Catalog No.
Product Name
Application
Product Information
Citations
-
PPAR agonist
Lobeglitazone is a novel thiazolidinedione-class compound and an orally active dual agonist of peroxisome proliferator-activated receptors (PPARs), with EC₅₀ values of 137.4 nM for PPARγ and 546.3 nM for PPARα. In addition to its metabolic effects, Lobeglitazone functions as an inhibitor of multiple pro-inflammatory and pro-fibrotic signaling pathways, including ERK, JNK, Smad, and NF-κB. Lobeglitazone exhibits a broad range of pharmacological activities, including anti-inflammatory, anti-diabetic, anti-fibrotic, and anti-atherosclerotic effects. These properties make it a promising candidate for therapeutic research in metabolic syndrome, type 2 diabetes, cardiovascular disease, and fibrosis-related conditions. - 6-Hydroxyflavone is an orally active flavonoid with diverse pharmacological properties. It exhibits anti-inflammatory activity by inhibiting lipopolysaccharide (LPS)-induced nitric oxide (NO) production and also promotes osteoblast differentiation through activation of the AKT, ERK1/2, and JNK signaling pathways, supporting its role in bone health. Additionally, 6-Hydroxyflavone inhibits the glycosylation of bovine hemoglobin (BHb), suggesting potential in managing glycation-related complications. It demonstrates kidney-protective effects and modulates GABAergic neurotransmission by enhancing GABA-induced currents via the benzodiazepine binding sites on GABAA receptors
-
Endogenous Metabolite
Gamma-linolenic acid (γ-linolenic acid, GLA) is an orally active omega-6 unsaturated fatty acid with broad pharmacological activities. It exhibits anti-inflammatory effects by inhibiting the NF-κB signaling pathway and suppressing the phosphorylation of ERK1/2 and JNK, key mediators of inflammatory responses. GLA also induces apoptosis in cancer cells, contributing to its anticancer potential. Additionally, it possesses antioxidant properties and has been shown to improve memory function, suggesting neuroprotective benefits. These multifunctional effects position gamma-linolenic acid as a promising compound for research in inflammation, oncology, and neurological disorders. -
Microglial inhibitor
Inflachromene is a microglial inhibitor that exerts anti-inflammatory effects by directly binding to high mobility group box proteins HMGB1 and HMGB2. Through this interaction, it effectively downregulates the proinflammatory activities of HMGB proteins, leading to reduced microglial activation and neuronal damage. Inflachromene holds promise as a therapeutic candidate for the treatment of neuroinflammatory disorders, including neurodegenerative diseases and central nervous system injuries. -
BMP receptor agonist
SY-LB-35 is a potent agonist of bone morphogenetic protein (BMP) receptors, capable of activating both canonical and non-canonical signaling pathways. In the C2C12 myoblast cell line, SY-LB-35 significantly enhances cell proliferation and viability, promoting cell cycle progression by increasing the proportion of cells in the S and G2/M phases. Mechanistically, it activates the canonical Smad pathway as well as non-canonical PI3K/Akt, ERK, p38, and JNK signaling cascades. These properties make SY-LB-35 a valuable tool for studying BMP-related cellular processes and a potential therapeutic candidate for tissue regeneration and muscle repair. -
JNK Inhibitor
(3S)-Tanzisertib hydrochloride is a selective inhibitor of c-Jun N-terminal kinases (JNK), demonstrating IC50 values of 61, 7, and 6 nM for JNK1, JNK2, and JNK3, respectively. This compound also exhibits inhibition of ERK1, p38α, and EGFR with IC50 values of 0.48, 3.4, and 0.38 μM, respectively. (3S)-Tanzisertib hydrochloride effectively reduces LPS-induced TNFα production in an acute rat pharmacokinetic-pharmacodynamic model, making it a valuable tool in idiopathic pulmonary fibrosis research and other inflammatory disease studies. -
JNK Inhibitor, ERK Inhibitor, TGFβ signaling Activator
(+)-Columbianetin targets JNK and ERK signaling pathways while acting as a TGFβ signaling activator. This compound effectively inhibits UVA-induced phosphorylation of JNK and ERK, decreases MMP-1 production, and reverses collagen degradation. In addition, it mitigates UVA-mediated suppression of Smad2/3 phosphorylation and translocation, providing protective effects against UV-induced cellular damage. (+)-Columbianetin is an essential tool for research focused on skin aging and oxidative stress responses in keratinocytes. -
