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557354

Sigma-Aldrich

ROS Inhibitor, YCG063

The ROS Inhibitor, YCG063, also referenced under CAS 330997-95-0, controls the biological activity of ROS.

Synonym(s):

ROS Inhibitor, YCG063, YCG063ROS Inhibitor

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About This Item

Empirical Formula (Hill Notation):
C19H25N5O4S
CAS Number:
Molecular Weight:
419.50
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

Assay

≥95% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

white

solubility

DMSO: 50 mg/mL
ethanol: soluble

shipped in

ambient

storage temp.

−20°C

General description

A cell-permeable acetohydrazide that dose-dependently inhibits hypoxia-induced mitochondrial ROS generation (≤ 10 µM) in HepG2 and other cells, and suppresses cellular growth (≤ 50 µM) in HUVEC, HeLa, and HCT15 cultures. At ≤ 10 µM, this compound strongly inhibits VGFR-induced tube formation and invasive activity in HUVECs in vitro without obvious toxicity. It is also shown to hinder capillary formation in a chick embryo CAM assay without any sign of thrombosis and hemorrhage in vivo. Furthermore, it attenuates the expression levels HIF-1α and its target gene VEGF (0–10 µM). dose-dependently.
A cell-permeable acetohydrazide that dose-dependently inhibits hypoxia-induced mitochondrial ROS generation (≤10 µM) in HepG2 and other cells, and suppresses cellular growth (≤50 µM) in HUVEC, HeLa, and HCT15 cultures. At ≤10 µM, this compound strongly inhibits VGFR-induced tube formation and invasive activity in HUVECs in vitro without obvious toxicity. It is also shown to hinder capillary formation in a chick embryo CAM assay without any sign of thrombosis and hemorrhage in vivo. Furthermore, it attenuates the expression levels HIF-1α and its target gene VEGF (0–10 µM) dose-dependently.

Packaging

Packaged under inert gas

Warning

Toxicity: Standard Handling (A)

Reconstitution

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Other Notes

Kim, K.H., et al. 2011. Biochem. Biophys. Res. Commun.404, 541.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Regulatory Listings

Regulatory Listings are mainly provided for chemical products. Only limited information can be provided here for non-chemical products. No entry means none of the components are listed. It is the user’s obligation to ensure the safe and legal use of the product.

JAN Code

557354-5MG:
557354-MG:


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Katiria Soto-Diaz et al.
Frontiers in immunology, 12, 734349-734349 (2021-12-14)
Microglia activation and proliferation are hallmarks of many neurodegenerative disorders and may contribute to disease pathogenesis. Neurons actively regulate microglia survival and function, in part by secreting the microglia mitogen interleukin (IL)-34. Both IL-34 and colony stimulating factor (CSF)-1 bind
Tomoya Sasahara et al.
STAR protocols, 3(1), 101053-101053 (2022-01-11)
Reactive oxygen species (ROS) are important physiological molecules, and identifying agonists for ROS production can yield useful tools for future research. Here we present an optimized protocol for high-throughput screening for agonists that induce ROS production. We describe the use
Minhua Yao et al.
PloS one, 18(4), e0285016-e0285016 (2023-04-28)
Guinea pigs are a valuable animal model for studying various diseases, including reproductive diseases. However, techniques for generating embryos via embryo engineering in guinea pigs are limited; for instance, in vitro maturation (IVM) technique is preliminary for guinea pig oocytes.
Tomoya Sasahara et al.
iScience, 24(9), 102936-102936 (2021-08-31)
Amyloid β-protein (Aβ) may contribute to worsening of Alzheimer's disease (AD) through vascular dysfunction, but the molecular mechanism involved is unknown. Using ex vivo blood vessels and primary endothelial cells from human brain microvessels, we show that patient-derived Aβ assemblies, termed

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