A selective, irreversible JNK inhibitor
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JNK Inhibitor XVI

Item No. 18096

Technical Information
Formal Name
3-[[4-(dimethylamino)-1-oxo-2-buten-1-yl]amino]-N-[3-methyl-4-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]-benzamide
CAS Number
1410880-22-6
Synonyms
  • JNK-IN-8
  • c-Jun N-terminal Kinase Inhibitor XVI
Molecular Formula
C29H29N7O2
Formula Weight
Purity
≥95%
A crystalline solid
DMF: 20 mg/mlDMF:PBS (pH 7.2) (1:1): 0.5 mg/mlDMSO: 16 mg/mlEthanol: 2 mg/ml
λmax
277 nm
SMILES
CN(C)C/C=C/C(NC1=CC=CC(C(NC2=CC=C(NC3=NC=CC(C4=CN=CC=C4)=N3)C(C)=C2)=O)=C1)=O
InChi Code
InChI=1S/C29H29N7O2/c1-20-17-24(11-12-25(20)34-29-31-15-13-26(35-29)22-8-5-14-30-19-22)33-28(38)21-7-4-9-23(18-21)32-27(37)10-6-16-36(2)3/h4-15,17-19H,16H2,1-3H3,(H,32,37)(H,33,38)(H,31,34,35)/b10-6+
InChi Key
GJFCSAPFHAXMSF-UXBLZVDNSA-N
Shipping & Storage Information
Storage
-20°C
Shipping
Room temperature in continental US; may vary elsewhere
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    Product Description

    c-Jun N-terminal kinases (JNKs) are MAP kinase family members that become highly activated after cells are exposed to stress conditions and are poorly activated by exposure to growth factors or mitogens. JNK inhibitor XVI is a selective, irreversible JNK inhibitor (IC50s = 4.67, 18.7, and 0.98 nM for JNK1, 2, and 3, respectively) that prevents phosphorylation of c-Jun in A375 and HeLa cells with EC50 values of 338 and 486 nM, respectively.1 It has been shown to inhibit JNK kinase activity by a mechanism that depends on covalent modification of cysteine116 in the ATP-binding motif.1 This compound has been used to explore the role of JNK in mediating cancer cell death.2,3

    WARNING This product is not for human or veterinary use.

    References & Product Citations
    Product Description References

    1. Zhang, T., Inesta-Vaquero, F., Niepel, M., et alDiscovery of potent and selective covalent inhibitors of JNK. Chem. Biol. 19(1), 140-154 (2012).

    2. Li, Q., Song, X.m., Ji, Y.y., et alThe dual mTORC1 and mTORC2 inhibitor AZD8055 inhibits head and neck squamous cell carcinoma cell growth in vivo and in vitro. Biochem. Biophys. Res. Commun. 440(4), 701-706 (2013).

    3. Fallahi-Sichani, M., Moerke, N.J., Niepel, M., et alSystematic analysis of BRAFV600E melanomas reveals a role for JNK/c-Jun pathway in adaptive resistance to drug-induced apoptosis. Mol. Syst. Biol. 11(3), 797 (2015).