JNK/c-Jun Activator
Ophiopogonin B primarily activates the JNK/c-Jun signaling pathway. This saponin compound, derived from Radix Ophiopogonjaponicus, demonstrates significant biological activity by inducing autophagy and apoptosis in colon cancer cells. It serves as a valuable reagent for researchers investigating mechanisms of cancer cell death and the therapeutic potential of autophagy modulation. -
JNK Inhibitor
JNK-IN-26 is a potent inhibitor of c-Jun N-terminal kinase (JNK), a key signaling enzyme involved in various cellular processes such as apoptosis, inflammation, and stress response. This compound exhibits significant biological activity by selectively inhibiting JNK signaling pathways, making it a valuable tool for studying JNK-related mechanisms in cellular and molecular biology. JNK-IN-26 is utilized in research applications focused on cancer, neurodegenerative diseases, and other conditions involving JNK activation. -
CDK/GSK3β/JNK Inhibitor
Indirubin-3′-oxime (IDR3O) is a synthetic derivative of indirubin that functions as a potent inhibitor of cyclin-dependent kinases (CDKs), glycogen synthase kinase 3β (GSK3β), and all three isoforms of c-Jun N-terminal kinases (JNK1, JNK2, JNK3). It demonstrates inhibitory activity with IC50 values of 0.8 μM, 1.4 μM, and 1.0 μM for each JNK isoform, respectively. Indirubin-3′-oxime is also known to promote chondrocyte height growth through the activation of Wnt/β-catenin signaling, making it relevant for studies in cellular growth and differentiation. -
JNK Inhibitor
J30-8 is a potent and isoform-selective inhibitor of c-Jun N-terminal kinase 3 (JNK3), exhibiting an IC50 value of 40 nM and a remarkable 2500-fold selectivity over JNK1α1 and JNK2α2 isoforms. This compound demonstrates significant neuroprotective activity in vitro, making it a valuable tool for researching neurodegenerative diseases and their therapeutic interventions. -
JNK Activator
CMX-8933 is a JNK activator derived from an octapeptide fragment of the goldfish brain neurotrophic factor ependymin. This compound enhances the enzymatic activity of c-Jun N-terminal kinase (JNK), leading to increased phosphorylation of JNK and c-Jun proteins, as well as elevated cellular levels of c-Jun and c-Fos mRNA. CMX-8933 serves as a valuable tool for investigating the roles of ependymin in neuroplasticity, learning processes, memory formation, and neural regeneration. -
JNK Inhibitor
SR-3306 is a selective pan-JNK (JNK1/2/3) inhibitor with notable brain-penetrating properties. It serves as a neuroprotective agent, making it valuable for investigating neurodegenerative diseases such as Parkinson's disease, as well as conditions related to ischemia/reperfusion (I/R) injury and obesity. Its targeted inhibition of JNK pathways offers potential insights into therapeutic strategies for these disorders. -
JNK3 Inhibitor
JNK3 inhibitor-4 is a selective inhibitor targeting JNK3 (IC50 = 1.0 nM), derived from a 2-aryl-1-pyrimidinyl-1H-imidazole-5-yl acetonitrile scaffold. It demonstrates remarkable selectivity over JNK1 (IC50 = 143.9 nM) and JNK2 (IC50 = 298.2 nM). This compound exhibits neuroprotective properties and shows potential for effective delivery across the blood-brain barrier, making it valuable for research in neurodegenerative diseases and other neurological disorders. -
JNK Inhibitor
JNK3 inhibitor-1 is a potent and selective inhibitor of c-Jun N-terminal kinase 3 (JNK3), exhibiting an IC50 of 0.005 μM. It demonstrates oral bioavailability and the ability to penetrate the blood-brain barrier, making it suitable for neurological research. JNK3 inhibitor-1 is utilized in studies investigating the role of JNK3 in neurodegenerative disorders and various cellular processes. -
JNK1 Inhibitor
JNK-1-IN-3 is a selective inhibitor of JNK1 that effectively downregulates JNK1 gene expression and decreases the levels of its phosphorylated form. This compound concurrently reduces the expression of key downstream targets, including c-Jun and c-Fos, while enhancing p53 activity. JNK-1-IN-3 demonstrates significant antiproliferative effects, especially against renal and breast cancer cell lines, showcasing both in vitro and in vivo anticancer activity, making it a valuable tool for cancer research and therapeutic investigations. -
JNK Inhibitor
