2. Signaling Pathways
  3. MAPK/ERK Pathway
  4. JNK

JNK

c-Jun N-terminal kinase

JNK

Related Products

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JNK (c-Jun N-terminal kinase), a kinase subfamily belonging to the MAPK, is activated in response to various stress stimuli and possesses a wide variety of regulatory functions. The JNK family of serine/threonine protein kinases comprises three isoforms (JNK1, JNK2 and JNK3). JNKs are involved in the emergence and progression of diverse pathologies such as neurodegenerative, cardiovascular and metabolic disorders as well as inflammation and cancer.

Similar to the other MAP kinases, JNKs are activated by a phosphorylation cascade generally involving two types of upstream kinases, the so-called MAP kinase kinase kinases (MAP3K, MKKK) and the MAP kinase kinases (MAP2K; MKK). At the MAP2K level, JNKs are activated by MKK4 and MKK7, the former is a common activator of the JNK and the p38 MAP kinase signaling pathway. The JNK cascade shares various intersection points with other pathways making it a part of a complex signaling network.

JNK Isoform Specific Products:

JNK Isoform Comparison
Cat. No. Product Name Effect Purity Chemical Structure
  • HY-N6576
    Hellebrigenin
    		Inhibitor 99.69%
    Hellebrigenin is an inhibitor that selectively targets the MAPK signaling pathway (ERK, p38, JNK) and XIAP, and can inhibit Akt expression and phosphorylation. Hellebrigenin can activate endogenous apoptosis pathways (such as mitochondrial membrane potential disruption, Caspase family activation, PARP cleavage), downregulate anti-apoptotic proteins (Bcl-2, Bcl-xL) and upregulate pro-apoptotic proteins (Bax, Bak). Hellebrigenin can also induce DNA double-strand breaks to activate the ATM pathway. Hellebrigenin can inhibit tumor cell proliferation and clone formation, and is mainly used in the study of oral squamous cell carcinoma, liver cancer and other cancers.
    Hellebrigenin
  • HY-N7695
    Physalin B
    		Modulator
    Physalin B is an orally active anti-inflammatory and anticancer agent. Physalin B can be isolated from Physalis alkekengi L. var. Franchetii. Physalin B inhibits the activation of the NF-κB, NLRP3 inflammasome, STAT3, PI3K/Akt and Hedgehog signaling pathways, regulates the phosphorylation levels of GSK-3β, p38 MAPK, ERK1/2 and JNK, and promotes the nuclear translocation of NRF2. Physalin B reduces the levels of pro-inflammatory cytokines and factors, induces mitochondrial reactive oxygen species (mito-ROS) production, Apoptosis, G2/M cell cycle arrest and incomplete Autophagy, alters cytoskeleton structure and alleviates oxidative stress. Physalin B reduces cancer cell viability, ameliorates liver and lung tissue damage and alleviates liver fibrosis. Physalin B can be used in research related to ulcerative colitis, breast cancer, acute lung injury, colon cancer, non-alcoholic steatohepatitis, liver fibrosis, lung cancer, pancreatic cancer, lymphoma, ovarian cancer, sarcoma and leukemia.
    Physalin B
  • HY-18982R
    Anisomycin (Standard)
    		Activator
    Anisomycin (Standard) is the analytical standard of Anisomycin. This product is intended for research and analytical applications. Anisomycin is a potent protein synthesis inhibitor which interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system[1]. Anisomycin is a JNK activator, which increases phospho-JNK[2][3]. Anisomycin is a bacterial antibiotic[4].
    Anisomycin (Standard)
  • HY-W004283R
    Pentadecanoic acid (Standard)
    		Activator
    α-Linolenic acid (Standard) is the analytical standard of α-Linolenic acid. This product is intended for research and analytical applications. α-Linolenic acid, isolated from Perilla frutescens, is an essential fatty acid that cannot be synthesized by humans. α-Linolenic acid can affect the process of thrombotic through the modulation of PI3K/Akt signaling. α-Linolenic acid possess the anti-arrhythmic properties and is related to cardiovascular disease and cancer.
