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Merck

SML0521

Sigma-Aldrich

ML 210

≥98% (HPLC)

Sinónimos:

CID 49766530, ML-210, [4-[Bis(4-chlorophenyl)methyl]piperazin-1-yl]-(5-methyl-4-nitro-1,2-oxazol-3-yl)methanone

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About This Item

Fórmula empírica (notación de Hill):
C22H20Cl2N4O4
Número de CAS:
Peso molecular:
475.32
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Quality Level

assay

≥98% (HPLC)

form

powder

color

white to beige

storage temp.

2-8°C

SMILES string

Cc1onc(C(=O)N2CCN(CC2)C(c3ccc(Cl)cc3)c4ccc(Cl)cc4)c1[N+]([O-])=O

InChI

1S/C22H20Cl2N4O4/c1-14-20(28(30)31)19(25-32-14)22(29)27-12-10-26(11-13-27)21(15-2-6-17(23)7-3-15)16-4-8-18(24)9-5-16/h2-9,21H,10-13H2,1H3

InChI key

VIBHJPDPEVVDTB-UHFFFAOYSA-N

Application

ML 210 has been used as a glutathione peroxidase 4 (GPX4) inhibitor to induce ferroptosis in cancer cells. It has also been used as a GPX4 inhibitor to examine whether pharmacological inhibition of GPX4 altered prominin2 expression and impacted ferroptosis in adherent MCF10A and Hs578t cells.

Biochem/physiol Actions

ML 210 acts as a selenoenzyme glutathione peroxidase 4 (GPX4) inhibitor. It exhibits cytotoxicity against few ovarian cancer cell lines.
ML 210 induces non-apoptotic cell death in tumor cells expressing the RAS oncogene.

pictograms

Exclamation mark

signalword

Warning

hcodes

Hazard Classifications

Acute Tox. 4 Oral

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Amrita Basu et al.
Cell, 154(5), 1151-1161 (2013-09-03)
The high rate of clinical response to protein-kinase-targeting drugs matched to cancer patients with specific genomic alterations has prompted efforts to use cancer cell line (CCL) profiling to identify additional biomarkers of small-molecule sensitivities. We have quantitatively measured the sensitivity
Jianling Bi et al.
Cell death & disease, 10(10), 682-682 (2019-09-19)
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death driven by lipid hydroperoxides within biological membranes. Although therapy-resistant mesenchymal-high cancers are particularly vulnerable to ferroptosis inducers, especially phospholipid glutathione peroxidase 4 (GPx4) inhibitors, the underlying mechanism is yet to
Matthew J Hangauer et al.
Nature, 551(7679), 247-250 (2017-11-02)
Acquired drug resistance prevents cancer therapies from achieving stable and complete responses. Emerging evidence implicates a key role for non-mutational drug resistance mechanisms underlying the survival of residual cancer 'persister' cells. The persister cell pool constitutes a reservoir from which
Yilong Zou et al.
Nature, 585(7826), 603-608 (2020-09-18)
Ferroptosis-an iron-dependent, non-apoptotic cell death process-is involved in various degenerative diseases and represents a targetable susceptibility in certain cancers1. The ferroptosis-susceptible cell state can either pre-exist in cells that arise from certain lineages or be acquired during cell-state transitions2-5. However
Leslie Magtanong et al.
Cell chemical biology, 29(9), 1409-1418 (2022-07-10)
Ferroptosis is an important mediator of pathophysiological cell death and an emerging target for cancer therapy. Whether ferroptosis sensitivity is governed by a single regulatory mechanism is unclear. Here, based on the integration of 24 published chemical genetic screens combined

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