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-112402
    SP 600125, negative control
    		Control 98.05%
    SP 600125, negative control (SPM1) is an alkyl derivative of pyrazoloanthrone, which can be used as a negative control for SP600125 (HY-12041).
    SP 600125, negative control
  • HY-126858
    Ambuic acid
    		Inhibitor 98.00%
    Ambuic acid exhibits antimicrobial activity against Staphylococcus aureus, with IC50 of 43.9 μM for strain ATCC 6538. Ambuic acid is an inhbitor for the biosynthesis of cyclic peptide quorum sensing molecules (quormones) in gram-positive bacteria. Ambuic acid exhibits anti-inflammatory activity through ERK/JNK/MAPK signaling pathway.
    Ambuic acid
  • HY-148066
    DB0662
    		Degrader 99.66%
    DB0662 is a multi-target kinase-directed PROTAC degrader, targeting kinases including PTK2B, MAPK9, BLK, CSK, LIMK1, etc.
    DB0662
  • HY-108646
    SX 011
    		Inhibitor 99.33%
    SX 011 is a p38 inhibitor with IC50s of 9 nM and 90 nM against p38α and p38β, respectively. SX 011 also inhibits JNK-2 with an IC50 of 100 nM. SX-011 is orally bioavailable.
    SX 011
  • 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.
    IQ-3
  • HY-170420
    JNK-1-IN-5
    		Inhibitor 99.63%
    JNK-1-IN-5 (Compound 14) is a potent JNK1 inhibitor with sub-nanomolar efficacy. JNK-1-IN-5 suppresses TGF-β-induced epithelial-mesenchymal transition. JNK-1-IN-5 is promising for research of anti-pulmonary fibrosis agent targeting JNK1.
    JNK-1-IN-5
  • HY-170879
    JD123
    		Inhibitor
    JD123 inhibits JNK1 activity and the expression of cJun (1-135). JD123 is a ATP-competitive p38-γ MAPK inhibitor, but not effect to ERK1, ERK2, or p38-α, p38-β or p38-δ..
    JD123
  • HY-W026930
    Benzanthrone
    		Activator 99.69%
    Benzanthrone is an immunotoxic, pro-inflammatory Photosensitizer. Benzanthrone upregulates iNOS, COX-2 and inflammatory cytokines; activates ERK1/2, p38, JNK, AP-1 and NF-κB; inhibits Nrf2; and induces oxidative stress and DNA damage. Upon radiation exposure, Benzanthrone generates singlet oxygen and superoxide anion radicals, induces photohemolysis and lipid peroxidation, and alters the levels of skin xenobiotic enzymes. Benzanthrone exhibits differential genotoxicity in different cell lines. Benzanthrone possesses skin tumor-initiating and promoting activities. Benzanthrone can be used in skin tumor-related studies.
    Benzanthrone
  • HY-B1135R
    Benzbromarone (Standard)
    Benzbromarone (Standard) is the analytical standard of Benzbromarone. This product is intended for research and analytical applications. Benzbromarone is an orally active anti-gout agent. Benzbromarone has anti-infammatory, anti-oxidative stress and nephroprotective effects. Benzbromarone can be used for the research of hyperuricemia and gout.
    Benzbromarone (Standard)
  • HY-113509B
    15(R)-Lipoxin A4
    		Inhibitor 98.3%
    15 (R)-Lipoxin A4 (15-epi-LXA4) is a specialized pro-resolving mediator and an acetylated derivative of COX2. 15 (R)-Lipoxin A4 is present in neurons. 15 (R)-Lipoxin A4 induces the SPM synthases ALOX12 and ALOX15, as well as the pro-resolving receptor ALX. 15 (R)-Lipoxin A4 inhibits protein kinases, including JNK1/2/3, Lyn, STAT-3 and STAT-6. 15 (R)-Lipoxin A4 enhances the release of pro-resolving mediators. 15 (R)-Lipoxin A4 alleviates the pro-inflammatory phenotype of tendon-derived stromal cells. 15 (R)-Lipoxin A4 promotes the resolution of neuroinflammation. 15 (R)-Lipoxin A4 is applicable to research related to achilles tendinitis, achilles tendon rupture and Alzheimer’s disease.
