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567417

Sigma-Aldrich

SOD1 Inhibitor, LCS-1

The SOD1 Inhibitor, LCS-1, also referenced under CAS 41931-13-9, controls the biological activity of SOD1.

Sinónimos:

SOD1 Inhibitor, LCS-1, lung cancer screen 1, 4,5-dichloro-2-m-tolylpyridazin-3(2H)-one, 4,5-dichloro-2-(3-methylphenyl)-3(2H)-pyridazinone, Superoxide dismutase 1 inhibitor

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About This Item

Fórmula empírica (notación de Hill):
C11H8Cl2N2O
Número de CAS:
Peso molecular:
255.10
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.28

Quality Level

assay

≥99% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

white

solubility

DMSO: 50 mg/mL, clear, colorless

shipped in

ambient

storage temp.

−20°C

InChI

1S/C11H8Cl2N2O/c1-7-3-2-4-8(5-7)15-11(16)10(13)9(12)6-14-15/h2-6H,1H3

InChI key

SYUPLLHVMCLXEM-UHFFFAOYSA-N

General description

A 2-phenylpyridazin-3(2H)-one based non-copper chelater that selectively inhibits the activity of Superoxide dismutase 1 (Cu/Zn-SOD) (IC50 = 1.07 µM). Cells over-expressing SOD1 show reduced sensitivity to LCS-1. Shown to preferably inhibit the growth of a variety of human lung adenocarinoma cell lines with EGFR and KRAS mutations (IC50 = 200 nM). Prevents serum-induced activation of the ERK and PI 3-kinase/AKT signaling thereby affecting cell growth and survival. Apparent half-life of this compound is reported to be 6.6 min in human liver microsomes.

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

Somwar, R., et al. 2011, PNAS in press.
Somwar, R., et al. 2009. J. Biomol. Screen14, 1176

Legal Information

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

Storage Class

11 - Combustible Solids

wgk_germany

WGK 2

flash_point_f

Not applicable

flash_point_c

Not applicable


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Min Ling et al.
Frontiers in oncology, 12, 937444-937444 (2022-08-19)
Gliomas are characterized by high morbidity and mortality, and have only slightly increased survival with recent considerable improvements for treatment. An innovative therapeutic strategy had been developed via inducing ROS-dependent cell death by targeting antioxidant proteins. In this study, we

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