SP600125
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- LARVOL DELTA
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December 04, 2025
AP-1 promotes oncogenic transcription in lung cancer cells by bridging promoter-enhancer interactions.
(PubMed, Cancer Gene Ther)
- "Pharmacological inhibition of AP-1, either directly via AP-1 inhibitor SR11302 or indirectly through its upstream JNK pathway inhibition via SP600125, suppressed AP-1-driven oncogenic transcription and reduced promoter-enhancer looping. Our findings highlight the pivotal role of AP-1 in oncogenic transcription in NSCLC, revealing that transcription factors enhance oncogene expression by facilitating promoter-enhancer interactions."
Journal • Lung Cancer • Non Small Cell Lung Cancer • Oncology • Solid Tumor • Squamous Cell Carcinoma
November 26, 2025
Dexamethasone regulates gene expression in chondrocytes through MKP-1 and downregulates cholesterol hydroxylases CH25H and CYP7B1.
(PubMed, Inflamm Res)
- "In conjunction with previous findings, the current data substantiate the role of MKP-1 as a protective factor in chondrocytes and highlight its potential as a therapeutic target for the treatment of osteoarthritis, because increased levels of cholesterol and its metabolism by CH25H and CYP7B1 are involved in the pathogenesis of OA, particularly in its obesity-associated phenotype."
Journal • Genetic Disorders • Immunology • Obesity • Orthopedics • Osteoarthritis • Pain • Rheumatology • IL1B
November 23, 2025
Integrin-specific signaling drives ER stress-dependent atherogenic endothelial activation.
(PubMed, Redox Biol)
- "However, pharmacological inhibition of ER stress using TUDCA suppresses proinflammatory and metabolic gene expression (bulk RNA-seq), without affecting NF-κB activation. Blocking this pathway using a JNK inhibitor (SP600125) or dominant-negative c-Jun (TAM67) abrogates inflammatory gene expression following oxLDL or disturbed flow. Together, these findings identify a novel mechanism by which fibronectin-integrin signaling promotes ER stress in response to mechanical and metabolic stressors, amplifying endothelial inflammation through JNK-c-Jun signaling."
Journal • Atherosclerosis • Cardiovascular • Dyslipidemia • Inflammation • TLN1
November 22, 2025
RAB3GAP2 silencing alleviates oxidative stress in cataracts by enhancing Mfn2-mediated mitochondrial autophagy by activating JNK/STAT3.
(PubMed, Int J Biol Macromol)
- "Further in vitro studies revealed that SP600125 treatment reversed the effects of RAB3GAP2 silencing on cataract development, the promotion of Mfn2 and mitochondrial autophagy, and the activation and nucleation of STAT3...These findings suggest that RAB3GAP2 silencing can mitigate oxidative stress to prevent cataract development, probably by facilitating Mfn2-mediated mitochondrial autophagy by activating JNK/STAT3. It may be a promising target for treating cataracts."
Journal • Cataract • Ophthalmology • MFN2 • STAT3
November 21, 2025
Protopanaxadiol induces apoptosis through JNK signaling pathway and targeting MLK3 in human melanoma.
(PubMed, J Ginseng Res)
- "Inhibition of JNK with SP600125 reversed PPD-induced apoptosis, indicating that JNK signaling plays a critical role...Our findings revealed that PPD exerts potent anti-melanoma effects by directly targeting MLK3 and activating the MLK3-JNK signaling pathway, leading to apoptosis. These results provide novel insights into the molecular mechanism of PPD and suggest its potential as a therapeutic agent for melanoma treatment."
Journal • Genetic Disorders • Melanoma • Oncology • Skin Cancer • Solid Tumor • MAP3K11
November 21, 2025
DHCR24 knockdown-induced cellular cholesterol deficiency triggers tau hyperphosphorylation at Thr181, Ser199 and Ser202/Thr205 via p38 MAPK/JNK signaling.
(PubMed, Cell Signal)
- "Both compounds restored tau phosphorylation to baseline in a concentration-dependent manner, with maximal suppression at 40 μM (SB203580) and 20-40 μM (SP600125). Collectively, these data establish DHCR24-controlled cholesterol homeostasis as a molecular rheostat of tau pathology through p38/JNK signaling, and nominate this axis for therapeutic intervention in AD."
Journal • Alzheimer's Disease • CNS Disorders • Neuroblastoma • Oncology • Solid Tumor
October 06, 2025
Integrin–ER Stress Crosstalk Links Mechanical and Metabolic Stress to Vascular Inflammation
(AHA 2025)
- "However, pharmacological inhibition of ER stress using TUDCA suppresses proinflammatory and metabolic gene expression (bulk RNA-seq), without affecting NF-κB activation. Blocking this pathway using a JNK inhibitor (SP600125) or dominant-negative c-Jun (TAM67) abrogates inflammatory gene expression following oxLDL or disturbed flow. Together, these findings identify a novel mechanism by which fibronectin–integrin signaling promotes ER stress in response to mechanical and metabolic stressors, amplifying endothelial inflammation through JNK–c-Jun signaling and contributing to atherogenesis."
