SP600125

For research use only.

Catalog No.S1460 Synonyms: Nsc75890

715 publications

SP600125 Chemical Structure

CAS No. 129-56-6

SP600125 (Nsc75890) is a broad-spectrum JNK inhibitor for JNK1, JNK2 and JNK3 with IC50 of 40 nM, 40 nM and 90 nM in cell-free assays, respectively; 10-fold greater selectivity against MKK4, 25-fold greater selectivity against MKK3, MKK6, PKB, and PKCα, and 100-fold selectivity against ERK2, p38, Chk1, EGFR etc. SP600125 is also a broad‐spectrum inhibitor of serine/threonine kinases including Aurora kinase A，FLT3 and TRKA with of IC50 of 60 nM, 90 nM and 70 nM. SP600125 inhibits autophagy and activates apoptosis.

Size Price Stock Quantity  
10mM (1mL in DMSO) USD 191 In stock
USD 77 In stock
USD 147 In stock
USD 247 In stock
USD 587 In stock
Bulk Discount
Bulk Inquiry

Free Overnight Delivery on orders over $ 500
Next day delivery by 10:00 a.m. Order now.

Selleck's SP600125 has been cited by 715 publications

Purity & Quality Control

Choose Selective JNK Inhibitors

Biological Activity

Description SP600125 (Nsc75890) is a broad-spectrum JNK inhibitor for JNK1, JNK2 and JNK3 with IC50 of 40 nM, 40 nM and 90 nM in cell-free assays, respectively; 10-fold greater selectivity against MKK4, 25-fold greater selectivity against MKK3, MKK6, PKB, and PKCα, and 100-fold selectivity against ERK2, p38, Chk1, EGFR etc. SP600125 is also a broad‐spectrum inhibitor of serine/threonine kinases including Aurora kinase A，FLT3 and TRKA with of IC50 of 60 nM, 90 nM and 70 nM. SP600125 inhibits autophagy and activates apoptosis.
Targets
JNK1 [1]
(Cell-free assay)		 JNK2 [1]
(Cell-free assay)		 Aurora A [4]
(Cell-free assay)		 TrkA [4]
(Cell-free assay)		 JNK3 [1]
(Cell-free assay)
40 nM 40 nM 60 nM 70 nM 90 nM
In vitro

