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Results for "

JNK/c-Jun

" in MedChemExpress (MCE) Product Catalog:

21

Inhibitors & Agonists

1

Screening Libraries

6

Peptides

6

Recombinant Proteins

3

Antibodies

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-P1190

    JNK Apoptosis Inflammation/Immunology
    c-JUN peptide is a cell-permeable c-JUN-JNK interaction inhibitor. c-JUN peptide inhibits serum-induced c-Jun phosphorylation. c-JUN peptide induces apoptosis .
    c-JUN peptide
  • HY-138304
    CC-90001
    1 Publications Verification

    JNK Inflammation/Immunology
    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 .
    CC-90001
  • HY-P10506

    JNK Neurological Disease
    CMX-8933 is an octapeptide fragment of the goldfish brain neurotrophic factor ependymin. CMX-8933 increases the enzymatic activity of c-Jun N-terminal kinase (JNK), increases the phosphorylation of JNK and c-Jun proteins, and increases the cellular levels of c-Jun and c-Fos mRNA. CMX-8933 can be used to study the role of ependymin in neuroplasticity, learning, memory formation, and neural regeneration .
    CMX-8933
  • HY-107598
    JNK Inhibitor VIII
    2 Publications Verification

    TCS JNK 6o

    JNK Cancer
    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 .
    JNK Inhibitor VIII
  • HY-107600
    IQ-3
    2 Publications Verification

    JNK Inflammation/Immunology
    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-125838

    JNK Neurological Disease
    J30-8 is a potent and isoform-selective inhibitor of c-Jun N-terminal kinase 3 (JNK3) with an IC50 of 40 nM, which 2500-fold isoform selectivity against JNK1α1 and JNK2α2. J30-8 exhibits neuroprotective activity in vitro and potential for the treatment of neurodegenerative diseases .
    J30-8
  • HY-155593

    JNK Inflammation/Immunology
    JNK-1-IN-2 (Compound c6) is a JNK-1 inhibitor (IC50: 33.5 nM). JNK-1-IN-2 also inhibits JNK-2 and JNK-3 with IC50s of 112.9 nM and 33.2 nM. JNK-1-IN-2 inhibits the phosphorylation of c-Jun. JNK-1-IN-2 reverses lung impairment. JNK-1-IN-2 can be used for research of pulmonary fibrosis .
    JNK-1-IN-2
  • HY-151928

    JNK Neurological Disease
    JNK3 inhibitor-3 (compound 15g) is a selective, BBB permeable and orally active c-Jun N-terminal kinase 3 (JNK3) inhibitor. JNK3 inhibitor-3 has inhibitory activities to JNK1, JNK2 and JNK3 with IC50 values of 147.8, 44.0 and 4.1 nM, respectively. JNK3 inhibitor-3 significantly improves the memory in mouse dementia model. JNK3 inhibitor-3 can be used for the research of Alzheimer’s disease .
    JNK3 inhibitor-3
  • HY-169021

    JNK Cancer
    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-169177

    JNK Inflammation/Immunology
    JNK-1-IN-4 (Compound E1) is an inhibitor for JNK, that inhibits JNK-1, JNK-2 and JNK-3 with IC50s of 2.7, 19.0 and 9.0 nM, respectively. JNK-1-IN-4 inhibits the phosphorylation of c-Jun, and reduces the expression of TGF-β1-induced EMT marker proteins, such as fibronectin and α-SMA. JNK-1-IN-4 exhibits good pharmacokinetic characteristics with a bioavailability of 69%. JNK-1-IN-4 exhibits anti-fibrotic effect in Bleomycin (HY-17565)-induced mice idiopathic pulmonary fibrosis models .
    JNK-1-IN-4
  • HY-101287

    Microtubule/Tubulin JNK Apoptosis Caspase Cancer
    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-13241
    Ralimetinib dimesylate
    Maximum Cited Publications
    12 Publications Verification

    LY2228820 dimesylate

    p38 MAPK Autophagy Apoptosis Inflammation/Immunology Cancer
    Ralimetinib dimesylate (LY2228820 dimesylate) is a selective, ATP-competitive inhibitor of p38 MAPK α/β with IC50s of 5.3 and 3.2 nM, respectively. Ralimetinib (LY2228820) selectively inhibits phosphorylation of MK2 (Thr334), with no effect on phosphorylation of p38a MAPK, JNK, ERK1/2, c-Jun, ATF2, or c-Myc.
    Ralimetinib dimesylate
  • HY-13241A