JNK-IN-11 is a selective JNK inhibitor, exhibiting IC50 values of 2.2 µM, 21.4 µM, and 1.8 µM for JNK1, JNK2, and JNK3, respectively. This compound demonstrates significant potential in research applications targeting neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease, by modulating pathways involved in cell stress and apoptosis. JNK-IN-11 serves as a valuable tool for investigating therapeutic strategies in these conditions. -
JNK Inhibitor
JNK-IN-13 is a selective inhibitor of the c-Jun N-terminal kinases (JNK), demonstrating IC50 values of 290 nM for JNK3 and 500 nM for JNK2. This compound exhibits significant biological activity in modulating cellular stress responses, apoptosis, and inflammation pathways. JNK-IN-13 is valuable for research applications focused on cancer, neurodegenerative diseases, and metabolic disorders, providing insights into JNK signaling mechanisms. -
JNK Inhibitor
Salicortin is a phenolic glycoside that functions as a JNK inhibitor. It effectively inhibits osteoclast differentiation and bone resorption by down-regulating the JNK and NF-κB/NFATc1 signaling pathways. Salicortin exhibits a range of biological activities, including anti-amnesic, anti-adipogenic, and immune-modulatory effects, making it a valuable tool for research in bone metabolism, neurobiology, and immunology. -
JNK/CYP Inhibitor
JNK-IN-14 is a potent inhibitor of the c-Jun N-terminal kinase (JNK) family, demonstrating IC50 values of 1.81 nM for JNK1, 12.7 nM for JNK2, and 10.5 nM for JNK3. This compound effectively induces early apoptosis and causes cell cycle arrest in the G2/M phase. Additionally, JNK-IN-14 exhibits a modest inhibition of beclin-1 expression in K562 leukemia cells, indicating its potential application in cancer research and therapeutic strategies targeting JNK signaling pathways. -
JNKs Inhibitor
(-)-Zuonin A is a selective inhibitor of c-Jun N-terminal kinases (JNKs), demonstrating IC50 values of 1.7 μM, 2.9 μM, and 1.74 μM for JNK1, JNK2, and JNK3, respectively. As a naturally occurring lignin, it exhibits potent inhibitory activity, making it a valuable reagent for studies investigating JNK signaling pathways. This compound is applicable in research areas including cancer biology, neuroprotection, and inflammation. -
JNK1 Inhibitor
JNK-1-IN-5 is a selective JNK1 inhibitor exhibiting sub-nanomolar activity. This compound effectively suppresses TGF-β-induced epithelial-mesenchymal transition, making it a valuable tool in research focused on pulmonary fibrosis. JNK-1-IN-5 provides a promising avenue for investigating the role of JNK1 in fibrogenic processes and related therapeutic interventions. -
JNK1 Inhibitor
JD123 is a selective inhibitor of JNK1, demonstrating ATP-competitive inhibition of p38-γ MAPK. It effectively reduces the activity of JNK1 and the expression of cJun (1-135), while exhibiting no inhibitory effects on ERK1, ERK2, or the other p38 MAPK isoforms (α, β, and δ). JD123 is primarily utilized in research applications focused on cell signaling pathways, apoptosis, and inflammatory responses. -
JNK Inhibitor
JNK-1-IN-1 is a potent inhibitor of c-Jun N-terminal kinase 1 (JNK-1), demonstrating additional inhibitory effects on MKK7 with an IC50 of 7.8 μM. This compound selectively targets the JNK signaling pathway, which is crucial in regulating various cellular processes such as apoptosis, inflammation, and differentiation. JNK-1-IN-1 is valuable for research applications in cancer biology, neurodegenerative diseases, and inflammatory disorders, providing insights into the modulation of JNK-related signaling pathways. -
JNK-1 Inhibitor
JNK-IN-22 is a selective inhibitor of JNK-1, a key regulator in the stress-activated protein kinase signaling pathway. This compound demonstrates potent inhibition of JNK-1 activity, which is implicated in various cellular processes, including apoptosis, differentiation, and inflammation. JNK-IN-22 is utilized in research to explore its role in neurodegenerative diseases, cancer, and metabolic disorders, making it a valuable tool for understanding JNK-mediated signaling pathways. -
JNK1/2/3 Inhibitor
JNK-IN-25 is a highly selective inhibitor of JNK1, JNK2, and JNK3, exhibiting IC50 values of 1.54 nM, 1.99 nM, and 0.75 nM, respectively. This compound acts by covalently binding to the conserved cysteine residue in the JNK isoforms, thereby obstructing the phosphorylation of c-Jun. JNK-IN-25 is valuable for investigating pathways involved in cancer, as well as in inflammatory and neurodegenerative diseases. -
JNK Inhibitor
