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567417

SOD1 Inhibitor, LCS-1

Name: SOD1 Inhibitor, LCS-1
Brand: MM

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

Synonym(s):

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

Empirical Formula (Hill Notation):

C₁₁H₈Cl₂N₂O

CAS Number:

41931-13-9

Molecular Weight:

255.10

MDL number:

MFCD00814448

UNSPSC Code:

12352200

NACRES:

NA.28

Quality Level

100

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

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

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LCS-1 inhibition of superoxide dismutase 1 induces ROS-dependent death of glioma cells and degradates PARP and BRCA1.

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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