    15(R)-Lipoxin A4
  • HY-B1839R
    Fluazinam (Standard)
    		Activator
    Fluazinam (Standard) is the analytical standard of Fluazinam (HY-B1839). This product is intended for research and analytical applications. Fluazinam is a broad spectrum pyridinamine fungal inhibitor. Fluazinam is an orally active dinitroaniline fungicide. Fluazinam induces phosphorylation of JNK, activates p38 pathway, decreases Bcl-2, activates caspase-3, decreases complex I activity, increases Autophagy and Apoptosis. Fluazinam has strong antifungal activity against F. fujikuroi and B. maydis. Fluazinam has a negative impact on Brachydanio rerio and worker bees.
    Fluazinam (Standard)
  • HY-150053
    JNK-IN-11
    		Inhibitor 98.01%
    JNK-IN-11 (compound 1) is a potent JNK inhibitor with an IC50 value of 2.2, 21.4, 1.8 µM for JNK1, JNK2, JNK3, respectively. JNK-IN-11 has the potential for the research of alzheimer and parkinson disease.
    JNK-IN-11
  • HY-121683
    (E)-2-Hexadecenal
    		Activator 99.9%
    (E)-2-Hexadecenal (trans-2-Hexadecenal) is an MLK3 activator that induces cytoskeletal remodeling, leading to cell rounding, detachment, and ultimately apoptosis in human and mouse cells. (E)-2-Hexadecenal activates the MLK3 signaling pathway, phosphorylating MKK4/7 and JNK, subsequently activating downstream targets of JNK, such as c-Jun phosphorylation, cytochrome c release, Bax activation, Bid cleavage, and Bim translocation to mitochondria. (E)-2-Hexadecenal has potential applications in research related to sphingolipid signaling pathways.
    (E)-2-Hexadecenal
  • HY-77009
    JNK-IN-13
    		Inhibitor
    JNK-IN-13 (compound 1) is a potent and selective JNK inhibitor with IC50s of 290 nM and 500 nM for JNK3 and JNK2, respectively.
    JNK-IN-13
  • HY-171980
    OZO-H
    		Inducer
    OZO-H is a GST inhibitor. OZO-H is an OZO derivative with potent anti-cancer effects. OZO-H releases JNK1 from GST-JNK1 complex. OZO-H induces JNK1 phosphorylation and activates c-Jun in cancer cells.
    OZO-H
  • HY-10851
    JNK-9L
    		Inhibitor 98.06%
    JNK-9L (Compound 9l) is a BBB-penetrable and ATP-competitive JNK inhibitor with IC50s of 0.099 and 0.148  μM for JNK1 and JNK3, respectively. JNK-9L significantly inhibits c-jun phosphorylation and Streptozotocin (HY-13753)-induced ROS generation with an IC50 of 0.8  nM. JNK-9L can be used for neurodegenerative disorders like Parkinson’s disease research.
    JNK-9L
  • HY-Y1322S
    Triphenyl phosphate-d15
    		Activator 99.74%
    Triphenyl phosphate-d15 is the deuterium labeled Triphenyl phosphate. Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.
    Triphenyl phosphate-d<sub>15</sub>
  • HY-120349
    LL-Z1640-4
    		Inhibitor 99.0%
    LL-Z1640-4 is a potent p38/JNK signaling inhibitor. LL-Z1640-4 significantly diminishes p38 and JNK activation in HCC cells transfected with MLK4 siRNA. LL-Z1640-4 markedly attenuates ROS production induced by MLK4 knockdown. LL-Z1640-4 significantly reduces the apoptotic cells in HCC cells transfected with siMLK4.
    LL-Z1640-4
  • HY-15035
    S-Diclofenac
    		Inhibitor 99.20%
    S-Diclofenac (ACS 15) is a hybrid molecule of an H2S donor and the NSAID diclofenac. S-Diclofenac activates the p53 signaling pathway, and inhibits the activation of JNK. S-Diclofenac exhibits antioxidant and anti-inflammatory activities.
    S-Diclofenac
  • HY-123503
    Salicortin
    		Inhibitor
    Salicortin, a phenolic glycoside, has been isolated from many plants such as Populus and Salix species. Salicortin inhibits osteoclast differentiation and bone resorption by down-regulating JNK and NF-κB/NFATc1 signaling pathways. Salicortin has anti-amnesic, anti-adipogenic, and immune-modulatory activity.
    Salicortin
Cat. No. Product Name / Synonyms Application Reactivity
JNK Isoform Comparison

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