jnk in 8

JNK-IN-8 (JNK Inhibitor XVI) is an irreversible JNK1/2/4 inhibitor (IC50: 4.7/18.7/1 nM) with over 10-fold selectivity compared to MNK2 and Fms, and no inhibition of Met, c-Kit, or PDGFRβ in the A375 cell line.

JNK3 Inhibitor-8 is a potent, selective, and orally active inhibitor that can cross the blood-brain barrier, targeting JNK3 with IC50 values of 21 nM for JNK3, 2203 nM for JNK2, and >10000 nM for JNK1. This compound demonstrates significant neuroprotective effects and holds promise for Alzheimer's disease (AD) research [1].

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).

αMβ2integrinagonist-1 (Compound 8) is a highly selective αMβ2 integrin agonist with anti-inflammatory properties (EC50=1.4 nM). It activates integrin-mediated cell adhesion and the JNK/ERK signaling pathway. Additionally, αMβ2integrinagonist-1 induces polarization of tumor-associated macrophages and enhances antitumor T-cell immune responses. This compound holds potential for research in cancer and chronic inflammatory diseases such as pancreatic cancer and rheumatoid arthritis.

Icaritin (Standard) is a reference standard for research and analysis in studies involving Icaritin. Icaritin (Anhydroicaritin) has hormone regulation activity and cardiovascular function improvement activity. Icaritin has anticancer activity, can induce S phase arrest and apoptosis, inhibit ENKL cell proliferation. Icaritin has anti-multiple myeloma activity, mainly mediated by inhibiting IL-6/JAK2/STAT3 signaling. Icaritin at low concentration (4 or 8 μMol/L) can promote rat chondrocyte proliferation and inhibit cell apoptosis, while the effect of Icaritin on rat chondrocyte at high concentration was reversed.

Hellebrigenin, as a selective inhibitor of MAPK signaling pathways (ERK, p38, JNK) and XIAP, effectively suppresses Akt expression and phosphorylation. This compound activates endogenous apoptosis pathways (including mitochondrial membrane potential disruption, Caspase family activation, and PARP cleavage) while modulating apoptosis-related protein expression. Hellebrigenin also induces DNA double-strand breaks to activate the ATM pathway, inhibiting tumor cell proliferation and clonogenesis, primarily applied in research of oral squamous cell carcinoma and liver cancer.

CMX-8933 is an 8-peptide fragment of the goldfish brain neurotrophic ependymin protein. This compound enhances the enzymatic activity of c-Jun N-terminal kinase (JNK), promotes the phosphorylation of JNK and c-Jun proteins, and increases the cellular levels of c-Jun and c-Fos mRNA. CMX-8933 is utilized for investigating the role of ependymin proteins in neural plasticity, learning, memory formation, and neural regeneration.