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Merck

SML0808

Sigma-Aldrich

JIB-04

≥98% (HPLC)

Synonym(e):

(E)-N-(5-Chloro-pyridin-2-yl)-N′-(phenyl-pyridin-2-yl-methylene)-hydrazine

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About This Item

Empirische Formel (Hill-System):
C17H13ClN4
CAS-Nummer:
Molekulargewicht:
308.76
UNSPSC-Code:
12352200
NACRES:
NA.77

Assay

≥98% (HPLC)

Form

powder

Farbe

white to beige

Löslichkeit

DMSO: 10 mg/mL, clear

Lagertemp.

2-8°C

InChI

1S/C17H13ClN4/c18-14-9-10-16(20-12-14)21-22-17(13-6-2-1-3-7-13)15-8-4-5-11-19-15/h1-12H,(H,20,21)/b22-17+

InChIKey

YHHFKWKMXWRVTJ-OQKWZONESA-N

Anwendung

JIB-04 has been used in sulforhodamine B cell growth assay. It has also been used as a control to determine the inhibitory action of ML324 on KDM4A (histone lysine demethylase 4A).

Biochem./physiol. Wirkung

JIB-04 is a selective inihibitor of Jumonji demethylases without inhibiting other α-ketoglutarate-dependent hydroxylases or histone-modifying enzymes including amine oxidase LSD1 (also known as KDM1A), which demethylates histone lysines. JIB-04 is a pan-inhibitor of Jumonji demethylases with JARID1A (KDM5A) being the most sensitive (IC50=230 nM) followed by JMJD2D (IC50=290 nM) and JMJD3 (KDM6B) and JMJD2C (KDM4C) more resistant (IC50 855 and 1100 nM, respectively). JIB-04 selectively inhibited viability of several human cancer cell lines with little toxicity towards normal cells, and also diminished tumor growth in two separate xenograft mouse models.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


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KDM4A regulates HIF-1 levels through H3K9me3
Dobrynin G, et al.
Scientific Reports, 7(1), 11094-11094 (2017)
Characterization of a linked Jumonji domain of the KDM5/JARID1 family of histone H3 lysine 4 demethylases.
Horton JR, et al.
The Journal of Biological Chemistry, 291(6), 2631-2646 (2016)
Grzegorz Dobrynin et al.
Scientific reports, 7(1), 11094-11094 (2017-09-13)
Regions of hypoxia (low oxygen) occur in most solid tumours and cells in these areas are the most aggressive and therapy resistant. In response to decreased oxygen, extensive changes in gene expression mediated by Hypoxia-Inducible Factors (HIFs) contribute significantly to
Alyssa A Lombardi et al.
Nature communications, 10(1), 4509-4509 (2019-10-06)
Fibroblast to myofibroblast differentiation is crucial for the initial healing response but excessive myofibroblast activation leads to pathological fibrosis. Therefore, it is imperative to understand the mechanisms underlying myofibroblast formation. Here we report that mitochondrial calcium (mCa2+) signaling is a

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