Late-breaking abstract • Atherosclerosis • Dyslipidemia • Inflammation • TLN1
November 14, 2025
c-Jun inhibition mitigates chemotherapy-induced neurotoxicity in iPSC-derived sensory neurons.
(PubMed, Cell Death Discov)
- "Administration of various chemotherapeutic agents (i.e., paclitaxel, vincristine, bortezomib and cisplatin) at clinically applicable concentrations resulted in reduced cell viability, axonal degeneration, electrophysiological dysfunction and increased levels of phosphorylated c-Jun in iPSC-DSN...To test whether c-Jun plays a central role in the development of CIPN, we applied the small molecule inhibitor of the Jun N-terminal kinase, SP600125, to iPSC-DSN treated with neurotoxic chemotherapy. c-Jun inhibition prevented chemotherapy-induced neurotoxicity by preserving cell viability, axonal integrity and electrophysiological function of iPSC-DSN. These findings identify c-Jun as a key mediator of CIPN pathophysiology across multiple drug types and present preclinical evidence that c-Jun inhibition is an attractive therapeutic target to prevent CIPN."
Journal • Oncology • Pain
November 13, 2025
Ursolic acid sensitizes bladder cancer to gemcitabine chemotherapy by concurrently targeting PI3K/AKT and JNK pathways.
(PubMed, Transl Androl Urol)
- "Pharmacological modulators (SC79, SP600125) were used to verify pathway roles. UA sensitizes BCa to GEM chemotherapy by promoting apoptosis, mediated through PI3K/AKT inactivation and JNK activation. These findings highlight UA as a promising adjunct to GEM therapy, warranting further clinical exploration."
Journal • Bladder Cancer • Genito-urinary Cancer • Oncology • Solid Tumor • CASP3 • MAPK8
November 10, 2025
Chemical Genetics with SP600125 Reveals That Mps1 Protein Kinase Works as a Regulatory Element in Post-embryonic Development of the Arabidopsis thaliana Root SystemAn Insight into Plant Cell Cycle Control.
(PubMed, ACS Omega)
- "Our experiments open new possibilities for understanding the mechanisms of the Mps1 protein using plants as experimental models. They also show that chemical genetics is a robust alternative for studies of plant development."
Journal • Oncology
November 06, 2025
SARM1 deficiency promotes depressive-like behavior and neuroinflammation through JNK/STING/TBK1 signaling.
(PubMed, Int Immunopharmacol)
- "Furthermore, Pharmacological inhibition of JNK with SP600125 in SARM1 knockdown mice effectively alleviated depressive-like behaviors, reduced hippocampal ROS and IL-1β, suppressed p-p38/p-NF-κB/NLRP3, and unexpectedly downregulated p-STING/p-TBK1 while improving PSD95 levels. These findings suggest that SARM1 deficiency drives neuroinflammation and depressive phenotypes through dysregulated JNK/STING/TBK1 signaling, highlighting this pathway as a potential therapeutic target for neuroinflammation-associated depression."
Journal • CNS Disorders • Depression • Inflammation • Psychiatry • DLG4 • IL1B • NLRP3 • SOD2 • STING • TBK1
October 27, 2025
Synthesis and evaluation of 8-(benzyloxy)-5,7-dibromo-2-methylquinoline derivatives as inducers of apoptosis in triple-negative breast cancer MDA-MB-468 cells via MKK7-JNK pathway activation.
(PubMed, Bioorg Chem)
- "Treatment with 10l significantly increased phospho-JNK (p-JNK) levels, and blockage of JNK signaling by either pharmacological inhibitor SP600125 or JNK siRNA abolished its pro-apoptotic effect, demonstrating that JNK activation was critical for 10l-induced cell death. Notably, the major kinase upstream of JNK MKK7 was activated under 10l treatment. All these data suggested that compound 10l was capable of inducing apoptosis via activating MKK7-JNK pathway, supporting its potential as a therapeutic candidate for TNBC treatment."
Journal • Breast Cancer • Liver Cancer • Lung Cancer • Oncology • Solid Tumor • Triple Negative Breast Cancer
October 22, 2025
Deubiquitinating enzyme USP42 promotes breast cancer progression by inhibiting JNK/p38-mediated apoptosis.
