1. Signaling Pathways
  2. MAPK/ERK Pathway
  3. JNK
  4. JNK2 Isoform

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].

JNK2 Related Products (42):

Cat. No. Product Name Effect Purity
  • HY-12041
    SP600125
    Inhibitor 99.55%
    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.
  • HY-13319
    JNK-IN-8
    Inhibitor 99.67%
    JNK-IN-8 (JNK Inhibitor XVI) is a potent JNK inhibitor with IC50s of 4.7 nM, 18.7 nM, and 1 nM for JNK1, JNK2, and JNK3, respectively.
  • HY-N0773
    Isovitexin
    Inhibitor 99.90%
    Isovitexin is a flavonoid isolated from passion flower, Cannabis and, and the palm, possesses anti-inflammatory and anti-oxidant activities; Isovitexin acts like a JNK1/2 inhibitor and inhibits the activation of NF-κB.
  • HY-107598
    JNK Inhibitor VIII
    Inhibitor 99.58%
    JNK 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.
  • HY-14761
    Bentamapimod
    Inhibitor 99.23%
    Bentamapimod (AS 602801) is an ATP-competitive JNK inhibitor with IC50 of 80 nM, 90 nM, and 230 nM for JNK1, JNK2, and JNK3, respectively.
  • HY-181812
    JNK2/MKK7 PPI-IN-1
    Inhibitor
    JNK2/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.
  • HY-12041G
    SP600125 (GMP)
    Inhibitor
    SP600125 (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.
  • HY-15495
    Tanzisertib
    Inhibitor 99.98%
    Tanzisertib (CC-930) is a potent JNK1/2/3 inhibitor with IC50s of 61/7/6 nM, respectively.
  • HY-15617
    JNK-IN-7
    Inhibitor 98.17%
    JNK-IN-7 is a potent JNK inhibitor with IC50 of 1.5, 2 and 0.7 nM for JNK1, JNK2 and JNK3, respectively.
  • HY-138304
    CC-90001
    Inhibitor 99.98%
    CC-90001 is a potent, selective and orally active inhibitor of c-Jun N-terminal kinase (JNK). CC-90001 shows 12.9-fold selectivity for JNK1 over JNK2 in a cell-based model. CC-90001 can be used for the research of idiopathic pulmonary fibrosis.
  • HY-11010
    AS601245
    Inhibitor 98.19%
    AS601245 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.
  • HY-N0541
    Pseudoginsenoside F11
    Inhibitor 99.87%
    Pseudoginsenoside F11 is an orally active neuroprotective agent. Pseudoginsenoside F11 reduces the expression of β-amyloid precursor protein, inhibits the production of 1-40, 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.
  • HY-15881
    TCS JNK 5a
    Inhibitor 99.40%
    TCS JNK 5a is a potent JNK3 inhibitor with a pIC50 of 6.7. TCS JNK 5a also inhibits JNK2 with a pIC50 of 6.5.
  • HY-N0631
    Cornuside
    Inhibitor 99.99%
    Cornuside 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.
  • HY-139254
    Indirubin-3′-oxime
    Inhibitor 99.10%
    Indirubin-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.
  • HY-167832
    PT109
    Inhibitor 99.20%
    PT109 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.
  • HY-151929
    JNK3 inhibitor-4
    Inhibitor 99.37%
    JNK3 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.
  • HY-100233
    IQ-1S free acid
    Inhibitor 99.28%
    IQ-1S free acid is a prospective inhibitor of NF-κB/activating protein 1 (AP-1) activity with an IC50 of 2.3±0.41 μM. IQ-1S free acid has binding affinity (Kd values) in the nanomolar range for all three JNKs with Kds of 100 nM, 240 nM, and 360 nM for JNK3, JNK1, and JNK2, respectively.
  • HY-N1195
    Sugiol
    Inhibitor 99.88%
    Sugiol is an abietane diterpenoid, can be isolated from Calocedrus formosana bark. Sugiol has anti-inflammatory activity, could effectively reduce intracellular reactive oxygen species (ROS) production in lipopolysaccharide (LPS)-stimulated macrophages.
  • HY-107600
    IQ-3
    Inhibitor 99.61%
    IQ-3 is a specific inhibitor of the c-Jun N-terminal kinase (JNK) family, with preference for JNK3. IQ-3 exhibits Kd values of 0.24 μM, 0.29 μM and 0.066 μM for JNK1, JNK2 and JNK3, respectively.
Cat. No. Product Name / Synonyms Application Reactivity