7-Cl-O-Nec1, metabolically stable RIP1 inhibitor (ab221984)
Key features and details
- Potent, selective, metabolically stable RIP1 inhibitor
- CAS Number: 852391-15-2
- Purity: > 98%
- Soluble in DMSO to 90 mM
- Form / State: Solid
- Source: Synthetic
Overview
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Product name
7-Cl-O-Nec1, metabolically stable RIP1 inhibitor -
Description
Potent, selective, metabolically stable RIP1 inhibitor -
Alternative names
- Nec-1s
- Necrostatin-2 racemate
- RIP1 Inhibitor II
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Biological description
Necrostatin-1 (ab141053) analog with superior selectivity and metabolic stability in blocking RIP1. No off-target inhibition of indolamine-2,3-deoxygenase (IDO) in contrast to Necrostatin-1. Higher activity in inhibiting necroptosis in Jurkat cells than Necrostatin-1 (EC50 = 210 nM vs. EC50 = 490 nM).
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Purity
> 98% -
CAS Number
852391-15-2 -
Chemical structure
Properties
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Chemical name
5-((7-Chloro-1H-indol-3-yl)methyl)-3-methylimidazolidine-2,4-dione -
Molecular weight
277.71 -
Molecular formula
C13H12ClN3O2 -
PubChem identifier
643953 -
Storage instructions
Shipped at room temperature. Store at -20°C. -
Solubility overview
Soluble in DMSO to 90 mM -
Handling
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20°C. Generally, these will be useable for up to one month. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please visit our frequently asked questions (FAQ) page for more details.
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SMILES
CN1C(=O)C(NC1=O)CC2=CNC3=C2C=CC=C3Cl -
Source
Synthetic
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Research areas
Protocols
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
Datasheets and documents
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SDS download
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Datasheet download
References (9)
ab221984 has been referenced in 9 publications.
- Puylaert P et al. Effect of erythrophagocytosis-induced ferroptosis during angiogenesis in atherosclerotic plaques. Angiogenesis 26:505-522 (2023). PubMed: 37120604
- Egorshina AY et al. Necroptosis as a Novel Facet of Mitotic Catastrophe. Int J Mol Sci 23:N/A (2022). PubMed: 35409093
- Henning Y et al. Hypoxia aggravates ferroptosis in RPE cells by promoting the Fenton reaction. Cell Death Dis 13:662 (2022). PubMed: 35906211
- Kieckhöfer E et al. Primary cilia suppress Ripk3-mediated necroptosis. Cell Death Discov 8:477 (2022). PubMed: 36460631
- Peek SL et al. p53-mediated neurodegeneration in the absence of the nuclear protein Akirin2. iScience 25:103814 (2022). PubMed: 35198879
- Chen IT et al. Promyelocytic leukemia protein targets MK2 to promote cytotoxicity. EMBO Rep 22:e52254 (2021). PubMed: 34633746
- Muendlein HI et al. Constitutive Interferon Attenuates RIPK1/3-Mediated Cytokine Translation. Cell Rep 30:699-713.e4 (2020). PubMed: 31968247
- Wandel MP et al. Guanylate-binding proteins convert cytosolic bacteria into caspase-4 signaling platforms. Nat Immunol 21:880-891 (2020). PubMed: 32541830
- Yambire KF et al. Impaired lysosomal acidification triggers iron deficiency and inflammation in vivo. Elife 8:N/A (2019). PubMed: 31793879