JNK Activator

ML-7 is a selective and highly specific myosin light chain kinase (MLCK) inhibitor that acts as a trabecular meshwork (TM) relaxant. ML-7 enhances Quinocetone (HY-123581)-induced phosphorylation of ERK, p38 MAPK and JNK, attenuates Akt activation, and promotes apoptosis of hepatocellular carcinoma cells. ML-7 reduces Th2 cytokine secretion by inhibiting MLCK, while alleviating smooth muscle hyperplasia and collagen deposition. As a non-antibiotic adjuvant, ML-7 restores the sensitivity of drug-resistant bacteria to Tigecycline (HY-B0117). ML-7 can be used in research related to glaucoma, hepatocellular carcinoma, asthma, and Klebsiella pneumoniae infection.

Parbendazole hydrochloride (SKF‑29044 hydrochloride) is an orally active benzimidazole carbamate compound with multiple biological activities. Parbendazole hydrochloride binds to free tubulin and inhibits microtubule polymerization; it also activates the JNK/c‑Jun signaling axis and upregulates the expression of the downstream axonal repulsion factor Sema3A. Parbendazole hydrochloride upregulates KAL-1 mRNA expression, reduces nerve growth factor levels, and promotes the terminal differentiation of normal human epidermal keratinocytes. Parbendazole hydrochloride induces apoptosis in differentiated acute myeloid leukemia monocytes and exerts antileukemic activity in a mouse xenograft model of acute myeloid leukemia. Parbendazole hydrochloride exhibits broad-spectrum anthelmintic activity against various animal nematodes. Parbendazole hydrochloride is used in research related to acute myeloid leukemia and parasitic infections.

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.

Guggulsterone (Standard) is the analytical standard of Guggulsterone (HY-107738). This product is intended for research and analytical applications. Guggulsterone is a plant sterol derived from the gum resin of the tree Commiphora wightii. Guggulsterone inhibits the growth of a wide variety of tumor cells and induces apoptosis through down regulation of antiapoptotic gene products (IAP1, xIAP, Bfl-1/A1, Bcl-2, cFLIP and survivin), modulation of cell cycle proteins (cyclin D1 and c-Myc), activation of caspases and JNK, inhibition of Akt. Guggulsterone, a farnesoid X receptor (FXR) antagonist, with IC₅₀s of 24.06 μM and 39.05 μM for (-)-(E)-Guggulsterone (HY-N7781) and (Z)-Guggulsterone (HY-110066), respectively.

CGC-11144 hydrochloride is a polyamine analog. CGC-11144 hydrochloride reduces the kinase activities of CDK4, CDK2 and CDK6, induces activation of the p53 pathway and p53-dependent p21 expression, and mediates cell cycle regulation, growth inhibition and apoptosis. CGC-11144 hydrochloride induces G1 phase cell cycle arrest, downregulates cyclin D1 and cyclin B1, upregulates cyclin E, induces dephosphorylation of pRb, and inhibits ERα-mediated transcriptional activity by disrupting the DNA binding of Sp1/Sp3 to the ERα promoter, while also stimulating activation of the JNK/AP-1 pathway. CGC-11144 hydrochloride can be used in research related to breast cancer, choroidal neovascularization and cancer.

MPT0B392 (Standard) is the analytical standard of MPT0B392 (HY-101287). This product is intended for research and analytical applications. MPT0B392, an orally active quinoline derivative, induces c-Jun N-terminal kinase (JNK) activation, leading to apoptosis. MPT0B392 inhibits tubulin polymerization and triggers induction of the mitotic arrest, followed by mitochondrial membrane potential loss and caspases cleavage by activation of JNK and ultimately leads to apoptosis. MPT0B392 is demonstrated to be a novel microtubule-depolymerizing agent and enhances the cytotoxicity of sirolimus in sirolimus-resistant acute leukemic cells and the multidrug resistant cell line.