CC-401 dihydrochloride is a potent inhibitor of c-Jun N-terminal kinases (JNK) with an inhibition constant (Ki) ranging from 25 to 50 nM. This compound effectively modulates JNK signaling pathways, making it valuable in studies related to cellular stress responses, apoptosis, and inflammatory processes. CC-401 dihydrochloride is applicable in various research areas, including cancer biology and neurodegenerative disease investigations. -
JNK-1 Inhibitor
JNK-IN-21 is a selective inhibitor of JNK-1, a member of the c-Jun N-terminal kinase family, which plays a crucial role in various cellular processes such as apoptosis and inflammation. By blocking JNK-1 activity, JNK-IN-21 demonstrates potential for modulating signaling pathways associated with stress responses and cellular differentiation. This compound is utilized in biological research to investigate JNK-related signaling mechanisms and their implications in disease models. -
JNK2 Inhibitor
JNK2-IN-1 is a selective inhibitor of JNK2, displaying a dissociation constant (Kd) of 79.2 μM. This compound exhibits anti-inflammatory properties by reducing the secretion of pro-inflammatory cytokines TNF-α and IL-6 through the inhibition of the NF-κB/MAPK signaling pathway. JNK2-IN-1 has demonstrated therapeutic potential in alleviating symptoms associated with LPS-induced acute lung injury (ALI) and sepsis, making it valuable for research in inflammation and related diseases. -
JNK Inhibitor
JNK-IN-23 is a potent inhibitor of c-Jun N-terminal kinases (JNK), demonstrating significant antiproliferative activity against MDA-MB-231 cells with a GIC50 of 30 nM. It effectively impedes metastatic growth in triple-negative breast cancer (TNBC) models in vivo, significantly reducing lung metastasis rates. JNK-IN-23 functions through the dual targeting of glutaminase-1 (GLS) and pyruvate dehydrogenase complex (PDHC), making it a valuable tool for research into cancer metabolism and metastasis. -
Inhibitor of the Phosphorylation of c-jun
TAT-JIP is an effective inhibitor of the phosphorylation of endogenous c-jun, particularly following activation by PHA-PMA. This compound is useful for studying the role of c-jun in various signaling pathways and cellular processes. Its application in research may extend to investigating the regulatory mechanisms involved in cell proliferation, differentiation, and response to stress. -
JNK3 Inhibitor
JNK3 Inhibitor-7 is a selective inhibitor of the c-Jun N-terminal kinase 3 (JNK3) pathway, exhibiting potent activity with IC50 values of 53 nM for JNK3, while demonstrating lesser inhibition against JNK2 and JNK1 at 973 nM and 1039 nM, respectively. This compound effectively crosses the blood-brain barrier and exhibits significant neuroprotective properties. JNK3 Inhibitor-7 holds potential for research applications related to neurodegenerative disorders, particularly Alzheimer's disease. -
JNK Inhibitor
JNK-IN-24 is a selective inhibitor of c-Jun N-terminal kinase (JNK), demonstrating significant anti-metastatic properties in cancer research. By downregulating JNK and matrix metalloproteinase 1 (MMP1) expression in Scrib knockdown-induced cancer models, JNK-IN-24 facilitates recovery from tumorous phenotypes. This compound is suitable for investigations into a range of epithelial cell-derived cancers, contributing to the understanding of JNK's role in tumor progression and metastasis. -
c-Jun N-terminal Kinase Inhibitor
JNK-IN-19 is a selective inhibitor of c-Jun N-terminal kinase (JNK), an important regulator in cellular stress responses. This compound demonstrates significant biological activity by modulating pathways associated with apoptosis, inflammation, and cell survival. JNK-IN-19 shows potential utility in research focused on surgical interventions, neuroprotection, and conditions characterized by oxidative stress. It provides a valuable tool for investigating the role of JNK in various physiological and pathological processes. -
p38 MAPK Inhibitor, JNK Inhibitor
HE4-1 leech peptide is a selective inhibitor of p38 MAPK and c-Jun N-terminal kinase (JNK). It effectively suppresses macrophage migration while maintaining normal macrophage immunological functions, such as phagocytosis, lysozyme activity, and the expression of various inflammatory factors. This peptide is primarily utilized in research focused on atherosclerosis and inflammation-related studies. -
JNK3 Inhibitor
JNK3 Inhibitor-8 is a selective, orally bioavailable inhibitor targeting the c-Jun N-terminal kinase 3 (JNK3) with an IC50 of 21 nM. It demonstrates pronounced neuroprotective effects and effectively crosses the blood-brain barrier. This compound is relevant for research applications related to neurodegenerative disorders, particularly Alzheimer’s disease. -
