jnk/c-jun

JNK-IN-7 (JNK inhibitor) is a selective JNK1 2 3 inhibitor (IC50: 1.54 1.99 0.75 nM). It can also inhibit phosphorylation of c-Jun, which is a substrate of JNK kinase.

Pinostilbene obviously attenuates the phosphorylation of c-Jun and JNK triggered by 6-OHDA.

10-Gingerol-induced apoptosis was accompanied by phosphorylation of the mitogen-activated protein kinase (MAPKs) family, p38 MAPK (p38), c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK).

IMM-H007 is a novel lipid-lowering agent, increasing abca1 protein expression

NBDHEX is a potent inhibitor of glutathione S-transferase P1-1 (GSTP1-1) .

MPT0B392 is an orally active quinoline derivative, induces c-Jun N-terminal kinase (JNK) activation.

Ralimetinib selectively inhibits phosphorylation of MK2 (Thr334) and has no effect on phosphorylation of p38α MAPK, JNK, ERK1 2, c-Jun, ATF2, or c-Myc. Ralimetinib is an effective and selective, ATP-competitive inhibitor of p38 MAPK α β (IC50s: 5.3 and 3.

JNK-1-IN-3 (Compound 9e) acts as a JNK1 inhibitor, both reducing JNK1 gene expression and lowering the protein levels of its phosphorylated form. It concurrently diminishes the expression of downstream targets c-Jun and c-Fos in tumors, while also restoring p53 activity. Exhibiting broad-spectrum antiproliferative effects, JNK-1-IN-3 is particularly effective against renal and breast cancer cell lines, showing significant anticancer activity both in vivo and in vitro.

JNK-1-IN-4 (Compound E1) is an inhibitor of JNK, targeting JNK-1, JNK-2, and JNK-3 with IC50 values of 2.7, 19.0, and 9.0 nM, respectively. This compound inhibits the phosphorylation of c-Jun and reduces the expression of TGF-β1-induced EMT markers (such as fibronectin and α-SMA). JNK-1-IN-4 exhibits favorable pharmacokinetic properties with a bioavailability of 69%. Additionally, it demonstrates antifibrotic effects in a Bleomycin-induced mouse model of idiopathic pulmonary fibrosis.

JNK-IN-19 (Compound Q8) is an inhibitor of c-Jun N-terminal kinase, utilized for the treatment and or prevention of injuries prior to, during, or following surgery.

SET-171 is a JNK (c-Jun N-terminal kinase) inhibitor that exhibits significant anticancer activity by suppressing the expression of hepatic pyruvate kinase (PKL) and offers potential in regulating lipid metabolism. In antitumor studies, SET-171 shows notable cytotoxicity against human liver cancer cell lines HepG2 and Huh7, with IC50 values of 8.82 μM and 2.97 μM, respectively. Additionally, in research related to non-alcoholic fatty liver disease (NAFLD), SET-171 significantly reduces triglyceride (TAG) levels and inhibits the expression of proteins associated with steatosis. This compound holds promise for hepatocellular carcinoma (HCC) and NAFLD research.

3-AP-Me is the dimethyl derivative of the ribonucleotide reductase inhibitor 3-AP (SML0568). It activates the endoplasmic reticulum (ER) stress pathway by promoting eIF2α phosphorylation and upregulating gene expression of transcription factors ATF4 and ATF6, thereby inducing apoptosis. Additionally, 3-AP-Me activates cellular stress kinases c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase, leading to the upregulation of spliced mRNA variant XBP1. It is applicable in cancer research.

Ezatiostat hydrochloride (TLK199 HCl) is an effective inhibitor of glutathione S-transferase. Ezatiostat hydrochloride is a novel glutathione analog and the potential treatment of cytopenias. In addition, Ezatiostat hydrochloride has been revealed to selectively bind to and thus inhibit GSTP1-1.

AS601245 is an inhibitor of the c-Jun NH2-terminal kinase (JNK), with neuroprotective properties.