SP600125 is originally characterized as a selective ATP-competitive inhibitor of c-Jun N-terminal kinase JNK. In Jurkat T cells, SP600125 inhibits the phosphorylation of c-Jun with IC50 of 5 μM to 10 μM. 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] However, later studies reveal that SP600125 also suppresses aryl hydrocarbon receptor (AhR) [2], Mps1 [3], and a panel of other serine/threonine kinases, including Aurora kinase A, FLT3, MELK, and TRKA [4]. In a mouse beta cells MIN6, SP600125 (20 μM) induces the phosphorylation of p38 MAPK and its downstream CREB-dependent promoter activation. [5] 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. [6]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
Plasmodium falciparum HB3 Ml6yRY51cWKjY4TldolidCCDc4PhfS=> MXW3NkBp MVjEUXNQ MWXBcpRqeGyjc33v[IlidCCjY4Tpeol1gSC5aYToJGlEPTBib3[gO{46PDN{ODFOwG0> NUjlephsOTl5M{S5NVA>
Plasmodium falciparum W2 NF22e2xCdnSrYnHjeIVzcWGuIFHzd4F6 NFO3R5I4OiCq M2jtVGROW09? NVTJ[VM1SW62aYDsZZNud2SrYXygZYN1cX[rdImge4l1cCCLQ{WwJI9nKDdwOUSzNlgh|ryP M3PSNVE6PzN2OUGw
Plasmodium falciparum 7G8 MXPBcpRq[mGldHXybYFtKEG|c3H5 M4TVO|czKGh? MXPEUXNQ NVf6dIxmSW62aYDsZZNud2SrYXygZYN1cX[rdImge4l1cCCLQ{WwJI9nKDFyIN88US=> Ml73NVk4OzR7MUC=
Plasmodium falciparum 3D7 NFfjflhCdnSrYnHjeIVzcWGuIFHzd4F6 M2LWTVczKGh? Moe0SG1UVw>? M{GyOGFvfGmybHHzcY9lcWGuIHHjeIl3cXS7IIfpeIghUUN3MDDv[kAyOi53OEmzJO69VQ>? NXnPXIZvOTl5M{S5NVA>
Plasmodium falciparum GB4 MYLBcpRq[mGldHXybYFtKEG|c3H5 NUP5V4NvPzJiaB?= NYexbotkTE2VTx?= MVjBcpRqeGyjc33v[IlidCCjY4Tpeol1gSC5aYToJGlEPTBib3[gNVIvPTh7M988US=> M33iTVE6PzN2OUGw
RAW264.7 M{XvTWZ2dmO2aX;uJGF{e2G7 NGXkXWQyOCEQvF2= MkXqNVIhcA>? MoDBRY51cWmwZnzhcY1ifG:{eTDhZ5Rqfmm2eTDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oIFzQV{1qdmS3Y3XkJG5QKHC{b3T1Z5Rqd25id3n0bEBKSzVyIH;mJFE4|ryP MX2xPVQ6PzRzOB?=
SH-SY5Y NUn4WnI2TnWwY4Tpc44hSXO|YYm= MnXsNVAh|ryP NEjTSIgyKGh? MYrEUXNQ MVLO[ZVzd3C{b4TlZ5RqfmViYXP0bZZqfHliYYPz[ZN{\WRiYYOgdoVlfWO2aX;uJI9nKGGwaYPvcZlkcW5vaX7keYNm\CClZXzsJIRm[XSq NHqwfXIzOzR7OEmxOC=>
SH-SY5Y MWnLbY5ie2ViQYPzZZk> M1j5V|ExKM7:TR?= MlXkNUBp MnXHSG1UVw>? MYPJcohq[mm2aX;uJI9nKEqQS{OgZZN{\XO|ZXSgZZMh[myxY3vh[IUhd2ZiYX7pd49ugWOrbj3pcoR2[2WmIHOtbpVvKHCqb4PwbI9zgWyjdHnvckBifCC|ZYK3Ny=> NIDPdnozOzR7OEmxOC=>
RAW264.7 MVLGeY5kfGmxbjDBd5NigQ>? NGjoNmIyOCEQvF2= M3XVWVI1KGh? MkDqRY51cWmwZnzhcY1ifG:{eTDhZ5Rqfmm2eTDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oIFnMMVFj\XSjIILlcIVie2V? MWmyN|c6OTB5OB?=
RAW264.7 NET3emJHfW6ldHnvckBCe3OjeR?= NIjx[IwyOCEQvF2= NVL5N5djOjRiaB?= M1v5fGFvfGmrbn\sZY1u[XSxcomgZYN1cX[rdImgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDMVHMucW6mdXPl[EBqVk:VIHX4dJJme3Orb36= MlXWNlM4QTFyN{i=
RAW264.7 NFT6UItHfW6ldHnvckBCe3OjeR?= MoHwNVAh|ryP MkfkNkBp M2K0d2FvfGmrbn\sZY1u[XSxcomgZYN1cX[rdImgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDMVHMucW6mdXPl[EBPVyCycn;keYN1cW:w MVGyN|c6OTB5OB?=
