- Inhibitory Selectivity
|Catalog No.||Product Name||Solubility(25°C)|
|S1460||SP600125||<1 mg/mL||44 mg/mL||<1 mg/mL|
|S4901||JNK-IN-8||<1 mg/mL||100 mg/mL||<1 mg/mL|
|S7544||Vacquinol-1||<1 mg/mL||70 mg/mL||<1 mg/mL|
|S7409||Anisomycin||<1 mg/mL||41 mg/mL||17 mg/mL|
|S7508||JNK Inhibitor IX||<1 mg/mL||20 mg/mL||<1 mg/mL|
|S8490||Tanzisertib(CC-930)||4 mg/mL||89 mg/mL||89 mg/mL|
|S7637||DTP3||100 mg/mL||100 mg/mL||100 mg/mL|
|S8201||BI-78D3||<1 mg/mL||100 mg/mL||<1 mg/mL|
- JNK Inhibitors (8)
|Catalog No.||Information||Product Use Citations||Product Validations|
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.
Loss of DUSP4 function upregulates IL-6 and IL-8 and enhances mammosphere growth. Immunoblot analysis of MDA-231 cells after treatment of 24 hours with 1 umol/L selumetinib (MEKi) or 10 umol/L SP600125 (JNKi). I, MDA-231 mammosphere formation quantitated by GelCount software 7 days after siRNA transfection. Where indicated, selumetinib (MEKi) or SP600125 (JNK1) or the combination was added to the mammosphere cultures.
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.
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.
Vacquinol-1 is an MKK4 activator, which rapidly and selectively induces glioma cell death.
Anisomycin is an antibiotic, which inhibits protein synthesis, and also act as a JNK activator.
(c) Immunostaining of Cx32, ALB, CPS1, CK18 and ECAD in hESC-Heps induced with SB or anisomycin.
JNK inhibitor IX is a selective and potent JNK inhibitor with pIC50 of 6.5 and 6.7 for JNK2 and JNK3, respectively.
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).
CC-930 is kinetically competitive with ATP in the JNK-dependent phosphorylation of the protein substrate c-Jun and potent against all isoforms of JNK (Ki(JNK1) = 44 ± 3 nM, IC50(JNK1) = 61 nM, Ki(JNK2) = 6.2 ± 0.6 nM, IC50(JNK2) = 5 nM, IC50(JNK3) = 5 nM) and selective against MAP kinases ERK1 and p38a with IC50 of 0.48 and 3.4 μM respectively.
DTP3 is a selective GADD45β/MKK7 inhibitor, which inhibits cancer-selective NF-κB survival pathway.
BI-78D3 is a competitive JNK inhibitor with IC50 of 280 nM that displays > 100 fold selectivity over p38α and no activity at mTOR and PI-3K.