JNK-IN-8

Catalog No.S4901

JNK-IN-8 Chemical Structure

Molecular Weight(MW): 507.59

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.

Size Price Stock Quantity  
USD 170 In stock
Bulk Discount
Bulk Inquiry

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

Cited by 16 Publications

4 Customer Reviews

  • SCC-9 cells were pre-treated with JNK inhibitor SP 600125 (1 umol/L) or JNK-IN-8 (1 umol/L) for 1 h, cells were also stimulated with indicated AZD8055 and cultured for 72 h, cell survival was analyzed. Scramble RNAi or JNK1/2 RNAi (JNK RNAi-1 or JNK RNAi-2, see methods) transfected HEK-293 cells were stimulated with AZD8055, cells were further cultured for 72 h before cell survival was tested.

    Biochem Biophys Res Commun 2013 440(4), 701-6. JNK-IN-8 purchased from Selleck.

  • The viability of DLBCL cell lines was assessed after 72 h of treatment with the indicated concentrations of the JNK inhibitor JNK-IN-8. Mean + SEM of at least three independent experiments is shown.

    J Exp Med, 2015, 212(5): 775-92. JNK-IN-8 purchased from Selleck.

  • Striatal slices from 6-OHDA-lesion mice were incubated for 5 min with vehicle, SKF38393 (3 μM), or SKF38393 in the presence of SP600125 (20 μM) or JNK-IN-8 (10 μM). P-cJun and P-ERK 1/2 were determined by Western blotting (25 and 10 μg of protein were loaded, respectively). Note the reduction of SKF38393-induced P-cJun produced by the two JNK inhibitors (top panels). In contrast, SP600125 and JNK-IN-8 did not affect the increase in P-ERK 1/2 produced by SKF38393 (bottom panels). Summary of data were calculated as percentage of control and are represented as mean ± S.E.M. 1 W ANOVA indicated significant effect of the treatment for both P-cJun (F3,16 = 15.22, p < 0.0001, n = 5 slices from 5 mice) and P-ERK 1/2 (F3,16 =18.23, p < 0.0001, n= 5 slices from mice).

    Neurobiol Dis, 2018, 110:37-46. JNK-IN-8 purchased from Selleck.

  • ICT induces JNK activation, mediating mPTP opening and CRC cell necrosis. JNK expression (p- and regular) in HT-29 or the primary CRC cells stimulated with applied ICT was tested by Western blots (a). HT-29 cells were pre-treated with JNK inhibitors SP600125 (SP), JNK inhibitor IX (JNK-IX), and JNK-IN-8 (JNKi-8) (5 μM each) for 1 h, followed by ICT (25 μM) stimulation, MMP decrease was tested by JC-10 dye assay (b, after 12 h), and cell necrosis was tested by LDH release assay (c, after 72 h).

    Tumour Biol, 2016, 37(3):3135-44. JNK-IN-8 purchased from Selleck.

Purity & Quality Control

Choose Selective JNK Inhibitors

Biological Activity

Description 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.
Targets
JNK3 [1]
(A375 cells)		 JNK1 [1]
(A375 cells)		 JNK2 [1]
(A375 cells)		 Kit (V559D,T670I) [1]
(A375 cells)		 Kit (V559D) [1]
(A375 cells)
1 nM 4.7 nM 18.7 nM 56 nM 92 nM
In vitro

