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.

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Cited by 11 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.

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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.
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 Mn\zSpVv[3Srb36gZZN{[Xl? M4r1VFEhcA>? M{C2cmlvcGmkaYTpc44hd2ZiSl7LN{1u\WSrYYTl[EBkNWq3bjDwbI9{eGixconsZZRqd25iaX6gbJVu[W5iQUO3OUBk\WyuczDh[pRmeiBzIHjyJIlv[3WkYYTpc44tKEmFNUC9NE4{OzhizszN M3W4[|I2PDF3NUO1
human HeLa cells NWjVeo5KTnWwY4Tpc44h[XO|YYm= MmT0NUBp M2rFWWlvcGmkaYTpc44hd2ZiSl7LN{1u\WSrYYTl[EBkNWq3bjDwbI9{eGixconsZZRqd25iaX6gbJVu[W5iSHXMZUBk\WyuczDh[pRmeiBzIHjyJIlv[3WkYYTpc44tKEmFNUC9NE41QDZizszN NIrsTGkzPTRzNUWzOS=>

... Click to View More Cell Line Experimental Data


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.

* 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


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

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JNK Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID