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Merck
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Documenti fondamentali

SML0521

Sigma-Aldrich

ML 210

≥98% (HPLC)

Sinonimo/i:

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

Formula empirica (notazione di Hill):
C22H20Cl2N4O4
Numero CAS:
Peso molecolare:
475.32
Numero MDL:
Codice UNSPSC:
12352200
ID PubChem:
NACRES:
NA.77

Saggio

≥98% (HPLC)

Stato

powder

Colore

white to beige

Temperatura di conservazione

2-8°C

Stringa SMILE

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
VIBHJPDPEVVDTB-UHFFFAOYSA-N

Applicazioni

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.

Azioni biochim/fisiol

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

Pittogrammi

Exclamation mark

Avvertenze

Warning

Indicazioni di pericolo

Classi di pericolo

Acute Tox. 4 Oral

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


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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
Yinu Wang et al.
Cancer research, 81(2), 384-399 (2020-11-12)
Defining traits of platinum-tolerant cancer cells could expose new treatment vulnerabilities. Here, new markers associated with platinum-tolerant cells and tumors were identified using in vitro and in vivo ovarian cancer models treated repetitively with carboplatin and validated in human specimens.
Yilong Zou et al.
Nature chemical biology, 16(3), 302-309 (2020-02-23)
Ferroptosis is widely involved in degenerative diseases in various tissues including kidney, liver and brain, and is a targetable vulnerability in multiple primary and therapy-resistant cancers. Accumulation of phospholipid hydroperoxides in cellular membranes is the hallmark and rate-limiting step of
Nobuaki Takahashi et al.
Molecular cell, 80(5), 828-844 (2020-11-01)
Cancer-associated mutations that stabilize NRF2, an oxidant defense transcription factor, are predicted to promote tumor development. Here, utilizing 3D cancer spheroid models coupled with CRISPR-Cas9 screens, we investigate the molecular pathogenesis mediated by NRF2 hyperactivation. NRF2 hyperactivation was necessary for

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