(PubMed, Sci Rep)
- "Treatment with SP600125 (JNK inhibitor) or SB203580 (p38 MAPK inhibitor) effectively recused JNK and p38 activation. Both inhibitors also reduced the apoptotic cell population, which was upregulated by USP42 silencing. These findings highlight USP42 promotes breast cancer progression by reducing JNK and p38 activation and inhibiting apoptosis, suggesting its potential as a therapeutic target in breast cancer treatment."
IO biomarker • Journal • Breast Cancer • Oncology • Solid Tumor • Targeted Protein Degradation • BAX • BCL2 • CASP3 • USP4 • USP42
October 21, 2025
The skin hydration and anti-ageing benefits of Ectoine, achieved through enhanced Src-ERK-mediated HAS-2 and JNK-driven AQP-3 expression in human keratinocytes, along with the inhibition of MMP-1-induced collagen-I degradation in human fibroblasts, both with and without UVB irradiation.
(PubMed, Int J Cosmet Sci)
- "We demonstrated that Ectoine exerts skin hydration effects without or with UVB exposure in human skin keratinocyte (HaCaT) cells and anti-ageing in fibroblast (Hs68) cells. Therefore, Ectoine could serve as a potential natural compound in cosmetic preparations for skin hydration and anti-ageing."
Journal • MAPK1 • MMP1
October 16, 2025
Transcriptomic-Driven Drug Repurposing Reveals SP600125 as a Promising Drug Candidate for the Treatment of Glial-Mesenchymal Transition in Glioblastoma.
(PubMed, Int J Mol Sci)
- "Further ranking according to their blood-brain barrier permeability, as well as structural and transcriptomic similarities to known anti-GBM drugs, revealed SP600125, vemurafenib, FG-7142, dibenzoylmethane, and phensuximide as the most promising for GMT inhibition. In vitro validation showed that SP600125, which is most closely associated with GMT-related hub genes, effectively inhibited TGF-β1- and chemical hypoxia-induced GMT in U87 GBM cells by reducing morphological changes, migration, vasculogenic mimicry, and mesenchymal marker expression. These results clearly demonstrate the applicability of connectivity mapping as a powerful tool to accelerate the discovery of effective GMT-targeting therapies for GBM and significantly expand our understanding of the antitumor potential of SP600125."
Journal • Brain Cancer • Glioblastoma • Oncology • Solid Tumor • TGFB1
October 06, 2025
Elp3 activates the JNK/MAPK pathway through histone acetylation to promote gastric cancer proliferation, migration, and invasion.
(PubMed, Histol Histopathol)
- "Elp3 may be involved in GC progression by activating the JNK/MAPK pathway through histone acetylation."
Journal • Gastric Cancer • Oncology • Solid Tumor • MAPK8
October 15, 2025
Inhibition of DHHC9-mediated CD36 palmitoylation lessens high-fat diet (HFD)-induced impairment of pubertal mammary gland development through the JNK-ERK pathway.
(PubMed, Cell Mol Biol Lett)
- "This study revealed that inhibition of DHHC9-mediated CD36 palmitoylation mitigated HFD-induced impairment of pubertal mammary gland development via the JNK1-ERK1/2 pathway."
Journal • CD36 • LYN • MAPK8 • SCARB1
October 13, 2025
High levels of uric acid upregulate endothelin receptors: the role of MAPK pathways in an in vitro study.
(PubMed, Arch Med Sci)
- "Additionally, the up-regulation of ETB receptors induced by UA was inhibited by the p38 inhibitor SB203580, the JNK inhibitor SP600125, and the ERK1/2 inhibitor U0126...High levels of UA stimulate the up-regulation of ET receptors in rat cerebral arteries in vitro through MAPK pathways. This study may offer novel perspectives on hyperuricaemia-associated cerebrovascular diseases."
Journal • Preclinical • CNS Disorders • Vascular Neurology
October 06, 2025
Tetrahydrocurcumin Protects Microglial Cells Against Pseudomonas aeruginosa Lipopolysaccharide-Induced Reactive Oxygen Species Production and Cathepsin B to Activate NLRP3 Inflammasome-Mediated Pyroptosis Via the HO-1 and p38/JNK Pathway.
(PubMed, Int J Med Sci)
- "Furthermore, we used MAPKs (SB203580, SP600125, and U0126) and HO-1 (SnPP) inhibitors to demonstrate that THC modulated inflammasome-mediated pyroptosis may be related to p38 and JNK MAPK and HO-1-dependent inflammatory signaling. Overall, THC can inhibit ROS-triggered NLRP3 inflammasome-mediated pyroptosis by promoting GSH activity and HO-1 expression via modulating the p38 and JNK signaling pathways in P.a. LPS-treated BV-2 cells."
