JNK2
JNK2 (MAPK9) is a member of the c-Jun N-terminal kinase (JNK) family, a stress-activated branch of the mitogen-activated protein kinase (MAPK) network that transduces extracellular stress, cytokine, and growth-factor signals into cellular responses regulating proliferation, survival, apoptosis, differentiation, and inflammation[1][2]. Mechanistically, JNK signaling is activated through a kinase cascade involving MAP3Ks, MKK4, and MKK7, leading to phosphorylation of transcriptional regulators such as c-Jun and other stress-responsive substrates that control gene expression programs[3][4]. In disease-associated contexts, dysregulated JNK signaling has been linked to cancer, obesity, type 2 diabetes, inflammatory disorders, neurodegenerative diseases, and pathological cell death, making the pathway a widely studied experimental target[1][2][3]. Compared with related isoforms, JNK1 and JNK2 are broadly expressed across tissues, whereas JNK3 shows a more restricted distribution, primarily in the brain, heart, and testis[1][3]. Importantly, JNK1 and JNK2 can exhibit both redundant and opposing biological functions, and experimental studies have demonstrated that JNK1, but not JNK2, is required for specific TNF-α-induced responses including c-Jun kinase activation and apoptosis, highlighting isoform-specific signaling properties[1][4]. For experimental applications, the growing recognition of isoform-dependent JNK biology has stimulated the development of JNK inhibitors, with current research emphasizing improved selectivity and on-target specificity for mechanistic studies and therapeutic evaluation[1][2].
References:
- [1]. Harrison R, et al. Enacting open disclosure in the UK National Health Service: A qualitative exploration. J Eval Clin Pract. 2017 Aug;23(4):713-718. [Content Brief]
- [2]. Karnam S, et al. Biochemical and biomechanical characteristics of dystrophin-deficient mdx3cv mouse lens. Biochim Biophys Acta Mol Basis Dis. 2021 Jan 1;1867(1):165998. [Content Brief]
- [3]. Cui J, et al. JNK pathway: diseases and therapeutic potential[J]. Acta Pharmacologica Sinica, 2007, 28(5): 601-608.
- [4]. Das D, et al. Secondary Structure Preferences of the Anthrax Toxin Protective Antigen Translocase. J Mol Biol. 2017 Mar 10;429(5):753-762. [Content Brief]
All Product Categories
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JNK2 Related Products (44)
Related Products (44)
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Antibodies (1)
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JNK Inhibitor VIII
0 ImagesSynonyms: TCS JNK 6oJNK Inhibitor VIII (TCS JNK 6o) is a c-Jun N-terminal kinases (JNK-1, -2, and -3) inhibitor with Ki values of 2 nM, 4 nM, 52 nM, respectively, and has IC50 values of 45 nM and 160 nM for JNK-1 and -2, respectively.
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Tanzisertib
0 ImagesSynonyms: CC-930Tanzisertib (CC-930) is a potent JNK1/2/3 inhibitor with IC50s of 61/7/6 nM, respectively.
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JNK2/MKK7 PPI-IN-1
0 ImagesCat. No.: HY-181812JNK2/MKK7 PPI-IN-1 is an orally active JNK2 inhibitor with an IC50 of 0.99 μM and a Kd of 81.6 μM. JNK2/MKK7 PPI-IN-1 inhibits JNK2 kinase activity, disrupts JNK2-MKK7 protein-protein interaction, and reduces c-Jun phosphorylation. JNK2/MKK7 PPI-IN-1 inhibits LPS-induced overexpression of inflammatory cytokines IL-6 and TNF-α. JNK2/MKK7 PPI-IN-1 can be used for the research of acute lung injury.
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SP600125 (GMP)
0 ImagesSP600125 (GMP) is SP600125 (HY-12041) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. SP600125 is an orally active, reversible, and ATP-competitive JNK inhibitor with IC50s of 40, 40 and 90 nM for JNK1, JNK2 and JNK3, respectively. SP600125 is a potent ferroptosis inhibitor. SP600125 induces the transformation of bladder cancer cells from autophagy to apoptosis.
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Iso-AS601245 TFA
0 ImagesCat. No.: HY-10612ACAS No.: 1644386-60-6Iso-AS601245 TFA is an orally active JNK inhibitor, with IC50 values of 0.15 μM, 0.22 μM and 0.07 μM against JNK1, JNK2 and JNK3, respectively. Iso-AS601245 TFA reduces plasma TNF-α levels in mice and inhibits IL-2 secretion in activated T cells. Iso-AS601245 TFA alleviates adjuvant-induced rheumatoid arthritis in mice. Iso-AS601245 TFA can be used in studies related to rheumatoid arthritis.