B16-F10 NUXMWFBNTnWwY4Tpc44hSXO|YYm= NFjNXJMyKGh? NUe3TmZoUW6qaXLpeIlwdiCxZjDUUmYu[WyyaHGtbY5lfWOnZDDjMWpWViCyaH;zdIhwenmuYYTpc44> NXvoXnVYOjF6MUW2N|Q>
PC12 NW\GZ2xQTnWwY4Tpc44hSXO|YYm= MlrwNVAh|ryP M1zHcVUhcA>? M4i5[mROW09? NXnrOGo4SWO2aY\heIlwdiCxZjDOdoYzN0GURTDhd5Nme3OnZDDhd{BJVy1zIIDyc5RmcW5iaX7keYN1cW:wIIDy[ZRz\WG2ZXSge4l1cCCSREm4NFU6 MWSyNVM1PTZ6NR?=
PC12 M4rvd2Z2dmO2aX;uJGF{e2G7 M3rEVFExKM7:TR?= M2DRR|UhcA>? NVf4[VFNTE2VTx?= MV7BZ5RqfmG2aX;uJI9nKE6{ZkKvRXJGKGG|c3Xzd4VlKGG|IFjPMVEheHKxdHXpckBqdmS3Y4Tpc44heHKndILlZZRm\CC5aYToJHUxOTJ4 MnTjNlE{PDV4OEW=
PC12 M2nvVmZ2dmO2aX;uJGF{e2G7 MlKwNVAh|ryP Mm[2OUBp M{G1VmROW09? MULBZ5RqfmG2aX;uJI9nKE6{ZkKvRXJGKGG|c3Xzd4VlKGG|IFjPMVEheHKxdHXpckBqdmS3Y4Tpc44heHKndILlZZRm\CC5aYToJHNRPjByMUK1 M2XTRVIyOzR3Nki1
PC12 MYTGeY5kfGmxbjDBd5NigQ>? NHK0NXgyOCEQvF2= NYHrVoFPPSCq M4\JfGROW09? NYD0[49PSWO2aY\heIlwdiCxZjDOdoYzN0GURTDhd5Nme3OnZDDhd{BJVy1zIIDyc5RmcW5iaX7keYN1cW:wIIDy[ZRz\WG2ZXSge4l1cCCVQkKwN|U5OA>? Mle5NlE{PDV4OEW=
A549 NY[5fnJDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXmyNEDPxE1? MmTDO|IhcA>? NVW0RXRFTE2VTx?= M4DYVXJieGmmIHHu[EBxd3SnboSgbY5pcWKrdHnvckBw\iClZXzsJJBzd2yrZnXyZZRqd25? MX[yN|kyOjh2MB?=
PC3 NYjhR2xKTnWwY4Tpc44hSXO|YYm= M1jSWFI2KM7:TR?= M3TxdFI1KGh? NVjqU3NwUW6qaXLpeIlwdiCxZjDBVE0yKGGwZDDwNlEhdHWlaX\ldoF{\SCjY4Tpeol1gSCrbnT1Z4VlKGK7IGOxO|lFKFCUTB?= MYOyN|E3OjZ3Mh?=
THP-1 MU\GeY5kfGmxbjDBd5NigQ>? MnH5PVAhdk1? M{PwOFMxKG2rbh?= MnnITY5pcWKrdHnvckBw\iC2aYPzeYUh\mGldH;yJIV5eHKnc4Ppc44> NHi1WVMzOjl2MEC1PS=>
LoVo M1XpRmZ2dmO2aX;uJGF{e2G7 NWTwTmFrOSEQvF2= M4\ET|EhcA>? MWnJcohq[mm2aX;uJI9nKFCJRUKtbY5lfWOnZDDlfJBz\XO|aX;uJI9nKHWSQTDhcoQhVU2SLUmgd4lodmmoaXPhcpRtgQ>? MnzxNlE5PTl2N{m=
LoVo NVLnN5Z7TnWwY4Tpc44hSXO|YYm= MUmxJO69VQ>? NGWxS3UyKGh? NI\uZ|NDdG:la4PQS2UzNWmwZIXj[YQh[2WubDDtbYdz[XSrb36gd4lodmmoaXPhcpRtgQ>? MmTnNlE5PTl2N{m=
A549 NV7yXGFlTnWwY4Tpc44hSXO|YYm= NHTpV3ozOCEQvF2= NUfHVnBoOSCq MVnJcohq[mm2aX;uJI9nKFSSQT3pcoR2[2WmIF3NVE0zKGGwZDD1MXBCKGW6cILld5Nqd25? NWT3[nZlOjB2OUKxO|U>
HaCaT M3n6ZmZ2dmO2aX;uJGF{e2G7 MWeyNEDPxE1? NXzMfmV5PCCq NFLKOWFFVVOR MVvCcI9kc3NidHjlJHRPTi4QsT3pcoR2[2WmwrDDXXA1TjFzwrD0doFve2O{aYD0bY9v MkHvNVk5OTJ|NEm=
HaCaT M3[wfWZ2dmO2aX;uJGF{e2G7 MVSyNEDPxE1? M{HLTFI1KGh? NVnucFFUTE2VTx?= MXHCcI9kc3NidHjlJJBpd3OyaH;yfYxifGmxbjDv[kBkNUq3bjDwdo91\Wmw M3Hpe|E6QDF{M{S5
PC3 NVGyNFhWTnWwY4Tpc44hSXO|YYm= MWKyNEDPxE1? MV[xJIg> MYXE[YNz\WG|ZYOgeIhmKE2PUEKgZY5lKE2PUEmg[ZhxemW|c3nvci=> MoToNVk3OzN7N{W=
BV-2 NH\u[mxHfW6ldHnvckBCe3OjeR?= NHHqWWozKM7:TR?= M{fJfFEhcA>? M3vBO2lvcGmkaYTzJJRp\SCrbnPy[YF{\SCxZjDzRmFHTiC{ZXzlZZNmKGmwIFftbZgufHKnYYTl[EBDXi1{IHPlcIx{ NF;a[ZIyQTRyNkizNS=>
Hep3B NWHBVIIxTnWwY4Tpc44hSXO|YYm= M1XKVFExKM7:TR?= MW[xJIg> M3rCc2Jtd2OtczDheZRweGijZ4mgZY5lKHWycnXneYxifGmxbjDv[kBD\WOuaX6gNUBmgHC{ZYPzbY9vKGmwZIXj[YQh[nliY3XyZY1q\GV? NH:0OlMyQTB4MEmyNC=>

