1. MAPK/ERK Pathway
    Autophagy
  2. JNK
    Autophagy

SP600125 

Cat. No.: HY-12041 Purity: 98.69%
Data Sheet SDS Handling Instructions

SP600125 is a broad-spectrum JNK inhibitor for JNK1, JNK2 and JNK3 with IC50 of 40 nM, 40 nM and 90 nM, respectively.

For research use only. We do not sell to patients.
SP600125 Chemical Structure

SP600125 Chemical Structure

CAS No. : 129-56-6

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Free Sample (0.5-1 mg)   Apply now  
10 mM * 1 mL in DMSO $55 In-stock
10 mg $50 In-stock
50 mg $65 In-stock
100 mg $86 In-stock
200 mg $130 In-stock
500 mg $190 In-stock
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Customer Review

    SP600125 purchased from MCE. Usage Cited in: Elife. 2016 Apr 11;5. pii: e14087.

    Fbxo21-/- RAW264.7 cells are transfected with indicated amounts (0, 1 or 5 μg) Fbxo21-Myc and equal amounts of K29O-Ub-HA vectors for 48 hr, and then infected with VSV (MOI = 1) or HSV-1 (MOI = 5) for 2 hr in the presence or absence of MLN-4924 (10 nM). Then polyubiquitinated ASK1 is examined by immunoblot (IB) against HA after immuneprecipitations (IP).

    SP600125 purchased from MCE. Usage Cited in: Cell Death Differ. 2017 Mar;24(3):492-499.

    LPS stimulates ICER expression via p38-CREB pathway. Effect of MAPK and IKK inhibitors on LPS-induced CREB phosphorylation in peritoneal macrophages.

    SP600125 purchased from MCE. Usage Cited in: Int J Mol Med. 2017 Jan;39(1):71-80.

    Inhibition of c-Jun N-terminal kinase (JNK) expression enhances the promoting effects of miR-214 on adipocyte differentiation and decreases p-JNK protein expression in bone marrow-derived mesenchymal stem cells (BMSCs) following the overexpression of miR-214. p-JNK protein expression is even more significantly suppressed by treatment of the cells with JNK inhibitor as shown by (A) western blot analysis and (B) statistical analysis of p-JNK protein expression.

    SP600125 purchased from MCE. Usage Cited in: Int J Mol Med. 2017 Jan;39(1):71-80.

    Inhibition of p38 expression enhances the promoting effect of miR-214 on the adipocyte differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) following the overexpression of miR-214. p-p38 protein expression decreases following treatment with p38 inhibitor, as shown by (A) western blot analysis, and (B) statistical analysis of p-p38 protein expression.

    SP600125 purchased from MCE. Usage Cited in: Cancer Lett. 2017 Feb 16;393:22-32.

    Effects of p38 MAPK inhibitor (SB203580), ERK inhibitor (U0126), JNK inhibitor (SP600125), caspase inhibitor (Z-VAD-FMK) and NAC on SGC-7901 and MGC-803 treated with DOX/VCPA combination treatment. VCPA pretreatment strategy is the same as above. SB203580 (20 μM), U0126 (10 μM), SP600125 (20 μM), Z-VAD-FMK (10 μM) and NAC (5 mM) are treated 2 h before DOX (2 μg/mL) added into the culture, respectively. MAPK pathway protein levels are determined.

    SP600125 purchased from MCE. Usage Cited in: Oxid Med Cell Longev. 2017;2017:6175841.

    Involvements of MAPK signaling pathway in CPS-induced apoptosis in ALI cultures of sheep bronchial epithelial cells. Cells are pretreated with U0126 (an ERK1/2 inhibitor, 10 μM) for 1 h, followed by exposure to CPS (100 ng/mL) or MO (MOI = 30) for 48 h. Cell lysates are subjected to Western blotting analysis using indicated antibodies.

    SP600125 purchased from MCE. Usage Cited in: Oxid Med Cell Longev. 2017;2017:6175841.

    Involvements of MAPK signaling pathway in CPS-induced apoptosis in ALI cultures of sheep bronchial epithelial cells. Cells are pretreated with SP600125 (a JNK inhibitor, 20 μM) for 1 h, followed by exposure to CPS (100 ng/mL) or MO (MOI = 30) for 48 h. Cell lysates are subjected to Western blotting analysis using indicated antibodies.

    SP600125 purchased from MCE. Usage Cited in: Oxid Med Cell Longev. 2017;2017:6175841.

    Involvements of MAPK signaling pathway in CPS-induced apoptosis in ALI cultures of sheep bronchial epithelial cells. Cells are pretreated with SB203580 (a P38 inhibitor, 20 μM) for 1 h, followed by exposure to CPS (100 ng/mL) or MO (MOI = 30) for 48 h. Cell lysates are subjected to Western blotting analysis using indicated antibodies.

    SP600125 purchased from MCE. Usage Cited in: J Mol Cell Cardiol. 2015 Dec;89(Pt B):268-79.

    Dose response of MAPK and Akt inhibitors on cardiac fibroblast-derived exosomes (Exo)-induced activation of MAPKs and Akt. Neonatal rat cardiomyocytes are treated with or without Exo (50 μg/mL), U0126, SP600125, MK-2206, and SB023580 for 20 min and subjected to Western blot analysis. The results are from 4 separate experiments.

    SP600125 purchased from MCE. Usage Cited in: Oncotarget. 2016 Dec 20;7(51):85079-85096.

