss of ΔΨm, release of cytochrome c from mitochondria, activation of caspase-9 and -3, and cleavage of poly-ADP-ribose polymerase.

CONCLUSION:
Apicidin, an inhibitor of histone deacetylase obtained from the mangrove endophytic fungi Fusarium sp., not only inhibited proliferation and invasion of GLC-82 cells, but also induced apoptosis via the mitochondrial pathway.

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

KEYWORDS

Apicidin; Fusarium sp; apoptosis; histone deacetylase; invasion; mitochondrial pathway; proliferation

Title

Apicidin Inhibited Proliferation and Invasion and Induced Apoptosis via Mitochondrial Pathway in Non-small Cell Lung Cancer GLC-82 Cells.

Author

Zhang J1, Lai Z1, Huang W1, Ling H1, Lin M1, Tang S1, Liu Y1, Tao Y1.

Publish date

2017

PMID

30943400

Abstract

Recurrent epidemics of drug-resistant Staphylococcus aureus illustrate the rapid lapse of antibiotic efficacy following clinical implementation. Over the last decade, community-associated methicillin-resistant S. aureus (MRSA) has emerged as a dominant cause of infections, and this problem is amplified by the hyper-virulent nature of these isolates. Herein, we report the discovery of a fungal metabolite, apicidin, as an innovative means to counter both resistance and virulence. Owing to its breadth and specificity as a quorum-sensing inhibitor, apicidin antagonizes all MRSA agr systems in a non-biocidal manner. In skin challenge experiments, the apicidin-mediated abatement of MRSA pathogenesis corresponds with quorum-sensing inhibition at in vivo sites of infection. Additionally, we show that apicidin attenuates MRSA-induced disease by potentiating innate effector responses, particularly through enhanced neutrophil accumulation and function at cutaneous challenge sites. Together, these results indicate that apicidin treatment represents a strategy to limit MRSA virulence and promote host defense.

Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.

KEYWORDS

MRSA; Staphylococcus aureus; agr; apicidin; natural product; pathogenesis; quorum sensing; skin infection

Title

Apicidin Attenuates MRSA Virulence through Quorum-Sensing Inhibition and Enhanced Host Defense.

Author

Parlet CP1, Kavanaugh JS2, Crosby HA2, Raja HA3, El-Elimat T3, Todd DA3, Pearce CJ4, Cech NB3, Oberlies NH3, Horswill AR5.

Publish date

2019 Apr 2

PMID

11698395

Abstract

We previously reported that apicidin arrested human cancer cell growth through selective induction of p21(WAF1/Cip1). In this study, the apoptotic potential of apicidin and its mechanism in HL60 cells was investigated. Treatment of HL60 cells with apicidin caused a decrease in viable cell number in a dose-dependent manner and an increase in DNA fragmentation, nuclear morphological change, and apoptotic body formation, concomitant with progressive accumulation of hyperacetylated histone H4. In addition, apicidin converted the procaspase-3 form to catalytically active effector protease, resulting in subsequent cleavages of poly(ADP-ribose) polymerase and p21(WAF1/Cip1). Incubation of HL60 cells with z-DEVD-fmk, a caspase-3 inhibitor, almost completely abrogated apicidin-induced activation of caspase-3, DNA fragmentation, and cleavages of poly(ADP-ribose) polymerase and p21(WAF1/Cip1). Moreover, these effects were preceded by an increase in translocation of Bax into the mitochondria, resulting in the release of cytochrome c and cleavage of procaspase-9. The addition of cycloheximide greatly inhibited activation of caspase-3 by apicidin by interfering with cleavage of procaspase-3 and DNA fragmentation, suggesting that apicidin-induced apoptosis was dependent on de novo protein synthesis. Consistent with these results, apicidin transiently increased the expressions of both Fas and Fas ligand. Preincubation with NOK-1 monoclonal antibody, which prevents the Fas-Fas ligand interaction and is inhibitory to Fas signaling, interfered with apicidin-induced translocation of Bax, cytochrome c release, cleavage of procaspase-3, and DNA fragmentation. Taken together, the results suggest that apicidin might induce apoptosis through selective induction of Fas/Fas ligand, resulting in the release of cytochrome c from the mitochondria to the cytosol and subsequent activation of caspase-9 and caspase-3.

Title

Apicidin, a histone deacetylase inhibitor, induces apoptosis and Fas/Fas ligand expression in human acute promyelocytic leukemia cells.

Author

Kwon SH1, Ahn SH, Kim YK, Bae GU, Yoon JW, Hong S, Lee HY, Lee YW, Lee HW, Han JW.

Publish date

2002 Jan 18


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