    Pentadecanoic acid (Standard)
  • HY-113402R
    Gamma-glutamylcysteine (Standard)
    		Inhibitor
    Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide. Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine (Standard)
  • HY-N2026S1
    Propylparaben-d4
    		99.55%
    Propylparaben-d4 (Propyl parahydroxybenzoate-d4) is the deuterium labeled Propylparaben (HY-N2026). Propylparaben (Propyl parahydroxybenzoate) is an antibacterial preservative that can be produced by plants and bacteria. Propylparaben is an orally active weak estrogen receptor agonist. Propylparaben regulates the PI3K-AKT and JNK signaling pathways, and induces oxidative stress. Propylparaben is commonly used in cosmetics, pharmaceuticals and foods, and can be used in studies related to ovarian aging and myocardial ischemia-reperfusion injury.
    Propylparaben-d<sub>4</sub>
  • 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.
    IQ-1S free acid
  • HY-108419
    WHI-P258
    		99.91%
    WHI-P258, a quinazoline compound, binds to the active site of JAK3 with an estimated Ki of 72 µM. WHI-P258 does not inhibit JAK3 and does not affect the thrombin-induced aggregation of platelets even at 100 μM.
    WHI-P258
  • HY-N7259
    (+)-Isomenthone
    		Inhibitor 99.13%
    (+)-Isomenthone is an enantiomer form of Menthone (HY-N2381). (+)-Isomenthone blocks TNF-α-triggered activation of the JNK and p38 MAPK pathways.(+)-Isomenthone inhibits TNF-α-mediated reductions in cell viability, increases in apoptosis, and downstream apoptotic events linked to pathway activation.(+)-Isomenthone protects human dermal fibroblasts against TNF-α-induced cell death under serum-deprived conditions.
    (+)-Isomenthone
  • HY-111254
    GQ-16
    		Modulator 98.12%
    GQ-16 is an orally active PPARγ partial agonist with an IC50 of 1.84 μM and a Ki of 160 nM against human PPARγ. GQ-16 inhibits Cdk5-mediated Ser-273 phosphorylation. GQ-16 improves insulin sensitivity and glucose tolerance in obese and diabetic mice. GQ-16 also exhibits certain cytotoxicity against tumor cells. GQ-16 can be used in research related to obesity, diabetes and cancer.
    GQ-16
  • HY-P991400
    GSK1995057
    		Inhibitor 99.09%
    GSK1995057 is a human monoclonal antibody (mAb) targeting TNFRSF1A. GSK1995057 selectively binds to TNFR1, blocks the binding of TNF-α and LT-α, and does not interfere with TNFR2 signaling. GSK1995057 inhibits the activation of NF-κB, JNK and MAPK pathways, alleviates apoptosis (apoptosis) and inflammatory responses (inhibiting IL-1β, IL-6, IL-10, TNF-α), and prevents viability loss of human nucleus pulposus cells. GSK1995057 inhibits the expression of cytokines and neutrophil adhesion molecules in human pulmonary microvascular endothelial cell monolayers, and reduces inflammatory responses and lung injury symptoms in non-human primates. GSK1995057 forms complexes with HAVH autoantibodies, thereby activating TNFR1 and triggering the release of cytokines and IL-8 in human cells. GSK1995057 can be used in research related to intervertebral disc degeneration and acute lung injury.
    GSK1995057
  • HY-111954
    (+)-Erinacin A
    		99.81%
    (+)-Erinacin A (Erinacine A) is a cyanoditerpenoid isolated from Hericium erinaceus with anticancer, anti-inflammatory and neuroprotective activities. (+)-Erinacin A can induce cancer cell death by activating extrinsic and intrinsic apoptosis pathways. (+)-Erinacin A can also inhibit the expression of NO synthase (iNOS) and the production of nitrotyrosine to exert inflammatory and neuroprotective effects, thereby reducing ischemic brain damage.
    (+)-Erinacin A
  • HY-10412
    CEP-1347
    		Inhibitor 98.50%
    CEP-1347 is an inhibitor of the JNK/SAPK pathway with neuroprotective effects. CEP-1347 blocks JNK1 activation induced by members of the mixed lineage kinase (MLK) family (MLK3, MLK2, MLK1, dual leucine zipper kinase, and leucine zipper kinase). As an inhibitor of MDM4, CEP-1347 can more effectively inhibit the growth of glioma cells expressing wild-type p53.