    LY2228820

    p38 MAPK Autophagy Inflammation/Immunology Cancer
    Ralimetinib (LY2228820) is a potent and selective, ATP-competitive inhibitor of p38 MAPK α/β, with IC50s of 5.3 and 3.2 nM, respectively. Ralimetinib (LY2228820) selectively inhibits phosphorylation of MK2 (Thr334), with no effect on phosphorylation of p38α MAPK, JNK, ERK1/2, c-Jun, ATF2, or c-Myc .
    Ralimetinib
  • HY-11010
    AS601245
    5+ Cited Publications

    JNK Neurological Disease Inflammation/Immunology Cancer
    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 .
    AS601245
  • HY-11010A

    JNK Neurological Disease Inflammation/Immunology Cancer
    AS601245 TFA 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 TFA 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 .
    AS601245 TFA
  • HY-P10401

    Apoptosis iGluR Cardiovascular Disease Neurological Disease
    TAT-GluR6-9c is a GluR6-PSD95 interaction blocker. By regulating the GluR6 mediated signaling pathway, TAT-GluR6-9c inhibits the activation of JNK and phosphorylation of c-Jun, reduces the expression of Fas L and thus reduces the occurrence of apoptosis. TAT-GluR6-9c can be used to study cerebral ischemia and neuroprotective strategies .
    TAT-GluR6-9c
  • HY-P6177

    Dipeptidyl Peptidase Inflammation/Immunology
    SGP8 (IAVPGEVA) is an octapeptide produced by hydrolysis of soybean 11S globulin, which has the effects of regulating lipid metabolism, inflammation and fibrosis. SGP8 (IAVPGEVA) exhibits inhibitory activity against DPP4 and inhibits the JNK-c-Jun signaling pathway, and has the ability to inhibit non-alcoholic steatohepatitis (NASH) .
    SGP8
  • HY-148510

    Phosphatase Cancer
    HKB99 is an allosteric inhibitor of phosphoglycerate mutase 1 (PGAM1). HKB99 inhibits the formation of invasive pseudopodia and increases the level of PAI-2 in vitro. HKB99 increases the oxidative stress, activates JNK/c-Jun and suppresses AKT and ERK. HKB99 can be used for the research of non-small-cell lung cancer (NSCLC) .
    HKB99
  • HY-13634A
    Ezatiostat
    5+ Cited Publications

    TER199(free base); TLK199

    Glutathione S-transferase Apoptosis Cancer
    Ezatiostat (TER199 free base; TLK199) is a tripeptide analog of glutathione and is a selective and orally active glutathione S-transferase P1-1 (GSTP1) inhibitor. Ezatiostat leads to JNK activation by inhibiting GSTP1. Ezatiostat stimulates both lymphocyte production and bone marrow progenitor proliferation. Ezatiostat has the potential for myelodysplastic syndrome (MDS) treatment .
    Ezatiostat
  • HY-13634

    TER199; TLK199 hydrochloride

    Glutathione S-transferase Apoptosis Cancer
    Ezatiostat hydrochloride (TER199; TLK199 hydrochloride) is a tripeptide analog of glutathione and is a selective and orally active glutathione S-transferase P1-1 (GSTP1) inhibitor. Ezatiostat hydrochloride leads to JNK activation by inhibiting GSTP1. Ezatiostat hydrochloride stimulates both lymphocyte production and bone marrow progenitor proliferation. Ezatiostat hydrochloride has the potential for myelodysplastic syndrome (MDS) treatment .
    Ezatiostat hydrochloride
  • HY-135318
    NBDHEX
    1 Publications Verification

    Apoptosis Autophagy Glutathione S-transferase Cancer
    NBDHEX is a potent glutathione S-transferase P1-1 (GSTP1-1) inhibitor. NBDHEX induces apoptosis of tumor cells. NBDHEX acts as an anticancer agent by inhibiting GSTs catalytic activity, avoiding inconvenience of the inhibitor extrusion from the cell by specific pumps and disrupting the interaction between the GSTP1-1 and key signaling effectors. NBDHEX can also act as late-phase autophagy inhibitor .
    NBDHEX

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