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JNKs (c-Jun N-terminal kinases) belong to the mitogen-activated protein kinase family, and are responsive to stress stimuli, such as cytokines,ultraviolet irradiation, heat shock, and osmotic shock. JNKs play a role in T cell differentiation and the cellular apoptosis pathway. Activation occurs through a dual phosphorylation of threonine (Thr) and tyrosine (Tyr) residues within a Thr-Pro-Tyr motif located in kinase subdomain VIII. Activation is carried out by two MAP kinases, MKK4 and MKK7 and JNK can be inactivated by Ser/Thr and Tyr protein phosphatases. Downstream molecules that are activated by JNK include c-Jun, ATF2, ELK1, SMAD4, p53 and HSF1. JNKs can associate with scaffold proteins JNK interacting proteins as well as their upstream kinases JNKK1 and JNKK2 following their activation. JNK activity regulates several important cellular functions including cell growth, differentiation, survival and apoptosis.

Cat. No. Product Name CAS No. Information

CC-401 hydrochloride


CC-401 hydrochloride is a potent, selective, ATP-competitive pan-JNK inhibitor with Ki of 25-50 nM, displays >40-fold selectivity over other related kinases, including p38, ERK, IKK2, PK C, Lck, and ZAP70; decreases hepatic necrosis and apoptosis after orthotopic liver transplantation in vivo; blocks JNK signaling in the rat obstructed kidney and significantly inhibits renal fibrosis in terms of interstitial myofibroblast accumulation and collagen IV deposition, also significantly reduces tubular apoptosis in the obstructed kidney; sensitizes hypoxic colon cancer cells to DNA-damaging agents, potentiates the effect of bevacizumab and oxaliplatin in HT29-derived mouse xenografts.




A small molecule JIP1 mimic that functions as substrate competitive inhibitor of JNK with IC50 of 500 nM; targets the JNK-JIP interaction site and dose-dependently inhibits the phosphorylation of JNK substrates both in vitro and in cell; blocks JNK dependent Con A-induced liver damage, restores insulin sensitivity in mouse models of type 2 diabetes.




CC-401 (JNK-401) is a potent, selective, ATP-competitive pan-JNK inhibitor with Ki of 25-50 nM, displays >40-fold selectivity over other related kinases; blocks JNK signaling and renal fibrosis in a rat obstructed kidney model, decrease hepatic necrosis and apoptosis after orthotopic liver transplantation and prevent acute renal failure following ischemia/reperfusion associated with renal transplantation in rats.




AS601245 is a potent and selective inhibitor of JNK with IC50s of 70/220/150 nM for JNK1/2/3 respectively; less potent for c-Src, c-Raf, p38a; exhibits in vitro and in vivo anti-inflammatory potential.




JNK-IN-8 is a potent, selective, pan-JNK inhibitor with IC50 of 4.7 nM, 18.7 nM and 1 nM for JNK1, JNK2 and JNK3, respectively; exhibits exceptional selectivity based upon KinomeScan and enzymatic profiling; inhibits c-Jun phosphorylation in HeLa and A375 cells with EC50 of 486 nM and 338 nM, respectively.




SP600125 is a potent, selective, reversible, ATP-competitive inhibitor of JNK with IC50 of 40, 40 and 90 nM for JNK1, JNK2 and JNK3, respectively; displays 300-fold selectivity against related MAP kinases ERK1 and p38, and PKA; dose dependently inhibits the phosphorylation of c-Jun, the expression of inflammatory genes COX-2, IL-2, IFN-γ, TNF-α, and prevents the activation and differentiation of primary human CD4 cell cultures; blocks LPS-induced expression of TNF-α and inhibits anti-CD3-induced apoptosis of CD4+ CD8+ thymocytes in vivo model of endotoxin-induced inflammation.




SR-3306(SR3306) is a highly selective, brain penetrant, potent inhibitor of JNK with IC50 of 67, 283 and 159 nM for JNK1, JNK2 and JNK3, >100-fold selectivity over p38; shows cell-based IC50 of 216 nM, protects dopaminergic neurons against MPTP neurotoxicity in vitro and in vivo, achieves dopaminergic neuronal survival in the 6-OHDA model; also prevents ROS increases and mitochondrial dysfunction




Brimapitide (D-JNKI-1;AM-111;XG-102) is a cell-permeable peptide inhibitor of JNK kinase; blocks apoptotic JNK signaling in brain mitochondria; decreases the expression of CD4(+) and CD8(+) cells, effects T-cell activation, differentiation, and migration in a murine model of chronic colitis; prevents hearing loss from SC transection in the guinea pig model of PA-OM.




IQ-1S (IQ 1S free acid) is a potent, highly specific JNK inhibitor with IC50 of 390, 360, and 87 nM for JNK1, JNK2, and JNK3, respectively; does not inhibits other kinases that represent potential targets for RA treatment, including GSK-3beta, JAK2, JAK3, PI3Ks, Btk, IKK-2, etc.; inhibits pro-inflammatory cytokine (IL-1α, IL-1β, IL-6, IL-10, TNF-α, IFN-γ, and GM-CSF and nitric oxide production by human and murine monocyte/macrophages; inhibits LPS-induced TNF-α and IL-6 production in MonoMac-6 cells with IC50 of 0.25 and 0.61 uM, respectively; reduces inflammation and cartilage loss associated with CIA in mice model.

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