1. Signaling Pathways
  2. Apoptosis
  3. RIP kinase

RIP kinase

Receptor-interacting protein kinases; RIPK

Receptor-interacting protein (RIP) kinases are a group of threonine/serine protein kinases with a relatively conserved kinase domain but distinct non-kinase regions. There are seven members of the RIPK family, RIPK1-7, some of which have emerged as critical effectors of immunity to infection with a diverse array of bacterial, viral, and protozoal pathogens.

RIP kinases are cellular signaling molecules that are critical for homeostatic signaling in both communicable and non-communicable disease processes. RIPK1, RIPK2, RIPK3 and RIPK7 have emerged as key mediators of intracellular signal transduction including inflammation, autophagy and programmed cell death, and are thus essential for the early control of many diverse pathogenic organisms.

Cat. No. Product Name Effect Purity Chemical Structure
  • HY-175370
    PROTAC RIPK1 Degrader-1
    Degrader
    PROTAC RIPK1 Degrader-1 is a selective RIPK1 PROTAC degrader. PROTAC RIPK1 Degrader-1 degrades RIPK1 in multiple cancer cell lines (e.g., A375, B16F10 cells). PROTAC RIPK1 Degrader-1 enhances the anti-cancer effect of radiotherapy in syngeneic and humanized mouse models. PROTAC RIPK1 Degrader-1 can be used to study cancers such as melanoma. (Pink: RIPK1-ligand-2: HY-175371, Blue: (S,R,S)-AHPC-Me: HY-112078, Pink + Black: RIPK1 ligand-Linker Conjugate-1: HY-175374, Black: Bispiperidin-piperazin-acetater: HY-175373).
    PROTAC RIPK1 Degrader-1
  • HY-177119
    ZBP1 Covalent PROTAC-1
    Inhibitor
    ZBP1 Covalent PROTAC-1 is a covalent Z-DNA binding protein 1 ZBP1 PROTAC degrader, with its DC50 being 25.69 nM. ZBP1 Covalent PROTAC-1 integrates the ligand that recruits the VHL E3 ubiquitin ligase and the DNA aptamer (Aptamer Z3) with the specific Zα domain that can bind to ZBP1, which has a high affinity (KD = 2.71 nM) with ZBP1. After degrading ZBP1, the phosphorylation levels of downstream signaling molecules RIPK3 and MLKL significantly decrease. ZBP1 Covalent PROTAC-1, encapsulated by nano-liposomes, significantly improves the survival rate of mice infected with influenza A virus (IAV) after administration via the trachea.
    ZBP1 Covalent PROTAC-1
  • HY-N3417
    Kongensin A
    Inhibitor 98.0%
    Kongensin A is a natural product isolated from Croton kongensis. Kongensin A is an effective, covalent HSP90 inhibitor that blocks RIP3-dependent necroptosishas. Kongensin A is a potent necroptosis inhibitor and an apoptosis inducer. Kongensin A has potential anti-necroptosis and anti-inflammation applications.
    Kongensin A
  • HY-19628A
    OD36 hydrochloride
    Inhibitor
    OD36hydrochloride is a RIPK2 inhibitor with an IC50 of 5.3 nM. OD36 hydrochloride is a macrocyclic inhibitor with potent binding to the ALK2 kinase ATP pocket. OD36 hydrochloride shows ALK2-directed activity with KDs of 37 nM.
    OD36 hydrochloride
  • HY-RS11999
    Ripk3 Mouse Pre-designed siRNA Set A
    Inhibitor

    Ripk3 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Ripk3 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.