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AS601245
0 ImagesAS601245 is an orally active, selective, ATP competitive JNK (c-Jun NH2-terminal protein kinase) inhibitor with IC50s of 150, 220, and 70 nM for three JNK human isoforms (hJNK1, hJNK2, and hJNK3), respectively. AS601245 exhibits 10- to 20-fold selectivity over c-src, CDK2, and c-Raf and more than 50- to 100-fold selectivity over a range of Ser/Thr- and Tyr-protein kinases. Neuroprotective properties.
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Pseudoginsenoside F11
0 ImagesSynonyms: Ginsenoside A1Pseudoginsenoside F11 is an orally active neuroprotective agent. Pseudoginsenoside F11 reduces the expression of β-amyloid precursor protein, inhibits the production of Aβ1-40, downregulates the expression of JNK2, p53 and activated Caspase 3, and restores the activities of SOD and Glutathione peroxidase. Pseudoginsenoside F11 inhibits the excessive activation of μ-Calpain and restores the level of neuronal Nitric oxide synthase. Pseudoginsenoside F11 reduces infarct volume, alleviates cerebral edema, decreases neuronal loss, improves neurological deficits and enhances long-term functional outcomes in transient cerebral ischemia models. Pseudoginsenoside F11 antagonizes Methamphetamine-induced behavioral deficits, dopamine level reduction and neurotoxicity without altering the baseline behaviors of normal mice. Pseudoginsenoside F11 can be used in studies related to Alzheimer's disease, transient cerebral ischemic injury and Methamphetamine-induced neurotoxicity.
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Cornuside
0 ImagesCornuside is an iridoid glycoside with anti-allergic, anti-inflammatory, and neuroprotective activities. Cornuside exerts anti-allergic activity by downregulating the p38 MAPK, JNK, and NF-κB signaling pathways, and inhibits IgE-mediated histamine release from mast cells. Cornuside improves cognitive impairment in mice by inhibiting BACE1 activity (IC50 = 55.84 μg/mL) and enhancing ChAT activity. Cornuside inhibits LPS (HY-D1056)-induced inflammatory mediators, including iNOS, COX-2, PGE2, TNF-α, IL-6, and IL-1β, by suppressing NF-κB activation.
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Indirubin-3′-oxime
0 ImagesSynonyms: IDR3O; I3OIndirubin-3′-oxime (IDR3O), a synthetic derivative of indirubin, is a potent inhibitor of cyclin-dependent kinases (CDKs) and glycogen synthase kinase 3β (GSK3β). Indirubin-3′-oxime directly inhibits the activity of all three isoforms of JNK (JNK1, JNK2, and JNK3), with IC50s of 0.8 μM, 1.4 μM, and 1.0 μM, respectively. Indirubin-3′-oxime can enhance height growth via activation of Wnt/β-catenin signaling in chondrocytes.
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PT109
0 ImagesPT109 is an orally active, blood-brain barrier permeable multi-kinase inhibitor. By inhibiting PTBP1, PT109 promotes the switch of pyruvate kinase isoform from PKM2 to PKM1, thereby effectively inhibiting the proliferation and migration of glioblastoma multiforme and inducing its reprogramming into oligodendrocytes. PT109 also targets and regulates key signaling molecules such as JNK, SGK1, GSK3β to exert neuroprotective effects including promoting neurogenesis, inducing synapse formation and alleviating neuroinflammation. In Alzheimer's disease models, PT109 exhibits significant efficacy in improving spatial learning ability, along with excellent in vivo pharmacokinetic properties. PT109 can be used to investigate metabolic reprogramming of glioblastoma multiforme and neuroprotective mechanisms of Alzheimer's disease.
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Quin-C7
0 ImagesQuin-C7 is an orally active FPR2/ALX antagonist. Quin-C7 binds to the orthosteric ligand-binding pocket of FPR2/ALX, modulates receptor activation, and inhibits pro-inflammatory ERK signaling mediated by serum amyloid A (SAA). Quin-C7 reduces pro-inflammatory mediators TNF-α levels, increases anti-inflammatory IL-10, decreases inflammatory neutrophils and pro-inflammatory M1 macrophages, downregulates ERK1/2 phosphorylation, and upregulates JNK1/2/3 phosphorylation. Quin-C7 blocks FPR2/mFpr2 signaling, reduces brain lesion volume. Quin-C7 can be used for the research of inflammatory bowel disease and neuromyelitis optica spectrum disorder.
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JNK3 inhibitor-4
0 ImagesJNK3 inhibitor-4 is a potent and BBB-permeable inhibitor of JNK3 (IC50=1.0 nM) based on 2-aryl-1-pyrimidinyl-1H-imidazole-5-yl acetonitrile. JNK3 inhibitor-4 shows excellent selectivity over other protein kinases including isoforms JNK1 (IC50=143.9 nM) and JNK2 (IC50=298.2 nM). JNK3 inhibitor-4 has neuroprotective effect and predicated blood-brain barrier permeability.