    IL-37b inhibits TNF-α mediated activation of the pSmad3L/c-myc pathway but potentiates pSmad3C/ p21 expression in SMMC-7721 cells. Serum-starved LV_NC and LV_IL1F7b-infected SMMC-7721 cells are incubated for 8 h in the absence or presence of 10 μM SP600125 and are then treated for 30 mins with 400 pM TNF-α. Expression of endogenous Smad3 phosphorylation, p21, and c-myc is analyzed in Western blot using specific Abs.

    SP600125 purchased from MCE. Usage Cited in: Free Radic Biol Med. 2017 Jul 9;112:49-59.

    Cells are pre-treated with ERK (U1026) and p38 (SB203580) inhibitors, followed by GL-V9 treatment for 24 h. Western blot is performed to analyze NAG-1 expression.
    • Biological Activity

    • Protocol

    • Technical Information

    • Purity & Documentation

    • References

    Description

    SP600125 is a broad-spectrum JNK inhibitor for JNK1, JNK2 and JNK3 with IC50 of 40 nM, 40 nM and 90 nM, respectively.

    IC50 & Target

    IC50: 40/40/90 nM (JNK1/2/3)[1]

    In Vitro

    SP600125 is an ATP-competitive inhibitor of JNK2 with a Ki value of 0.19±0.06 μM. SP600125 inhibits the phosphorylation of c-Jun with IC50 of 5 μM to 10 μM in Jurkat T cells. In CD4+ cells, such as Th0 cells isolated from either human cord or peripheral blood, SP600125 blocks cell activation and differentiation and inhibits the expression of inflammatory genes COX-2, IL-2, IL-10, IFN-γ, and TNF-α, with IC50 of 5 μM to 12 μM[1]. In a mouse beta cells MIN6, SP600125 (20 μM) induces the phosphorylation of p38 MAPK and its downstream CREB-dependent promoter activation[2]. In HCT116 cells, SP600125 (20 μM) blocks the G2 phase to mitosis transition and induces endoreplication. This ability of SP600125 is independent of JNK inhibition, but due to its inhibition of CDK1-cyclin B activation upstream of Aurora A and Polo-like kinase 1[3].

    In Vivo

    Administration of SP600125 at 15 or 30 mg/kg i.v. significantly inhibits TNF-α serum levels, whereas oral administration dose-dependently blocks TNF-α expression with significant inhibition observed at 30 mg/kg per os[1]. SP600125 attenuates LPS-induced ALI in rats in vivo. The expression levels of TNF-α and IL-6 in the BALF in rats in the SP600125 group are significantly decreased[4].

    References
    Preparing Stock Solutions
    Concentration Volume (DMSO) Mass 1 mg 5 mg 10 mg
    1 mM 4.5407 mL 22.7035 mL 45.4071 mL
    5 mM 0.9081 mL 4.5407 mL 9.0814 mL
    10 mM 0.4541 mL 2.2704 mL 4.5407 mL
    Cell Assay
    [1]

    SP600125 is dissolved in DMSO (20 mM) and stored, and then diluted with appropriate media (DMSO 0.1%) befor use[1].

    Determination of mRNA half-life is performed essentially, except that CD14+ cells are stimulated with (bacterial) lipopolysaccharide (LPS; 50 ng/mL) for 2 h before addition of actinomycin D (5 μg/mL). SP600125 (25 μM) or vehicle (0.5% DMSO vol/vol) is added immediately following the actinomycin D. Analysis is performed by using real-time reverse transcription (RT)-PCR. Total RNA is extracted with an RNeasy Mini kit. TNF mRNA is measured by real time RT-PCR, using a TNF Taqman probe. All data are normalized by using glyceraldehyde-3-phosphate dehydrogenase (GAPDH) expression. The TNF-α forward primer is 5′-CTGGCCCAGGCAGTCAGAT-3′ and the reverse primer is 5′-TATCTCTCAGCTCCACGCCATT-3′. The Taqman probe sequence is 5′-FAM-CCTGTAGCCCATGTTGTAGCAAACCCTCA-TAMRA-3′[1]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration
    [1][4]

    SP600125 is dissolved in 30% PEG-400/20% polypropylene glycol/15% Cremophor EL/5% ethanol/30% saline (Mice)[1].

    Mice[1]
    Female CD-1 mice (8-10 weeks of age) are dosed i.v. or per oswith SP600125 in PPCES vehicle (30% PEG-400/20% polypropylene glycol/15% Cremophor EL/5% ethanol/30% saline), final volume of 5 mL/kg, 15 min before i.v. injection with LPS in saline (0.5 mg/kg). At 90 min, a terminal bleed is obtained from the abdominal vena cava, and the serum is recovered. Samples are analyzed for mouse TNF-α by using an ELISA.
    Rat[4]
    A total of 40 male Wistar rats are randomly divided into four groups (n=10): the control group, LPS group, normal saline group (NS) and the SP600125 group. Acute lung injury (ALI) is induced via intratracheal injection of LPS. Briefly, the rats are anesthetized with pentobarbital sodium followed by intratracheal injection of 5 mg/kg LPS. The rats are then placed in a vertical position and rotated for 1 min to distribute the LPS in the lungs. Normal saline or SP600125 is administered via intraperitoneal injection (15 mg/kg) 10 min after the LPS injection. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References
    Molecular Weight

    220.23

    Formula

    C₁₄H₈N₂O

    CAS No.

    129-56-6

    Storage
    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Shipping

    Room temperature in continental US; may vary elsewhere

    Solvent & Solubility

    DMSO: ≥ 45 mg/mL

    * "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

    Purity: 98.69%

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    SP600125
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