    Ripk3 Mouse Pre-designed siRNA Set A
  • HY-122665A
    HTH-01-091 TFA
    Inhibitor 99.48%
    HTH-01-091 TFA is a potent and selective maternal embryonic leucine zipper kinase (MELK) inhibitor, with an IC50 of 10.5 nM. HTH-01-091 TFA also inhibits PIM1/2/3, RIPK2, DYRK3, smMLCK and CLK2. HTH-01-091 TFA can be uesd for breast cancer research.
    HTH-01-091 TFA
  • HY-151369
    AV123
    Inhibitor 99.60%
    AV123 (compound 12) is a non-cytotoxic RIPK1 inhibitor (IC50=12.12 µM). AV123 blocks the TNF-α-induced necroptotic (EC50=1.7 μM) but not the apoptotic cell death. AV123 can be used in the study of necrotic chronic conditions such as ischemia-reperfusion injury of the brain, heart and kidney, inflammatory diseases, neurodegenerative diseases and infectious diseases.
    AV123
  • HY-15760R
    Necrostatin-1 (Standard)
    Inhibitor
    Necrostatin-1 (Standard) is the analytical standard of Necrostatin-1. This product is intended for research and analytical applications. Necrostatin-1 (Nec-1) is a potent and cross the blood-brain barrier necroptosis inhibitor with an EC50 of 490 nM in Jurkat cells. Necrostatin-1 inhibits RIP1 kinase (EC50=182 nM). Necrostatin-1 is also an IDO inhibitor.
    Necrostatin-1 (Standard)
  • HY-125466
    cRIPGBM
    cRIPGBM, a proapoptotic derivative of RIPGBM, a cell type-selective inducer of apoptosis in GBM cancer stem cells (CSCs) by binding to receptor-interacting protein kinase 2 (RIPK2), with an EC50 of 68 nM in GBM-1 cells.
    cRIPGBM
  • HY-133014
    RIP2 kinase inhibitor 1
    Inhibitor
    RIP2 kinase inhibitor 1 (compound 11) is a potent and selective receptor interacting protein 2 (RIP2) kinase inhibitor with an IC50 of 0.03 μM for RIP2 FP. RIP2 kinase inhibitor 1 is used for autoinflammatory disorders.
    RIP2 kinase inhibitor 1
  • HY-126296
    RIPK1-IN-3
    Inhibitor
    RIPK1-IN-3 (Example 38), a RIPK1 inhibitor, extracted from patent WO2018148626A1, possesses anti-inflammatory proprieties.
    RIPK1-IN-3
  • HY-143728
    RIPK1-IN-10
    Inhibitor 98.25%
    RIPK1-IN-10 is a potent RIPK1 inhibitor, example 37, extracted from patent WO2021160109.
    RIPK1-IN-10
  • HY-B0339S
    Primidone-d5
    Inhibitor 99.00%
    Primidone-d5 is the deuterium labeled Primidone. Primidone is the orally active inhibitor for TRPM3 (IC50 = 0.6 μM), RIP kinase and voltage-gated sodium channel, and the antagonist for GABA receptor. Primidone can be used as the analgesic and anticonvulsant agent.
    Primidone-d<sub>5</sub>
  • HY-173185
    RIP1-IN-1
    Inhibitor
    RIP1-IN-1 is an orally active RIP1 inhibitor with strong RIP1 binding affinity (Kd: 110 nM). RIP1-IN-1 exhibits strong anti-necroptosis activity. RIP1-IN-1 effectively inhibits the formation of necrosomes by blocking the phosphorylation of RIP1, RIP3 and MLKL signaling pathways. RIP1-IN-1 inhibits necroptosis and can be used in the study of acute liver injury.
    RIP1-IN-1
  • HY-179234
    LD5097
    Degrader
    LD5097 is a highly effective and selective PROTAC degrader targeting RIPK1. LD5097 can rapidly and efficiently downregulate RIPK1 and significantly enhance TNFα-mediated apoptosis in Jurkat cells. LD5097 significantly increases the levels of cleaved caspase-3/7 and PARP. LD5097 can be used for the study of acute T-lymphoblastic leukemia.
    LD5097
  • HY-169509
    Topoisomerase I/II inhibitor 8
    Activator
    Topoisomerase I/II Inhibitor 8 (Compound Ru7) is a dual catalytic inhibitor of Topoisomerase I/II, capable of inducing DNA damage and PARP-1 activation, which subsequently leads to the activation of RIPK1, RIPK3, and MLKL, ultimately triggering necroptosis. Topoisomerase I/II Inhibitor 8 demonstrates remarkable anticancer activity by effectively targeting the nuclei of cancer cells and inducing cell death through necroptosis, showing great clinical potential in circumventing drug resistance in cancer treatment.
    Topoisomerase I/II inhibitor 8
  • HY-173445
    RIPK1-IN-30
    Inhibitor
    RIPK1-IN-30 (compound 24) is a potent RIPK1 inhibitor with an IC50 of 2.01 μM. RIPK1-IN-30 exhibits protective effects in HT-29 cell model of TSZ-induced necroptosis with an EC50 of 6.77 μM.
    RIPK1-IN-30
  • HY-141453
    Desmethyl-WEHI-345 analog
    Inhibitor
    Desmethyl-WEHI-345 analog is a protein kinase inhibitor extracted from patent WO2012003544A1, example 12. Desmethyl-WEHI-345 analog can be used for the research of colon cancer.
    Desmethyl-WEHI-345 analog
  • HY-169107
    RIPK1-IN-25
    Inhibitor
    RIPK1-IN-25 (WL8) is a blood-brain permeable RIPK1 inhibitor with EC50 and Kd values are 19.9 and 25 nM, respectively. RIPK1-IN-25 can be used in the study of neurometabolic diseases.
    RIPK1-IN-25
  • HY-173454
    RIPK2/3-IN-2
    Inhibitor 99.67%
    RIPK2/3-IN-2 (29) is a dual RIPK2 and RIPK3 inhibitor, with IC50 values of 12 nM and 18 nM, respectively. RIPK2/3-IN-2 (29) induces necroptosis, with an EC50 of 0.16 μM.
    RIPK2/3-IN-2
Cat. No. Product Name / Synonyms Species Source
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