Tanzisertib (CC-930) is a potent JNK1/2/3 inhibitor with IC50s of 61/7/6 nM, respectively.
JNK Inhibitor VIII (TCS JNK 6o) is a c-Jun N-terminal kinases (JNK-1, -2, and -3) inhibitor with ki values of 2 nM, 4 nM, 52 nM, respectively[1].
MPT0B392, an orally active quinoline derivative, induces c-Jun N-terminal kinase (JNK) activation, leading to apoptosis. MPT0B392 triggers induction of the mitotic arrest, followed by mitochondrial membrane potential loss and caspases cleavage by activation of JNK and ultimately leads to apoptosis[1].
JNK3 inhibitor-1 is a potent and selective JNK3 inhibitor (IC50 = 0.005 μM). JNK3 inhibitor-1 is orally bioavailable and brain penetrant.
Tomatidine hydrochloride acts as an anti-inflammatory agent by blocking NF-κB and JNK signaling.
n-Butyl α-D-fructofuranoside, isolated from the root barks of Ulmus davidiana var. japonica, enhances Nrf2 activity through activation of JNK and has antiinflammation activity[1][2].
CC-401 hydrochloride is a potent inhibitor of all three forms of JNK with Ki of 25 to 50 nM.
JNK-IN-7 is a potent JNK inhibitor with IC50 of 1.5, 2 and 0.7 nM for JNK1, JNK2 and JNK3, respectively.
Astin B is a orally active and potent cyclic pentapeptide, that can be isolated from Aster tataricus. Astin B has hepatotoxic effects in vitro and in vivo and that hepatic injury was primarily mediated by apoptosis in a mitochondria/caspase-dependent manner. Astin B induces autophagy in L-02 cells, increases LC3-II and decreases p62 expression[1].
JNK-1-IN-1 is a JNK-1 inhibitor. JNK-1-IN-1 also inhibits MKK7 with an IC50 of 7.8μM. JNK-1-IN-1 bind to MKK7cp and acts as an inhibitor of JNK-1[1].
6,8-Diprenylorobol, a prenylated isoflavone, is a nature product that could be isolated from the leaves of Cudrania tricuspidata. 6,8-Diprenylorobol antiproliferative effect and induces apoptosis through activation of p53 and generation of ROS[1][2].
SR-3306 is a selective, potent, highly brain penetrant JNK inhibitor.