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Oxyphenisatin acetate
CAS No. 115-33-3
Oxyphenisatin acetate( —— )
Catalog No. M20707 CAS No. 115-33-3
Oxyphenisatin acetate inhibits the growth of the breast cancer cell lines MCF7 T47D HS578T and MDA-MB-468.
Purity : >98% (HPLC)
COA
Datasheet
HNMR
HPLC
MSDS
Handing Instructions
| Size | Price / USD | Stock | Quantity |
| 1 mL x 10 mM in DMSO | 29 | In Stock |
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| 10MG | 29 | In Stock |
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| 25MG | 36 | In Stock |
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| 50MG | 43 | In Stock |
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| 100MG | 60 | In Stock |
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| 200MG | 86 | In Stock |
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| 500MG | Get Quote | In Stock |
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| 1G | Get Quote | In Stock |
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Biological Information
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Product NameOxyphenisatin acetate
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NoteResearch use only, not for human use.
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Brief DescriptionOxyphenisatin acetate inhibits the growth of the breast cancer cell lines MCF7 T47D HS578T and MDA-MB-468.
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DescriptionOxyphenisatin acetate inhibits the growth of the breast cancer cell lines MCF7 T47D HS578T and MDA-MB-468.
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In VitroOxyphenisatin acetate inhibits the growth of the breast cancer cell lines MCF7, T47D, HS578T, and MDA-MB-468. In the estrogen receptor (ER) positive MCF7 and T47D cells, oxyphenisatin acetate induces TNFα expression and TNFR1 degradation, indicating autocrine receptor-mediated apoptosis in these lines. Ten micromoles per liter Oxyphenisatin acetate treatment results in autophagy and mitochondrial dysfunction.
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In VivoOxyphenisatin acetate (300 mg/kg, i.p.) delivers intraperitoneally inhibited tumor growth, accompanied by phosphorylation of eIF2α and degradation of TNFR1 in an MCF7 xenograft model.
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Synonyms——
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PathwayAutophagy
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TargetAutophagy
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RecptorAutophagy
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Research Area——
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Indication——
Chemical Information
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CAS Number115-33-3
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Formula Weight401.41
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Molecular FormulaC24H19NO5
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Purity>98% (HPLC)
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SolubilityDMSO:150 mg/mL (373.68 mM)
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SMILESCC(=O)Oc1ccc(cc1)C1(C(=O)Nc2ccccc12)c1ccc(OC(C)=O)cc1
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Chemical Name2-Indolinone 33-bis(p-hydroxyphenyl)- diacetate
Shipping & Storage Information
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Storage(-20℃)
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ShippingWith Ice Pack
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Stability≥ 2 years
Reference
1.Morrison B L Mullendore M E Stockwin L H et al. Oxyphenisatin acetate (NSC 59687) triggers a cell starvation response leading to autophagy mitochondrial dysfunction and autocrine TNFα-mediated apoptosis[J]. Cancer Medicine 2013:n/a-n/a.
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