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
p-JNK; 

PubMed: 25226534     


(A) HepG2 cells were treated with increasing doses of SP600125 for 48 h, followed by western blot analysis of c-Jun N-terminal kinases (JNK) phosphorylation;

p-IGF1R / IGF1R / p-Akt / Akt / p-ERK / ERK; 

PubMed: 25226534     


(B) HepG2 cells were treated with SP600125 for 48 h at the indicated doses, followed by western blot analysis of phosphorylated IGF-1R, Akt, Erk1/2 and total IGF-1R, Akt, Erk1/2; (C) HepG2 cells were treated with 15 µM SP600125 for indicated periods, followed by western blot analysis of phosphorylated IGF-1R, Akt, Erk1/2 and total IGF-1R, Akt, Erk1/2;

p-Src / Src; 

PubMed: 25226534     


HepG2 cells were treated with 15 µM SP600125 for the indicated time. Total protein extracts were harvested and subjected to western blot analysis of phosphorylated Src and total Src.

p-c-Jun / c-Jun / pJNK / JNK; 

PubMed: 27176481     


JNK inhibitor SP600125 suppressed JNK signaling via reducing c-Jun phosphorylation, whereas JNK phosphorylation was not affected

Survivin / Bcl-2 / PARP; 

PubMed: 22870247     


The effect of SP600125 on the apoptosis regulator proteins in SW1116/HCPT cells were measured by Western-blot analysis.

p-FADD / FADD / p-c-Jun / c-Jun ; 

PubMed: 21859840     


A549-FKR cells were treated as described for FKR reporter assay and lysates analyzed with specific antibodies by western blot. Treatment with FADD-kinase inhibitor SP600125 shows dose dependent decrease in phosphorylated FADD protein that correlates with FKR activity.

25226534 27176481 22870247 21859840
Immunofluorescence
AIF / Endo G; 

PubMed: 21738692     


Representative confocal images showing translocation of AIF and Endo G to the nucleus, and nuclear condensation, at the indicated times after treatment with 5 µM of β-lap for 6 h in the presence or absence of SP600125 (30 µM). Nuclear translocation of AIF and Endo G is demonstrated by overlap of AIF or Endo G (green) and nuclear staining (red), resulting in a yellow color. 

