AB221984

7-Cl-O-Nec1, metabolically stable RIP1 inhibitor

Name: 7-Cl-O-Nec1, metabolically stable RIP1 inhibitor (ab221984) | Abcam
Brand: Abcam Limited
SKU: AB221984
Price: 150 USD
Availability: InStock

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(11 Publications)

MW 277.7 Da, Purity >98%. 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).

View Alternative Names

Cell death protein RIP, FLJ39204, OTTHUMP00000039163, RIPK1_HUMAN, Receptor (TNFRSF) interacting serine threonine kinase 1, Receptor TNFRSF interacting serine threonine kinase 1, Receptor interacting protein, Receptor interacting protein kinase 1, Receptor interacting serine threonine protein kinase 1, Receptor-interacting protein 1, Receptor-interacting serine/threonine-protein kinase 1, Rinp, Rip-1, Serine threonine protein kinase RIP, Serine/threonine-protein kinase RIP

1 Images

Chemical Structure - 7-Cl-O-Nec1, metabolically stable RIP1 inhibitor (AB221984)

Chemical Structure

Lab

Chemical Structure - 7-Cl-O-Nec1, metabolically stable RIP1 inhibitor (AB221984)

2D chemical structure image of ab221984, 7-Cl-O-Nec1, metabolically stable RIP1 inhibitor

Key facts

Purity

>98%

Form

Solid

form

Molecular weight

277.7 Da

Molecular formula

C13H12ClN3O2

PubChem

643953

Nature

Synthetic

Solubility

Soluble in DMSO to 90 mM

Biochemical name

Necrostatin 2 racemate

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).

Canonical smiles

CN1C(=O)C(NC1=O)CC2=CNC3=C2C=CC=C3Cl

InChi

InChI=1S/C13H12ClN3O2/c1-17-12(18)10(16-13(17)19)5-7-6-15-11-8(7)3-2-4-9(11)14/h2-4,6,10,15H,5H2,1H3,(H,16,19)

InChiKey

WIKGAEMMNQTUGL-UHFFFAOYSA-N

IUPAC Name

5-[(7-chloro-1H-indol-3-yl)methyl]-3-methylimidazolidine-2,4-dione

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Properties and storage information

Shipped at conditions

Ambient - Can Ship with Ice

Appropriate short-term storage conditions

-20°C

Appropriate long-term storage conditions

-20°C

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Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

RIP also known as Receptor-Interacting Protein or RIPK1 is a serine/threonine-protein kinase with a mass of approximately 74 kDa. It plays an important role in cell death and survival signaling pathways. RIP is expressed ubiquitously across various tissues indicating its importance in many cellular functions. The protein contains a kinase domain an intermediate domain for protein-protein interactions and a death domain which facilitates its involvement in apoptotic signaling processes.

Biological function summary

Receptor-Interacting Protein Kinase 1 (RIPK1) participates in regulating both necroptosis and apoptosis distinguishing itself as an important mediator in cell death mechanisms. As part of the necrosome complex which includes RIPK3 and MLKL RIPK1 functions in necroptosis—a programmed form of necrosis. This characteristic involvement shows its dual role in maintaining cell fate decisions making it an integral part of immune response and inflammation control.

Pathways

RIPK1 strongly associates with the TNF signaling pathway and NF-kB pathway. Its interaction with TNF receptor 1 (TNFR1) and consequent involvement with TRADD and TRAF2 mediates the signal transduction necessary for the activation of NF-kB leading to transcription of genes involved in survival and inflammation. This connection illustrates its capability to switch between promoting cell survival through NF-kB and facilitating cell death via necroptosis or apoptosis depending on cellular context and cues.

RIPK1 plays a significant role in conditions such as inflammatory diseases and neurodegenerative disorders. Its overactivation results in excessive cell death implicated in inflammatory conditions; necrostatin a necroptosis inhibitor targets RIPK1 to potentially mitigate this damage. Furthermore RIPK1's dysregulation links to Alzheimer's disease where it can interact with components like RIPK3 to exacerbate neurodegenerative processes. This relationship underlines the potential of targeting RIPK1 therapeutically to manage inflammation and neurodegeneration.

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Product protocols

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Publications (11)

Recent publications for all applications. Explore the full list and refine your search

European journal of immunology 55:e51526 PubMed40498275

2025

Dipeptidyl Peptidase 9 in Human Leukocytes: Novel Inhibitors Induce Caspase-1- and Gasdermin-Dependent Cell Death.

Applications

Unspecified application

Species

Unspecified reactive species

Joni De Loose,Kathleen Mertens,Nicolò Filippi,Sam Corthaut,Siham Benramdane,Yani Sim,Yentl Van Rymenant,Karen Claesen,Gwendolyn Vliegen,Maya Berg,Tiphanie Gomard,Guy Caljon,Isabel Pintelon,Pieter Van Der Veken,Ingrid De Meester

Science advances 11:eadq1047 PubMed40053580

2025

TBK1 and IKKε prevent premature cell death by limiting the activity of both RIPK1 and NLRP3 death pathways.

