JNK inhibitors(c-Jun N-terminal kinase inhibitors), JNK1 inhibitors(c-Jun N-terminal kinase 1 inhibitors), JNK2 inhibitors(c-Jun N-terminal kinase 2 inhibitors)

Therapeutic Areas

Nervous System Diseases

Active Indication

Alzheimer Disease

Inactive Indication

Allograft RejectionAsthmaBrain Ischemia+ [1]

Originator Organization

Signal Research Corp.

Active Organization

Kafrelsheikh University

Inactive Organization

Signal Research Corp.

Drug Highest PhasePreclinical

First Approval Date-

Regulation-

100 Clinical Results associated with SP-600125

100 Translational Medicine associated with SP-600125

100 Patents (Medical) associated with SP-600125

3,686

Literatures (Medical) associated with SP-600125

01 May 2025·European Journal of Pharmacology

M084 causes cell cycle arrest and inhibits voltage-gated Na+ and K+ channels in neuronal N2A cells

Article

Author: Shiao, Lian-Ru ; Leong, Iat-Lon ; Chuang, Chin-Min ; Wu, Cheng-Hsun ; Leung, Yuk-Man ; Huang, Yi-Ping

The effects of M084, an inhibitor of transient receptor potential (TRP) channels TRPC4 and TRPC5, on cell proliferation, voltage-gated K⁺ (Kv) channels and voltage-gated Na⁺ (Nav) channels were investigated in mouse neuronal N2A cells. Cell proliferation was measured by MTT assay and trypan blue exclusion test. Mitochondrial membrane potential was measured using JC-1 as a fluorescent probe. Cell cycle and ion channel activities were studied, respectively, using flow cytometry and voltage-clamp method. M084 (10-100 μM) concentration-dependently suppressed cell proliferation; M084 at 100 μM also arrested cell cycle at the G1 phase, and caused a decrease in mitochondrial membrane potential. The anti-proliferative effect of M084 was not mitigated by dorsomorphine (AMPK inhibitor), sodium salicylate (NF-κB inhibitor) and SP600125 (JNK inhibitor), but was alleviated by SB203580 (p38 inhibitor). M084 (3-100 μM) suppressed Nav and Kv currents in a concentration-dependent fashion with IC₅₀ values of 9.1 and 29.2 μM, respectively. M084 (30 μM) caused left-shifts in inactivation curves of both Nav and Kv currents, and diminished peak amplitude of current injection-triggered membrane potential overshoot. In conclusion, M084 suppressed neuronal cell growth and inhibited their Nav and Kv channels.

01 Apr 2025·Chemico-Biological Interactions

Pulsatilla saponin D inhibited the growth of osteosarcoma by regulating the JNK/ATF3 signaling pathway

Article

Author: Tao, Huimin ; Lin, Jinti ; Yu, Wei ; Jin, Kaipeng ; Liu, Bing ; Shen, Chengchun ; Zhu, Jian

Osteosarcoma (OS) is a highly malignant and aggressive bone tumor associated with early lung metastasis and high mortality. Traditional chemotherapy does not effectively improve the efficacy and survival rate of patients with OS. Thus, it is vital to search for alternative therapies. Pulsatilla saponin D (PSD) is a potent bioactive compound that has been widely employed in cancer therapy due to its diverse bioactivities and minimal adverse effects. However, any effect on OS remains unclear. We found that PSD induced apoptosis of OS cells and investigated the mechanisms thereof. In vitro, PSD dose-dependently induced apoptosis and inhibited the viability of HOS and K7M2 cells. Furthermore, PSD significantly suppressed cell migration and invasion, and caused cell cycle arrest at the G0/G1 phase. Mechanistically, PSD upregulated ATF3 and JUN transcription by controlling JNK expression. Compared to cells treated with PSD alone, cells pre-treated with SP600125 (a JNK inhibitor), or in which ATF3 had been knocked down ATF3 with siRNA, did not exhibit PSD-mediated cell apoptosis. In a murine OS model, PSD exhibited a powerful anti-cancer effect and an excellent safety profile. Our data imply that PSD could effectively prevent OS occurrence and progression.

01 Apr 2025·Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids

D-allulose enhances lipid oxidation in HepG2 cells via peroxisome proliferator-activated receptor α (PPARα)

Article

Author: Haas, Michael J ; Mooradian, Arshag D ; Batch, Jennifer ; Graham, Lauren ; Warda, Firas

Lipid accumulation in hepatocytes in non-alcoholic steatohepatitis (NASH) is attributed partly to loss of insulin-responsiveness and/or an increased pro-inflammatory state. Since the rare sugar D-allulose has insulin mimetic and anti-inflammatory properties, its effects on lipid accumulation in liver-derived cells was tested. In HepG2 cells exposed to 200 μM oleic acid for 72 h, D-allulose treatment decreased intracellular lipid accumulation with an IC₅₀ = 0.45 ± 0.07 mM. A similar effect was observed in cells treated with 10 μM gemfibrozil. D-allulose and gemfibrozil treatment increased oleic acid β-oxidation. Both D-allulose and gemfibrozil increased peroxisome proliferator-activated receptor α (PPARα) expression (two-fold) relative to control cells, while retinoid X receptor was unchanged. D-allulose and gemfibrozil increased PPARα-dependent genes including those involved in fatty acid β-oxidation (acyl-coenzyme A oxidase 1, long-chain-fatty-acid-coenzyme A ligase 5, and carnitine palmitoyltransferase 1 A). D-allulose and gemfibrozil also increased PPARα reporter gene expression and phosphorylation (Serine 12) which were both inhibited by the mitogen-activated protein (MAP) kinase inhibitor PD098059. Other MAP kinase inhibitors, including SB203580, SP600125, and BIX10289 had no effect on reporter gene expression. Oleic acid treatment, but not D-allulose or gemfibrozil, decreased sterol response element binding protein 1 and sterol response element binding protein 2 expression relative to cells not exposed to oleic acid, while peroxisome proliferator-activated receptor γ expression did not change. These results indicate that D-alluose mimics gemfibrozil effects on lipid content in HepG2 cells by promoting fatty acid β-oxidation via PPARα .

100 Deals associated with SP-600125

R&D Status

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Alzheimer Disease	Preclinical	Egypt	Kafrelsheikh University	07 Oct 2024
Allograft Rejection	Preclinical	United States	Signal Research Corp.	-
Asthma	Preclinical	United States	Signal Research Corp.	-
Brain Ischemia	Preclinical	China	Signal Research Corp.	-
Rheumatoid Arthritis	Preclinical	United States	Signal Research Corp.	-

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