E-cadherin / β-catenin ; 

PubMed: 21030692     


Human primary keratinocytes were treated with 10 μM SP600125 for 30 min or transduced with recombinant lentivirus encoding for flag-JNK1DN. Confocal of cells stained for β-catenin (red) and E-cadherin (green). Cell nuclei were stained with Hoechst (blue). 

α-catenin / Actin ; 

PubMed: 21030692     


Confocal images of the cells stained with α-catenin (red) and actin phalloidin (green). Cell nuclei were stained with Hoechst (blue). Scale bars = 20 μm.

21738692 21030692
Growth inhibition assay
Cell viability (U-87 MG); 

PubMed: 27176481     


U-87 MG cells were treated with SP600125 at different concentrations for 48 h. DMSO was used as a carrier control. Cell viability of U-87 MG cells sharply decreased when treated with SP600125.

Cell viability (A549); 

PubMed: 24944614     


Cells were treated with different concentrations of SP600125 (between 0 and 40 nM). The Cell Counting kit (CCK)-8 assay were then performed to measure the A549 cell viability. *P<0.05 vs. control; #P<0.05 vs. ALI.

27176481 24944614
In vivo

In mice, SP600125 (15 mg/kg or 30 mg/kg) significantly inhibits lipopolysaccharide (LPS)-induced TNF-α expression and anti-CD3-induced apoptosis of CD4+ CD8+ thymocytes. [1]

Protocol

Kinase Assay:

[4]
- Collapse

In Vitro Kinase Assays :

The potency of SP600125 towards kinases, including MPS1, JNK, and Aurora kinase A, is determined based on the specific measurement of radioactive phosphotransfer to the substrate. For each enzyme, the absolute Km values for ATP and the specific substrate are initially determined and each assay is then run at optimized [ATP] (2·αKm) and [substrate] (5·Km) concentrations. MPS1 activity is measured using 5 nM of MPS1 recombinant protein in 50 mM HEPES pH 7.5, 2.5 mM MgCl2, 1 mM MnCl2, 1 mM DTT, 3 μM NaVO3, 2 mM β-glycerophosphate, 0.2 mg/mL BSA, 200 μM P38-βtide substrate-peptide (KRQADEEMTGYVATRWYRAE), and 8 μM ATP with 1.5 nM 33P-γ-ATP. Ten serial 1:3 dilutions (from 30 μM to 1.5 nM) of SP600125 are tested and IC50 determined.
Cell Research:

[4]
- Collapse
  • Cell lines: HCT116, A2780, and U2OS cells
  • Concentrations: 0–5 μM
  • Incubation Time: 72 hours
  • Method:

    Cells are seeded in 384 well-plates. One day after seeding, the cells are treated with SP600125 for 72 hours and the plates are then processed using a CellTiter-Glo assay. Inhibitory activity is evaluated comparing treated versus control data and IC50 value of proliferation is calculated.


    (Only for Reference)
Animal Research:

[1]
- Collapse
  • Animal Models: Mouse LPS/TNF model (female CD-1)
  • Dosages: 15 or 30 mg/kg
  • Administration: Administered via intravenous injection or orally
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 44 mg/mL (199.79 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5%DMSO+40%PEG300+5%Tween80+50%ddH2O
For best results, use promptly after mixing. 		2mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 220.23
Formula

C14H8N2O
CAS No. 129-56-6
Storage powder
in solvent
Synonyms Nsc75890
Smiles C1=CC=C2C(=C1)C3=NNC4=CC=CC(=C43)C2=O

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
Dosage mg/kg Average weight of animals g Dosing volume per animal ul Number of animals
Step 2: Enter the in vivo formulation ()
% DMSO % % Tween 80 % ddH2O
CalculateReset

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)

  • Mass
    Concentration
    Volume
    Molecular Weight

*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

  • C1
    V1
    C2
    V2

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

  • * Indicates a Required Field

Frequently Asked Questions

  • Question 1:

    how to reconstitute the inhibitor for in vivo studies?

