c-jun

Peptide comprising residues 33 - 57 of the JNK binding (δ) domain of human c-Jun. Disrupts JNK/c-Jun interaction leading to inhibition of serum-induced c-Jun phosphorylation, up-regulation of p21cip/waf and modulation of inflammatory gene expression. Spec

Methacycline hydrochloride (Rondomycin) is a broad-spectrum semisynthetic antibiotic related to TETRACYCLINE but excreted more slowly and maintaining effective blood levels for a more extended period.

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

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.

MOMIPP is a PIKfyve inhibitor and a macropinocytosis inducer. MOMIPP readily penetrates the blood-brain barrier and is moderately effective in suppressing progression of intracerebral glioblastoma xenografts[1][2].

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

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

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

Elgodipine significantly reduced the incidence and severity of exercise-induced angina pectoris systemically and was able to inhibit vascular smooth muscle proliferation through a mechanism independent of the expression of the transcription factors c-fos and c-jun. The Elgodipine-induced inhibition was voltage-dependent. Elgodipine is a potential compound for the treatment of angina pectoris.

DN-1289 is an orally available, blood-brain barrier-crossing, selective and potent inhibitor with an IC50 value of 17 nM for di-leucine zipper kinase (DLK) and 40 nM for leucine zipper-bearing kinase (LZK).DN-1289 significantly inhibited optic nerve crush (ONC)-induced p-c-Jun in a mouse model.

Ralimetinib is a selective inhibitor that blocks phosphorylation of MK2 at Thr334, without affecting the phosphorylation of p38α MAPK, JNK, ERK1/2, c-Jun, ATF2, or c-Myc. Ralimetinib functions as an ATP-competitive inhibitor of p38 MAPK α/β, demonstrating IC50 values of 5.3 and 3.2 nM, respectively, and is under investigation as an anti-inflammatory and anticancer therapeutic.

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

PBOX 6 is a pyrrolo-1,5-benzoxazepine (PBOX) compound exhibiting anticancer and antitumor activity by inhibiting breast cancer cell growth in vitro and selectively inducing apoptosis in leukemia cells through c-Jun NH2 terminal kinase-dependent phosphorylation and inactivation of Bcl-2 and Bcl-XL.

JNK-1-IN-3 (Compound 9e) is a JNK1 inhibitor that downregulates JNK1 and phosphorylated JNK1, reduces c-Jun and c-Fos expression in tumours, and restores p53 activity. JNK-1-IN-3 exhibits potent antiproliferative activity against renal carcinoma and breast cancer cell lines.

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.

MAP4K4-IN-6 (Compound 15f) is a MAP4K4 inhibitor with an IC50 of 80 nM. It reduces the phosphorylation of c-Jun and exhibits neuroprotective effects. Additionally, MAP4K4-IN-6 enhances the vitality of motor neurons and can be utilized in the study of amyotrophic lateral sclerosis (ALS).

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.

c-Fos-IN-1 (Compound P16) acts as a c-Jun inhibitor, effectively reducing the mRNA and protein levels of c-Fos. It also inhibits the phosphorylation activity of ERK and the transcriptional activity of AP-1. This compound demonstrates anticancer properties through the inhibition of the ERK/c-Fos/Jun pathway. c-Fos-IN-1 curbs the proliferation and migration of gastric cancer cells, with an IC50 of 2.31 μM for MGC-803 cells, causing cell cycle arrest at the G2/M phase and inducing apoptosis in cancer cells. Additionally, c-Fos-IN-1 hampers the growth of gastric cancer tumors.

JNK3inhibitor-9 (Compound 24a) is a potent, selective JNK3 inhibitor capable of crossing the blood-brain barrier (BBB), demonstrating an IC50 value of 12 nM. It effectively inhibits GSK3α/β, which is involved in Tau phosphorylation, with IC50 values of 14 nM and 35 nM, respectively. JNK3inhibitor-9 also reduces the phosphorylation of c-Jun and APP and protects neurons from Aβ1-42 toxicity.

2-Pyridinamine, 4-[3-fluoro-5-(4-morpholinyl)phenyl] (Compound 9l) is an ATP-competitive JNK (c-Jun N-terminal kinase) inhibitor with IC₅₀ values of 0.099 μM and 0.148 μM for JNK1 and JNK3 respectively, exhibiting the advantage of blood-brain barrier penetration. 2-Pyridinamine, 4-[3-fluoro-5-(4-morpholinyl)phenyl] inhibits c-Jun phosphorylation and reactive oxygen species (ROS) generation, making it suitable for neurodegenerative disease research.

ZAK-IN-1 is an orally active and selective inhibitor of the leucine zipper and sterile-alpha motif kinase ZAK, with an IC50 of 4 nM and a KD of 8 nM. It demonstrates exceptional selectivity against 403 types of wild-type kinases. ZAK-IN-1 effectively blocks the p38/GATA-4 and JNK/c-Jun signaling pathways, significantly suppressing cardiac hypertrophy. This compound is applicable in the study of hypertrophic cardiomyopathy (HCM).

JNK2/3-IN-1 (Compound 56d) is an irreversible covalent inhibitor of c-Jun N-terminal kinases 2/3 (JNK2/3), with IC50 values of 830 nM and 1909 nM, respectively. JNK2/3-IN-1 is potentially useful for research in neurodegenerative diseases such as Parkinson's and Alzheimer's, as well as fibrotic diseases.