Applications

Unspecified application

Species

Unspecified reactive species

Fabian A Fischer,Benjamin Demarco,Felicia Chan Hui Min,Hui Wen Yeap,Dominic De Nardo,Kaiwen W Chen,Jelena S Bezbradica

Angiogenesis 26:505-522 PubMed37120604

2023

Effect of erythrophagocytosis-induced ferroptosis during angiogenesis in atherosclerotic plaques.

Applications

Unspecified application

Species

Unspecified reactive species

Pauline Puylaert,Lynn Roth,Melissa Van Praet,Isabel Pintelon,Catalina Dumitrascu,Alexander van Nuijs,Greta Klejborowska,Pieter-Jan Guns,Tom Vanden Berghe,Koen Augustyns,Guido R Y De Meyer,Wim Martinet

Cell death discovery 8:477 PubMed36460631

2022

Primary cilia suppress Ripk3-mediated necroptosis.

Applications

Unspecified application

Species

Unspecified reactive species

Emilia Kieckhöfer,Gisela G Slaats,Lena K Ebert,Marie-Christine Albert,Claudia Dafinger,Hamid Kashkar,Thomas Benzing,Bernhard Schermer

Cell death & disease 13:662 PubMed35906211

2022

Hypoxia aggravates ferroptosis in RPE cells by promoting the Fenton reaction.

Applications

Unspecified application

Species

Unspecified reactive species

Yoshiyuki Henning,Ursula Sarah Blind,Safa Larafa,Johann Matschke,Joachim Fandrey

International journal of molecular sciences 23: PubMed35409093

2022

Necroptosis as a Novel Facet of Mitotic Catastrophe.

Applications

Unspecified application

Species

Unspecified reactive species

Aleksandra Yu Egorshina,Alexey V Zamaraev,Vitaliy O Kaminskyy,Tatiana V Radygina,Boris Zhivotovsky,Gelina S Kopeina

iScience 25:103814 PubMed35198879

2022

p53-mediated neurodegeneration in the absence of the nuclear protein Akirin2.

Applications

Unspecified application

Species

Unspecified reactive species

Stacey L Peek,Peter J Bosch,Ethan Bahl,Brianna J Iverson,Mrutyunjaya Parida,Preeti Bais,J Robert Manak,Jacob J Michaelson,Robert W Burgess,Joshua A Weiner

EMBO reports 22:e52254 PubMed34633746

2021

Promyelocytic leukemia protein targets MK2 to promote cytotoxicity.

Applications

Unspecified application

Species

Unspecified reactive species

I-Ting Chen,Hsiao-Chi Chen,Yu-Hsun Lo,Peng-Yeh Lai,Fu-Yi Hsieh,Yung-Hsuan Wu,Hsiu-Ming Shih,Ming-Zong Lai

Nature immunology 21:880-891 PubMed32541830

2020

Guanylate-binding proteins convert cytosolic bacteria into caspase-4 signaling platforms.

Applications

Unspecified application

Species

Unspecified reactive species

Michal P Wandel,Bae-Hoon Kim,Eui-Soon Park,Keith B Boyle,Komal Nayak,Brice Lagrange,Adrian Herod,Thomas Henry,Matthias Zilbauer,John Rohde,John D MacMicking,Felix Randow

Cell reports 30:699-713.e4 PubMed31968247

2020

Constitutive Interferon Attenuates RIPK1/3-Mediated Cytokine Translation.

Applications

Unspecified application

Species

Unspecified reactive species

Hayley I Muendlein,Joseph Sarhan,Beiyun C Liu,Wilson M Connolly,Stephen A Schworer,Irina Smirnova,Amy Y Tang,Vladimir Ilyukha,Jodie Pietruska,Soroush Tahmasebi,Nahum Sonenberg,Alexei Degterev,Alexander Poltorak

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7-Cl-O-Nec1, metabolically stable RIP1 inhibitor

Chemical Structure - 7-Cl-O-Nec1, metabolically stable RIP1 inhibitor (AB221984)

Key facts

Purity

Form

Molecular weight

Molecular formula

PubChem

Nature

Solubility

Biochemical name

Biological description

Canonical smiles

InChi

InChiKey

IUPAC Name

Properties and storage information

Shipped at conditions

Appropriate short-term storage conditions

Appropriate long-term storage conditions

Supplementary information

Biological function summary

Pathways

Product protocols

Publications (11)

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Biochemicals

Primary Antibodies

Biochemicals

Biochemicals

Product promise