  • Answer:

    S1460 can be dissolved in 5% DMSO/corn oil at 5 mg/ml as a clear solution for injection. The inhibitor dissolved in vehicle 30% PEG400/0.5% Tween80/5%Propylene glycol, at 30mg/ml is a suspension and can be used for oral administration.

selleck catalog

JNK Signaling Pathway Map

Related JNK Products

  • DTP3 New

    DTP3 is a selective GADD45β/MKK7 (growth arrest and DNA-damage-inducible β/mitogen-activated protein kinase kinase 7) inhibitor and is able to restore MKK7/JNK activation. DTP3 inhibits cancer-selective NF-κB survival pathway.

  • Anisomycin New

    Anisomycin (Flagecidin) is a bacterial antibiotic isolated from Streptomyces griseolus, which inhibits protein synthesis, and also act as a JNK activator. Anisomycin upregulates autophagy and increases apoptosis.

  • Ravoxertinib (GDC-0994) New

    GDC-0994 is a potent, orally available and highly selective ERK1/2 inhibitor with IC50 of 1.1 nM and 0.3 nM, respectively. Phase 1.

  • JNK-IN-8

    JNK-IN-8 is the first irreversible JNK inhibitor for JNK1, JNK2 and JNK3 with IC50 of 4.7 nM, 18.7 nM and 1 nM, >10-fold selectivity against MNK2, Fms and no inhibition to c-Kit, Met, PDGFRβin A375 cell line.

    Features:JNK-IN-8 and JNK-IN-7 are structurally very similar, but whereas the former is a specific covalent inhibitor of JNKs.

  • JNK Inhibitor IX

    JNK inhibitor IX is a selective and potent JNK inhibitor with pIC50 of 6.5 and 6.7 for JNK2 and JNK3, respectively.

  • Trametinib (GSK1120212)

    Trametinib (GSK1120212, JTP-74057, Mekinist) is a highly specific and potent MEK1/2 inhibitor with IC50 of 0.92 nM/1.8 nM in cell-free assays, no inhibition of the kinase activities of c-Raf, B-Raf, ERK1/2. Trametinib activates autophagy and induces apoptosis.

    Features:More potent than PD0325901 or AZD6244.

  • Mirdametinib (PD0325901)

    Mirdametinib (PD0325901) is a selective and non ATP-competitive MEK inhibitor with IC50 of 0.33 nM in cell-free assays, roughly 500-fold more potent than CI-1040 on phosphorylation of ERK1 and ERK2. Phase 2.

  • Vemurafenib (PLX4032)

    Vemurafenib (PLX4032, RG7204) is a novel and potent inhibitor of B-RafV600E with IC50 of 31 nM in cell-free assay. 10-fold selective for B-RafV600E over wild-type B-Raf in enzymatic assays and the cellular selectivity can exceed 100-fold. Vemurafenib (PLX4032, RG7204) induces autophagy.

    Features:A novel and potent inhibitor of the B-RAFV600E oncoprotein.

  • Selumetinib (AZD6244)

    Selumetinib (AZD6244, ARRY-142886) is a potent, highly selective MEK inhibitor with IC50 of 14 nM for MEK1 and Kd value of 530 nM for MEK2. It also inhibits ERK1/2 phosphorylation with IC50 of 10 nM, no inhibition to p38α, MKK6, EGFR, ErbB2, ERK2, B-Raf, etc. Selumetinib suppresses cell proliferation, migration and trigger apoptosis. Phase 3.

    Features:First MEK inhibitor being tested in Phase II clinical trials.

  • SB203580

    SB203580 (RWJ 64809, PB 203580) is a p38 MAPK inhibitor with IC50 of 0.3-0.5 μM in THP-1 cells, 10-fold less sensitive to SAPK3(106T) and SAPK4(106T) and blocks PKB phosphorylation with IC50 of 3-5 μM. SB203580 induces mitophagy and autophagy.

    Features:First reported p38 inhibitor.

Tags: buy SP600125 | SP600125 supplier | purchase SP600125 | SP600125 cost | SP600125 manufacturer | order SP600125 | SP600125 distributor
×
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID