S4068

Splitomicin

Name: Splitomicin
Brand: SIGMA
Price: 91.4 EUR

≥98% (HPLC), powder

Synonym(e):

1,2-Dihydro-3H-naphtho[2,1-b]pyran-3-one

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5 MG

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Über diesen Artikel

Empirische Formel (Hill-System):

C₁₃H₁₀O₂

CAS-Nummer:

5690-03-9

Molekulargewicht:

198.22

NACRES:

NA.77

PubChem Substance ID:

24724608

UNSPSC Code:

12352200

MDL number:

MFCD08705254

Assay:

≥98% (HPLC)

Form:

powder

Quality level:

100

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Quality Level

100

assay

≥98% (HPLC)

form

powder

storage temp.

2-8°C

SMILES string

O=C1CCc2c(O1)ccc3ccccc23

InChI

1S/C13H10O2/c14-13-8-6-11-10-4-2-1-3-9(10)5-7-12(11)15-13/h1-5,7H,6,8H2

InChI key

ISFPDBUKMJDAJH-UHFFFAOYSA-N

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Dieser Artikel	SML1767	567750	SML0376
Sigma-Aldrich S4068 Splitomicin	Sigma-Aldrich SML1767 Sparstolonin B	Sigma-Aldrich 567750 Splitomicin	Sigma-Aldrich SML0376 CGS 9895
form powder	form powder	form powder	form powder
assay ≥98% (HPLC)	assay ≥98% (HPLC)	assay ≥95% (HPLC)	assay ≥98% (HPLC)
Quality Level 100	Quality Level 100	Quality Level 100	Quality Level 100
storage temp. 2-8°C	storage temp. 2-8°C	storage temp. 2-8°C	storage temp. 2-8°C

Application

Splitomicin was used to inhibit SIRT1 in human aortic endothelial cells[1][2] and sirtuins in human breast cancer cells.[3] Mouse leukaemic monocyte macrophage cell line was treated with Splitomicin prior to cholesterol efflux studies.[4]

Biochem/physiol Actions

Sir2p (silent information regulator) and HDAC inhibitor.

Splitomicin, a derivative of β-naphthol is an inhibitor of Silent Information Regulator 2 (SIR2). It inhibits the NAD⁺-dependent deacetylase activity of Sir2 in vitro.[5] It increases the levels of cyclic AMP by inhibiting the activity of cyclic AMP phosphodiesterase, interferes with mobilization of intracellular Ca⁺² and ATP release. This results in inhibition of platelet aggregation that is effective in cardiovascular and cerebrovascular diseases.[6]

Features and Benefits

This compound is a featured product for Gene Regulation research. Click here to discover more featured Gene Regulation products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.

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EPI004

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Sirtuin 2 (SIRT2) Inhibitor Screening Assay Kit, 100 assays in 96 well plates

Lagerklasse

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)

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The Sir2 family of protein deacetylases.

Gil Blander et al.

Annual review of biochemistry, 73, 417-435 (2004-06-11)

The yeast SIR protein complex has been implicated in transcription silencing and suppression of recombination. The Sir complex represses transcription at telomeres, mating-type loci, and ribosomal DNA. Unlike SIR3 and SIR4, the SIR2 gene is highly conserved in organisms ranging

Splitomicin suppresses human platelet aggregation via inhibition of cyclic AMP phosphodiesterase and intracellular Ca++ release.

Fu-Chao Liu et al.

Thrombosis research, 124(2), 199-207 (2009-03-31)

Splitomicin is derived from beta-naphthol and is an inhibitor of Silent Information Regulator 2 (SIR2). Its naphthoic moiety might be responsible for its inhibitory effects on platelets. The major goal of our study was to examine possible mechanisms of action

Reduced thrombosis in Klkb1-/- mice is mediated by increased Mas receptor, prostacyclin, Sirt1, and KLF4 and decreased tissue factor.

Evi X Stavrou et al.

Blood, 125(4), 710-719 (2014-10-24)

The precise mechanism for reduced thrombosis in prekallikrein null mice (Klkb1(-/-)) is unknown. Klkb1(-/-) mice have delayed carotid artery occlusion times on the rose bengal and ferric chloride thrombosis models. Klkb1(-/-) plasmas have long-activated partial thromboplastin times and defective contact

Deacetylation of the DNA-binding domain regulates p53-mediated apoptosis.

Hestia S Mellert et al.

The Journal of biological chemistry, 286(6), 4264-4270 (2010-12-15)

In unstressed cells, the p53 tumor suppressor is highly unstable. DNA damage and other forms of cellular stress rapidly stabilize and activate p53. This process is regulated by a complex array of post-translational modifications that are dynamically deposited onto p53.

miR‑155‑5p downregulation inhibits epithelial‑to‑mesenchymal transition by targeting SIRT1 in human nasal epithelial cells.

Niannian Yang et al.

Molecular medicine reports, 22(5), 3695-3704 (2020-10-02)

Epithelial-to-mesenchymal transition (EMT) in nasal epithelial cells is involved with tissue remodeling of nasal polyps. The present study investigated the molecular mechanisms through which miR‑155‑5p regulated EMT in chronic rhinosinusitis (CRS). Patients were divided into the following groups: CRSsNP, CRS

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We offer a variety of small molecule research tools, such as transcription factor modulators, inhibitors of chromatin modifying enzymes, and agonists/antagonists for target identification and validation in gene regulation research; a selection of these research tools is shown below.

Global Trade Item Number

SKU	GTIN
S4068-5MG	04061832632728

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