IQ-1S free acid (IQ-1S) is an effective and specific c-Jun N-Terminal Kinase Inhibitor. IQ-1S inhibits murine delayed-type hypersensitivity. IQ-1S can reduce inflammation and cartilage loss associated with CIA and can serve as a small-molecule modulator for mechanistic studies of JNK function in rheumatoid arthritis. IQ-1S is highly specific for JNK and that its neutral form is the most abundant species at physiologic pH.

High affinity JNK inhibitor (Ki values are 25-50 nM). Inhibits JNK via competitive binding of the ATP-binding site of active, phosphorylated JNK. Exhibits > 40-fold selectivity for JNK over p38, ERK, IKK2, protein kinase C, Lck and ZAP70. Hepatoprotective. Also inhibits HCMV replication. Uehara et al (2004) c-Jun N-terminal kinase mediates hepatic injury after rat liver transplantation. Transplantation. 78 324 PMID:15316358 |Uehara et al (2005) JNK mediates hepatic ischemia reperfusion injury. J.Hepatol. 42 850 PMID:15885356 |Ma et al (2007) A pathogenic role for c-Jun amino-terminal kinase signaling in renal fibrosis and tubular cell apoptosis. J.Am.Soc.Nephrol. 18 472 PMID:17202416 |Ma et al (2009) Blockade of the c-Jun amino terminal kinase prevents crescent formation and halts established anti-GBM glomerulonephritis in the rat. Lab.Invest. 89 470 PMID:19188913 |Zhang et al (2015) The c-Jun N-terminal kinase inhibitor SP600125 inhibits human cytomegalovirus replication. J.Med.Virol. 87 2135 PMID:26058558 |Vasilevskaya et al (2015) Inhibition of JNK sensitizes hypoxic colon cancer cells to DNA-damaging agents. Clin.Cancer.Res. 21 4143 PMID:26023085

Ezatiostat (TER199(free base)) is a tripeptide analog of glutathione that can selectively inhibit GSTP1-1 catalytic activity.

CC-401 Hydrochloride (CC401 HCl) is a second generation ATP-competitive anthrapyrazolone c-Jun N terminal kinase (JNK) inhibitor (Ki of 25 to 50 nM.)with potential antineoplastic activity.

Erioflorin is an ATP-competitive selective c-Jun N-terminal kinase (JNK) inhibitor.

1. Mulberroside has nephroprotective, hypoglycemic, and antidiabetic effects. 2. Mulberroside A is a glycosylated stilbene of oxyresveratrol; thus, the deglycosylation of Mulberroside A resulted in enhanced inhibition of melanogenesis. 3. Mulberroside A has anti-inflammatory antiapoptotic effects. by decreasing the expressions of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 and inhibiting the activation of NALP3, caspase-1, and nuclear factor-κB and the phosphorylation of extracellular signal-regulated protein kinases, the c-Jun N-terminal kinase, and p38.

JNK Inhibitor VIII (TCS JNK 6o) is an ATP-competitive, selective inhibitor of c-Jun N-terminal kinase (JNK) with IC50 values of 45 nM for JNK-1 and 160 nM for JNK-2.

JNK-1-IN-2 (Compound c6) is a potent inhibitor of JNK-1 with an IC50 of 33.5 nM, and also exhibits inhibitory effects on JNK-2 and JNK-3 with IC50 values of 112.9 nM and 33.2 nM, respectively. This compound effectively inhibits the phosphorylation of c-Jun and has shown potential in reversing lung impairment, making it relevant for research into pulmonary fibrosis [1].

CC-90001 is an orally administered c-Jun N-terminal kinase (JNK) inhibitor with bias for JNK1 over JNK2.

Scandoside, a cyclic enolide that can be isolated from Haemophilus difficile, exhibits anti-inflammatory activity, inhibits the expression levels of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, and IL-6 messenger RNA (mRNA), and inhibits the nuclear transcription factor, kappa-B alpaha (IκB-α), p38, extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) inhibitor phosphorylation.