    CEP-1347
  • HY-169021
    JNK-1-IN-3
    		Inhibitor 98.44%
    JNK-1-IN-3 (Compound 9e) is an inhibitor of JNK1 that downregulates JNK1 gene expression and inhibits the protein levels of its phosphorylated form, concurrently reducing the expression of its downstream targets, c-Jun and c-Fos, in tumors while restoring p53 activity. JNK-1-IN-3 exhibits broad-spectrum antiproliferative activity, particularly with high inhibitory activity against renal and breast cancer cell lines, demonstrating both in vivo and in vitro anticancer activity.
    JNK-1-IN-3
  • 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.
    Sugiol
  • HY-N0854
    Alisol F
    		Inhibitor 99.89%
    Alisol F is a protostane-type triterpenoid with anti-inflammatory and anti-hepatitis B virus activities. Alisol F inhibits LPS (HY-D1056)-induced phosphorylation of ERK, JNK, p38, STAT3 and NF-κB (p65), suppresses the production of NO, IL-6, TNF-α and IL-1β, and also downregulates the levels of iNOS and COX-2. Alisol F reduces the serum alanine aminotransferase and aspartate aminotransferase levels in mice with acute liver injury and ameliorates their liver pathological damage.
    Alisol F
  • HY-W011398
    Linoleate sodium
    		99.88%
    Linoleate sodium is an orally active IL8 regulator via the JNK and NF-κB pathway. Linoleate sodium can change the composition of fatty acids and the production of metabolites in cells. Linoleate sodium has anti-inflammatory, immune-regulating, and tumor cell growth-affecting activities.
    Linoleate sodium
  • HY-111431AR
    p-Cresyl sulfate potassium (Standard)
    		Activator
    p-Cresyl sulfate (potassium) (Standard) is the analytical standard of p-Cresyl sulfate (potassium). This product is intended for research and analytical applications. p-Cresyl sulfate (p-Tolyl sulfate) potassium is a uremic toxin, that can cause renal damage and dysfunction. p-Cresyl sulfate potassium shows antiproliferation activity. p-Cresyl sulfate potassium increases the protein expression of HIF-1α and VHL, decreases the protein expression of HIF-2α. p-Cresyl sulfate potassium induces epithelial-mesenchymal transition (EMT). p-Cresyl sulfate potassium activates the JNK and p38 MAPK signaling pathways.
    p-Cresyl sulfate potassium (Standard)
  • HY-101287
    MPT0B392
    		Activator 99.63%
    MPT0B392, an orally active quinoline derivative, induces c-Jun N-terminal kinase (JNK) activation, leading to apoptosis. MPT0B392 inhibits tubulin polymerization and triggers induction of the mitotic arrest, followed by mitochondrial membrane potential loss and caspases cleavage by activation of JNK and ultimately leads to apoptosis. MPT0B392 is demonstrated to be a novel microtubule-depolymerizing agent and enhances the cytotoxicity of sirolimus in sirolimus-resistant acute leukemic cells and the multidrug resistant cell line.
    MPT0B392
  • HY-N6928
    Mogroside III-E
    		Inhibitor 99.30%
    Mogroside III-E is a cucurbitane-type triterpenoid glycoside extracted from Siraitia grosvenorii, and it is an orally active TLR4 inhibitor. Mogroside III-E downregulates the expression of TLR4 and MyD88, and blocks the phosphorylation of downstream ERK, JNK and p38 MAPK molecules; meanwhile, it inhibits TGF-β- or LPS-mediated transdifferentiation of primary pulmonary fibroblasts into myofibroblasts, reduces the content of fibrosis markers such as hydroxyproline, suppresses the pro-fibrotic TGF-β/Smad signaling pathway, and downregulates the levels of inflammatory factors MPO and IL-1β. Mogroside III-E alleviates Bleomycin (HY-108345)-induced pulmonary collagen deposition and inflammatory infiltration in mice. Mogroside III-E can be used in studies related to idiopathic pulmonary fibrosis.
    Mogroside III-E
Cat. No. Product Name / Synonyms Application Reactivity
JNK Isoform Comparison

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