JNK3 Inhibitor
JNK3 Inhibitor-3 is a selective inhibitor of c-Jun N-terminal kinase 3 (JNK3) that effectively permeates the blood-brain barrier and exhibits oral bioavailability. With IC50 values of 147.8 nM, 44.0 nM, and 4.1 nM for JNK1, JNK2, and JNK3 respectively, JNK3 Inhibitor-3 demonstrates significant inhibitory effects across these kinase targets. This compound has been shown to enhance memory performance in mouse models of dementia, making it a valuable tool for research in Alzheimer’s disease and related neurodegenerative disorders. -
JNK Inhibitor
JNK-1-IN-4 is a selective inhibitor of the c-Jun N-terminal kinase (JNK) family, targeting JNK-1, JNK-2, and JNK-3 with IC50 values of 2.7 nM, 19.0 nM, and 9.0 nM, respectively. This compound effectively inhibits the phosphorylation of c-Jun and decreases the expression of TGF-β1-induced epithelial-to-mesenchymal transition (EMT) marker proteins, including fibronectin and α-SMA. JNK-1-IN-4 demonstrates favorable pharmacokinetic properties, evidenced by a bioavailability of 69%, and has shown anti-fibrotic effects in bleomycin-induced models of idiopathic pulmonary fibrosis. -
TOPK-p38/JNK Inhibitor
TOPK-p38/JNK-IN-1 is an orally active inhibitor targeting the TOPK-p38/JNK signaling pathway, exhibiting an IC50 value of 2.14 µM for nitric oxide production. This compound demonstrates significant anti-inflammatory activity by inhibiting the phosphorylation of downstream proteins while preventing degradation of TOPK. Research applications include studies on inflammatory processes and cellular signaling mechanisms in various disease models. -
JNK Inhibitor
ZG-10 is a selective inhibitor of JNK (c-Jun N-terminal kinase), demonstrating IC50 values of 809 nM for JNK1, 1140 nM for JNK2, and 709 nM for JNK3. This compound exhibits potential therapeutic benefits in mitigating SARS-CoV-2 infection. Its biological activity positions it as a valuable tool for research into cellular signaling pathways and antiviral strategies. -
JNK3/p38 Inhibitor
SR-3737 is a potent inhibitor of JNK3 and p38 mitogen-activated protein kinases, with IC50 values of 12 nM and 3 nM, respectively. This compound exhibits significant biological activity by modulating pathways involved in stress responses and inflammation. SR-3737 is useful in research applications focusing on neuronal signaling, cytokine production, and the molecular mechanisms underlying various neurodegenerative diseases. -
JNK3 Inhibitor
JNK3 Inhibitor-2 is a selective inhibitor targeting c-Jun N-terminal kinase 3 (JNK3), demonstrating an IC50 of 0.25 µM for JNK3, with minimal activity against JNK1 and JNK2 (>100 µM). This compound exhibits additional inhibitory effects on DDR1 and EGFR variants (T790M, L858R). JNK3 Inhibitor-2 is valuable for research applications focusing on cellular stress response and cancer signaling pathways, particularly in studies investigating JNK3’s role in neurodegeneration and oncogenesis. -
JNK Inhibitor
JNK-IN-20 is a selective JNK inhibitor targeting the c-Jun N-terminal kinase pathway. This compound demonstrates significant anti-inflammatory properties and exhibits potential in cancer research by modulating cell signaling pathways involved in tumor progression. JNK-IN-20 is suitable for studies focusing on inflammatory diseases and tumorigenesis. -
JNK Inhibitor
JD118 is a selective JNK inhibitor that predominantly targets JNK1, effectively modulating its activity and downstream signaling pathways. This compound has been shown to inhibit the expression of cJun (1–135), making it a valuable tool for research in cellular stress responses and apoptosis. JD118 is suitable for studies investigating the role of JNK signaling in various disease models, including cancer and neurodegeneration. -
JNK Inhibitor
AS601245 TFA is a selective, ATP-competitive inhibitor of c-Jun NH2-terminal protein kinases (JNK), demonstrating IC50 values of 150 nM for hJNK1, 220 nM for hJNK2, and 70 nM for hJNK3. This compound exhibits significant selectivity, being 10- to 20-fold more selective for JNK over kinases such as c-src, CDK2, and c-Raf, and shows more than 50- to 100-fold selectivity against various Ser/Thr and Tyr-protein kinases. AS601245 TFA is suitable for applications involving neuroprotection and the study of cellular stress response pathways in research settings.