Journal • Inflammation • CTSB • HMOX1 • IL18 • MAPK8 • NLRP3
October 06, 2025
Pharmacological inhibition of JNK-MAPK disrupts cigarette smoke-induced RUNX2/Galectin-3 driven EMT and cancer stemness in lung adenocarcinoma.
(PubMed, Biochem Pharmacol)
- "A specific pharmacological inhibitor of JNK (SP600125) significantly attenuated CSE-induced RUNX2 and Galectin-3 expression, and also reversed CSE-driven EMT marker alterations, suppressed transcriptional EMT perturbations, and reduced proinflammatory cytokines, including monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α). In conclusion, this study identifies that ROS/JNK/RUNX2/Gal-3 axis drives CS-induced oncogenic plasticity, suggesting that targeted inhibition of this pathway could be an effective strategy for mitigating CS-related LC progression."
Journal • Lung Adenocarcinoma • Lung Cancer • Non Small Cell Lung Cancer • Oncology • Solid Tumor • CCL2 • CXCL8 • LGALS3 • MAPK8 • RUNX2 • TNFA
September 26, 2025
In Vitro Evaluation of the Inhibitory Effects of Linarin on Histamine-Induced Expression of Proinflammatory Cytokines, Mucin 5AC, and Aquaporin 5 in Human Nasal and Bronchial Epithelial Cells.
(PubMed, Kaohsiung J Med Sci)
- "Notably, the inhibitory effects of linarin were potentiated in the presence of specific inhibitors targeting NF-κB (PDTC), ERK (U0126), p38 (SB203580), and JNK (SP600125)...These effects are mediated through the inhibition of the NF-κB and MAPK pathways. Thus, linarin may serve as a promising therapeutic agent for the treatment of allergic rhinitis and asthma."
Journal • Preclinical • Allergic Rhinitis • Asthma • Immunology • Inflammation • Pulmonary Disease • Respiratory Diseases • CXCL8 • IL6 • MUC5AC • NFKBIA • RELA
September 18, 2025
Depletion of Mycobacterium tuberculosis transmembrane protein Rv3737 reduces pathogen survival and induces M1 macrophage polarization against tuberculosis.
(PubMed, Front Cell Infect Microbiol)
- "Colony-forming units (CFUs) and inducible nitric oxide synthase (iNOS) levels were examined in H37RvΔRv3737-infected macrophages pretreated with specific inhibitors (JSH-23, U0126-EtOH, SB203580, SP600125)...Its deletion enhances host antimicrobial activity by activating NF-κB and MAPK signaling pathways. Targeting Rv3737 may represent a novel strategy for tuberculosis therapy."
Journal • Infectious Disease • Pulmonary Disease • Respiratory Diseases • Tuberculosis • CD86 • IL10 • IL1B • IL6 • MRC1 • TGFB1 • TNFA
September 17, 2025
Resveratrol ameliorates osteogenic differentiation, calcification, and apoptosis of VSMCs through regulating JNK/Bax signaling.
(PubMed, Front Pharmacol)
- "Rat VSMCs were cultured in calcifying medium (CM) to induce calcification, and treated with resveratrol, the JNK inhibitor SP600125, or the JNK activator anisomycin...In vitamin D3-induced calcification models, resveratrol significantly reduced vascular calcification and osteogenic differentiation. Resveratrol exerted an inhibitory effect on VSMC calcification, osteogenic differentiation, and apoptosis through the inhibition of the JNK/Bax signaling pathway."
Journal • BMP2 • CASP3 • RUNX2
September 04, 2025
Inhibiting JNK and PI3K-Akt signaling pathways altered spontaneous network bursts and developmental trajectories of neuronal networks.
(PubMed, J Neural Eng)
- "This study investigates the roles of JNK and PI3K-Akt signaling in regulating spontaneous NBs dynamics and network organization in cultured neuronal networks. Approach: Using longitudinal microelectrode array (MEA) recordings from cultured cortical neurons (DIV14-49), we pharmacologically inhibited JNK (SP600125, JNK-IN-8) and PI3K-Akt (LY294002, GDC-0941) pathways. JNK signaling is crucial for maintaining early core-node functionality, whereas PI3K-Akt signaling promotes the development of mature modular architecture. Our findings enhance the understanding of how molecular signaling influences neuronal network dynamics, contributing to a broader framework for studying neurodevelopmental principles.
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Journal
September 12, 2025
Histamine regulates the activity and the expression of the Na+/H+ exchanger (NHE)3 in human epithelial HK-2 cells.
(PubMed, Inflamm Res)
- "Histamine shows early (within 60 min) and late (48 h) effects on NHE3 expression. The histamine H1 and H4 receptors are shown to contribute to these effects differentially. The findings of this study extends the evidence for a direct contribution of histamine on the renal reabsorptive machinery."
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