JNK Inhibitor

(+)-Columbianetin ((S)-Columbianetin) acts as an inhibitor of JNK/ERK. (+)-Columbianetin inhibits UVA-induced phosphorylation of JNK and ERK, reduces the production of MMP-1, reverses UVA-induced Collagen (HY-NP003) degradation, and alleviates UVA-mediated inhibition of Smad2/3 phosphorylation and translocation. (+)-Columbianetin regulates the AP-1 and ASK1-MAPK signaling pathways, inhibits the production of ROS and blocks sub-G₁ cell cycle arrest. (+)-Columbianetin is applicable to research related to skin aging.

Viridicatol is a quinolone alkaloid with anti-inflammatory, antibacterial, antifungal, osteogenic and chondrogenic activities. Viridicatol reduces the phosphorylation levels of ERK, JNK, p38 and STAT6; inhibits MMP-2, MMP-9, NF-κB signaling pathway and PTP1B; downregulates genes related to mast cell activation; and binds to SHN3 to activate the Wnt/SHN3 signaling pathway. Viridicatol inhibits the expression of pro-inflammatory mediators and cytokines, and promotes osteogenic/chondrogenic differentiation. Viridicatol can be used in studies related to fibrosarcoma, allergy, bacterial infection, fungal infection and osteoporosis.

CC-401 is a potent inhibitor of all three forms of JNK with K_i of 25 to 50 nM.

Acenocoumarol is an anticoagulant that functions as a Vitamin K antagonist. Acenocoumarol inhibits MAPK/ERK/JNK signaling pathway, reduces the nuclear translocation of NF-κB p65, activates Akt/GSK3β signaling pathway. Acenocoumarol induces apoptosis in cell A549, arrests cell cycle at S phase.

Nimustine hydrochloride (ACNU) is the hydrochloride salt form of Nimustine (HY-13703). Nimustine hydrochloride is an alkylating agent, which induces DNA double-strand breaks (DSBs) and inter-strand crosslinks (ICLs), thereby activating the DNA damage response (DDR) signaling pathway. Nimustine hydrochloride activates p38 MAPK/JNK signaling pathway, and exhibits antitumor activity.

1-Heptanol (n-Heptyl alcohol) is a linear primary fatty alcohol. 1-Heptanol selectively inhibits the activating phosphorylation of SAPK/JNK and reduces the phosphorylation level of IκB-α. 1-Heptanol increases plasma membrane fluidity, decreases membrane thermal stability, alters the coupling kinetics of STIM1-ORAI1, inhibits the production of ROS and LTC₄, and induces the expression of HSP70. 1-Heptanol is used in the fragrance industry due to its pleasant odor.

JNK3 inhibitor-4 is a potent and BBB-permeable inhibitor of JNK3 (IC₅₀=1.0 nM) based on 2-aryl-1-pyrimidinyl-1H-imidazole-5-yl acetonitrile. JNK3 inhibitor-4 shows excellent selectivity over other protein kinases including isoforms JNK1 (IC₅₀=143.9 nM) and JNK2 (IC₅₀=298.2 nM). JNK3 inhibitor-4 has neuroprotective effect and predicated blood-brain barrier permeability.

3′,4′,7-Trihydroxyflavone is an orally active inhibitor of OXA-48 (IC₅₀ = 1.89 μM) and COX-1 (IC₅₀ = 36.37 μM). 3′,4′,7-Trihydroxyflavone exhibits antioxidant and anti-inflammatory properties, inhibiting the release of inflammatory cytokines such as IL-6, IL-8, and TNF-α. 3′,4′,7-Trihydroxyflavone inhibits H₂O₂-induced neuronal apoptosis and ROS accumulation, and exerts anti-neuroinflammatory effects by suppressing the JNK-STAT1 pathway. 3′,4′,7-Trihydroxyflavone exhibits antimicrobial and antibiotic-modifying activities against multidrug-resistant Gram-negative enteric bacteria. 3′,4′,7-Trihydroxyflavone inhibits RANKL-induced osteoclast formation via NFATc1. 3′,4′,7-Trihydroxyflavone activates the CREB-BDNF axis and restores scopolamine (HY-N0296)-induced memory deficits in mice.

SR-3576 is a highly potent and selective JNK3 inhibitor with an IC₅₀ of 7 nM.