JNK-IN-8 inhibits c-Jun phosphorylation in HeLa and A375 cells with EC50 of 486 nM and 338 nM, respectively. JNK-IN-8 shows a dramatic improvement in selectivity and eliminated binding to IRAK1, PIK3C3, PIP4K2C, and PIP5K3. JNK-IN-8 requires Cys116 for JNK2 inhibition. [1] JNK-IN-8 (10 mM) suppresses the IL-1β-stimulated phosphorylation of c-Jun in IL-1R cells, an established substrate of the JNKs. JNK-IN-8 covalently attaches to the JNK isoforms caused a small retardation in the electrophoretic mobility of the JNK isoforms. [2] JNK-IN-8 is discovered to inhibit JNK kinase by broad-based kinase selectivity profiling of a library of acrylamide kinase inhibitors based on the structure of imatinib using the KinomeScan approach. JNK-IN-8 possesses distinct regiochemistry of the 1,4-dianiline and 1,3-aminobenzoic acid substructures relative to imatinib and uses an N,N-dimethyl butenoic acetamide warhead to covalently target Cys154. JNK-IN-8 adopts an L-shaped type I binding conformation to access Cys 154 located toward the lip of the ATP-binding site. [3]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human A375 cells M3TjW2Z2dmO2aX;uJIF{e2G7 NUDoRotWOSCq NVfVWlhIUW6qaXLpeIlwdiCxZjDKUms{NW2nZHnheIVlKGNvaoXuJJBpd3OyaH;yfYxifGmxbjDpckBpfW2jbjDBN|c2KGOnbHzzJIFnfGW{IEGgbJIhcW6ldXLheIlwdixiSVO1NF0xNjN|ODFOwG0> NHLYSJYzPTRzNUWzOS=>
human HeLa cells M1S5V2Z2dmO2aX;uJIF{e2G7 Mnv3NUBp MWDJcohq[mm2aX;uJI9nKEqQS{OtcYVlcWG2ZXSgZ{1rfW5icHjvd5Bpd3K7bHH0bY9vKGmwIHj1cYFvKEinTHGgZ4VtdHNiYX\0[ZIhOSCqcjDpcoN2[mG2aX;uMEBKSzVyPUCuOFg3KM7:TR?= MkfyNlU1OTV3M{W=

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
c-Jun / p-c-Jun / ATF2 / p-ATF2 / Elk-1 / pElk-1; 

PubMed: 27941886     


JNK-IN-8 treatment inhibited c-Jun phosphorylation at Ser63 and Ser73 by JNK in TNBC cells as analyzed by Western blotting.

Notch1 / c-Myc / Cyclin D1 / p21; 

PubMed: 27941886     


JNK-IN-8 treatment reduced expression of Notch1 and c-Jun phosphorylation at Ser63 and Ser73 as analyzed by Western blotting. JNK-IN-8 treatment also reduced expression of c-MYC, cyclin D1, and p21. Cells were treated with JNK-IN-8 for 48 h and then subjected to Western blotting. α-Tubulin was used as a loading control.

27941886
Growth inhibition assay
Cell viability; 

PubMed: 25847947     


The viability of DLBCL cell lines was assessed after 72 h of treatment with the indicated concentrations of JNK-IN-8. Mean + SEM of at least three independent experiments is shown.

25847947

Protocol

Solubility (25°C)

In vitro DMSO 100 mg/mL warmed (197.0 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+5% Tween 80+ddH2O
For best results, use promptly after mixing. 		10mg/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 507.59
Formula

C29H29N7O2
CAS No. 1410880-22-6
Storage powder
in solvent
Synonyms N/A

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
selleck catalog

JNK Signaling Pathway Map

Related JNK Products

  • DTP3 New

    DTP3 is a selective GADD45β/MKK7 inhibitor, which inhibits cancer-selective NF-κB survival pathway.

  • Anisomycin New

    Anisomycin is an antibiotic, which inhibits protein synthesis, and also act as a JNK activator.

  • 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.

  • SP600125

    SP600125 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.

  • 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) 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.

    Features:More potent than PD0325901 or AZD6244.

  • PD0325901

    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, RG7204)

    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.

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

  • Selumetinib (AZD6244)

    Selumetinib (AZD6244) 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. Phase 3.

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

  • SB203580

    SB203580 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.

    Features:First reported p38 inhibitor.

Tags: buy JNK-IN-8 | JNK-IN-8 supplier | purchase JNK-IN-8 | JNK-IN-8 cost | JNK-IN-8 manufacturer | order JNK-IN-8 | JNK-IN-8 distributor
×
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID