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SML2561

Sigma-Aldrich

ML162

≥98% (HPLC)

Sinônimo(s):

α-[(2-Chloroacetyl)(3-chloro-4-methoxyphenyl)amino]-N-(2-phenylethyl)-2-thiopheneacetamide, 2-Chloro-N-(3-chloro-4-methoxyphenyl)-N-(2-oxo-2-(phenethylamino)-1-(thiophen-2-yl)ethyl)acetamide, BRD-5421, BRD5421, CID 3689413, ML 162, ML-162, Molecular Libraries 162

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About This Item

Fórmula empírica (Notação de Hill):
C23H22Cl2N2O3S
Número CAS:
1035072-16-2
Peso molecular:
477.40
Número MDL:
MFCD03450805
Código UNSPSC:
12352200
NACRES:
NA.77

Ensaio

≥98% (HPLC)

forma

powder

cor

white to very dark brown

solubilidade

DMSO: 2 mg/mL, clear

temperatura de armazenamento

2-8°C

Ações bioquímicas/fisiológicas

ML162 is a small molecule that induces ferroptosis via covalent inhibition of cellular phospholipid glutathione peroxidase (GPX-4; GPX4; GSHPx-4; PHGPx; snGPx; snPHGPx). Synthetic lethality studies in cancer cultures identify contributing factors such as HRas(G12V) expression and fumarate hydratase (FH) deletion to ML162 sensitivity (IC50 = 25 nM & 35 nM, respectively, in BJeLR-HRas(G12V) & UOK262-FH-/- cultures).

Código de classe de armazenamento

11 - Combustible Solids

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable

Certificados de análise (COA)

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Michel Weïwer et al.
Bioorganic & medicinal chemistry letters, 22(4), 1822-1826 (2012-02-03)
Synthetic lethal screening is a chemical biology approach to identify small molecules that selectively kill oncogene-expressing cell lines with the goal of identifying pathways that provide specific targets against cancer cells. We performed a high-throughput screen of 303,282 compounds from
Emilie Logie et al.
International journal of molecular sciences, 22(22) (2021-11-28)
Disease relapse and therapy resistance remain key challenges in treating multiple myeloma. Underlying (epi-)mutational events can promote myelomagenesis and contribute to multi-drug and apoptosis resistance. Therefore, compounds inducing ferroptosis, a form of iron and lipid peroxidation-regulated cell death, are appealing
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
Vasanthi S Viswanathan et al.
Nature, 547(7664), 453-457 (2017-07-06)
Plasticity of the cell state has been proposed to drive resistance to multiple classes of cancer therapies, thereby limiting their effectiveness. A high-mesenchymal cell state observed in human tumours and cancer cell lines has been associated with resistance to multiple
Kenichi Shimada et al.
Cell chemical biology, 23(2), 225-235 (2016-02-09)
Precision medicine in oncology requires not only identification of cancer-associated mutations but also effective drugs for each cancer genotype, which is still a largely unsolved problem. One approach for the latter challenge has been large-scale testing of small molecules in
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