Homovanillyl alcohol is a biological metabolite of Hydroxytyrosol, and belongs to the class of phenolic organic compounds. Homovanillyl alcohol alleviates cellular oxidative stress and inflammatory responses by scavenging free radicals, inhibiting the phosphorylation of the p38 and JNK MAP kinase pathways, as well as suppressing NF-κB-driven transcription and nuclear translocation. It can be used in studies related to cardiovascular diseases and allergic asthma.

Strictosamide is a compound that can be isolated from Nauclea officinalis. Strictosamide has various activities such as anti-inflammatory, analgesic, anti-Plasmodium, antifungal, and promoting wound healing.

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.

Ombuoside has antioxidant properties, inhibiting ROS production and apoptosis. Ombuoside exerts neuroprotective effects through the ERK-JNK-caspase-3 system. Ombuoside promotes Dopamine biosynthesis through TH and CREB activation. Ombuoside exhibits antimicrobial activity against several Gram-positive and Gram-negative bacteria, as well as Candida albicans

SR-3306 is a brain-penetrant and selective pan-JNK (JNK1/2/3) inhibitor. SR-3306 is a neuroprotective agent that can be used for the study of Parkinson's disease, ischemia/reperfusion (I/R) injury and obesity.

MAPK-IN-1 (Compound 2) is a MAPK signaling pathway inhibitor. MAPK-IN-1 exhibits AChE inhibitory activity with an IC₅₀ of 23.84 μM. MAPK-IN-1 shows anti-neuroinflammatory and neuroprotective activity and can be used for Alzheimer's disease research.

5,7-Dihydroxy-4-methylcoumarin is an antioxidant. 5,7-Dihydroxy-4-methylcoumarin protects mouse cochlear hair cells from Cisplatin-induced damage, enhances cell viability and inhibits apoptosis. 5,7-Dihydroxy-4-methylcoumarin downregulates phosphorylated JNK levels, increases the ratio of phosphorylated FoxO1 to total FoxO1, scavenges free radicals, reduces ROS accumulation, maintains mitochondrial membrane potential and alleviates mitochondrial dysfunction. 5,7-Dihydroxy-4-methylcoumarin downregulates the expression of caspase-3 and improves cell viability. 5,7-Dihydroxy-4-methylcoumarin can be used in studies related to ototoxicity.

(2S)-2'-Methoxykurarinone (2'-O-Methylkurarinone) is a flavanone natural product found in the roots of Sophora flavescens, possessing anti-sepsis, inhibitory effects on osteoclast differentiation and bone resorption, anti-inflammatory, and anti-Plasmodium activities. (2S)-2'-Methoxykurarinone exhibits an EC₅₀ = 2.4 μM against the FCR-3 strain of Plasmodium falciparum. In sepsis models, (2S)-2'-Methoxykurarinone modulates immune cell function and inhibits inflammation and oxidative stress. In bone-related models, (2S)-2'-Methoxykurarinone blocks osteoclast differentiation and bone resorption, and inhibits RANKL-mediated Akt, p38, and JNK signaling pathways. In skin inflammation models, (2S)-2'-Methoxykurarinone inhibits NF-κB pathway activation, upregulates HO-1 expression, and suppresses CCL27 chemokine production in HaCaT cells. (2S)-2'-Methoxykurarinone is useful for research on osteoporosis, sepsis, inflammatory skin diseases (such as atopic dermatitis and allergic contact dermatitis), and malaria.

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.

GDC-0134 (RG6000) is a modulator targeting dual leucine zipper kinase (DLK) that can cross the blood-brain barrier. By inhibiting the kinase activity of DLK, GDC-0134 blocks the activation of the downstream JNK signaling pathway, suppresses DLK-dependent retrograde signal transduction of axon-to-soma degeneration, and exerts neuroprotective activity. GDC-0134 reduces TDP-43 protein aggregation and decreases the degree of neuromuscular junction denervation in motor neurons. GDC-0134 can be used in the research of amyotrophic lateral sclerosis (ALS), Alzheimer's disease and other DLK-related neurodegenerative diseases.

IMM-H007 (WS070117) is an orally active and potent AMPK (AMP-activated protein kinase) activator and TGFβ1 (transforming growth factor β1) antagonist. IMM-H007 has protective effects in cardiovascular diseases via activation of AMPK. IMM-H007 negatively regulates endothelium inflammation through inactivating NF-κB and JNK/AP1 signaling. IMM-H007 inhibits ABCA1 degradation. IMM-H007 resolves hepatic steatosis in HFD-fed hamsters by the regulation of lipid metabolism. IMM-H007 can be used for the research of nonalcoholic fatty liver disease (NAFLD) and inflammatory atherosclerosis.