Pratol (7-Hydroxy-4'-methoxyflavone) is an NF-κB inhibitor. Pratol also inhibits NO, PGE₂, TNF-α, IL-1β, and IL-6 production. Pratol increases the phosphorylation of p38 MAPK, JNK, and ERK, decreases AKT phosphorylation, and upregulates MITF, tyrosinase, TRP-1, and TRP-2 through a PKA-dependent signaling pathway. Pratol reduces iNOS and COX-2 protein expression, inhibits p65 phosphorylation, and protects IκBα from degradation, thereby inhibiting NF-κB nuclear translocation. Pratol can be used in research on hypopigmentary disorders, inflammatory diseases, cervical cancer, and colon cancer.

Ro 31-8220 mesylate (Standard) is the analytical standard of Ro 31-8220 mesylate (HY-13866). This product is intended for research and analytical applications. Ro 31-8220 mesylate is a potent PKC inhibitor, with IC₅₀s of 5, 24, 14, 27, 24 and 23 nM for PKCα, PKCβI, PKCβII, PKCγ, PKCε and rat brain PKC, respectively. Ro 31-8220 also significantly inhibits MAPKAP-K1b, MSK1, S6K1 and GSK3β (IC₅₀s, 3, 8, 15, and 38 nM, respectively), with no effect on MKK3, MKK4, MKK6 and MKK7. Ro 31-8220 mesylate can also inhibit the expression of MKP-1, induce the expression of c-Jun, and activate JNK, and these effects possess pharmacological properties independent of PKC.

Polyporenic acid C (Standard) is an analytical standard of Polyporenic acid C (HY-N2993). This product is intended for research and analytical applications. Polyporenic acid C is a lanostane-type triterpenoid. Polyporenic acid C can be isolated from Poria cocos. Polyporenic acid C causes the cleavage of caspase-8 and caspase-3, as well as the cleavage of PARP. Polyporenic acid C reduces the phosphorylation level of Akt (Ser473), increases the phosphorylation of PTEN and p53 (Ser15), and activates JNK. Polyporenic acid C induces Apoptosis. Polyporenic acid C shows anticancer activity against non-small cell lung cancer.

Bromuconazole is a triazole fungicide with oral efficacy and blood-brain barrier permeability. Bromuconazole protects crops from various fungal contaminations. Bromuconazole exhibits cytotoxicity against a variety of cancer cells, induces G0/G1 cell cycle arrest and inhibits DNA synthesis in cancer cells, and triggers cytoskeletal structural disorder, genotoxic damage, apoptotic (apoptosis) cell death, and mitochondrial membrane depolarization. Bromuconazole activates caspase-3, induces excessive production of ROS, p53 and Bax, lipid peroxidation, increased activities of SOD and CAT, and downregulates Bcl-2. By upregulating p-ERK1/2 and p-JNK, Bromuconazole disrupts the MAPK signaling pathway, impairs the cellular stress response of human trophoblast cells and endometrial cells, and damages the implantation process. Bromuconazole is applicable to research related to glioma, colon cancer, reproductive injury (implantation dysfunction), and cardiac dysfunction.

TASIN-1 hydrochloride is a selective inhibitor of truncated APC^TR (adenomatous polyposis coli gene) that exerts cytotoxic effects by inhibiting cholesterol biosynthesis. TASIN-1 hydrochloride specifically targets colorectal cancer (CRC) cells carrying APC truncated mutations, while having no significant toxicity to wild-type APC cells. TASIN-1 hydrochloride exerts cytotoxic effects by targeting Emopamil binding protein (EBP) to inhibit cholesterol biosynthesis, triggering endoplasmic reticulum (ER) stress, reactive oxygen species (ROS) generation, and JNK-mediated apoptosis, and inhibiting Akt survival signaling. TASIN-1 hydrochloride can be used to prevent and intervene in APC mutant colorectal cancer.

p-Cresol sulfate-d₄ (potassium) is deuterium labeled p-Cresyl sulfate (potassium). p-Cresyl sulfate potassium is a uremic toxin that binds to a prototype protein. p-Cresyl sulfate potassium activates the JNK and p38 MAPK signaling pathways. p-Cresyl sulfate potassium has pro-inflammatory activity.

Cantharidic acid is a selective inhibitor for protein phosphatase 2 (PP2A) and protein phosphatase 1 (PP1). Cantharidic acid inhibits cell viability and arrest cell cycle at sub G1 phase, induces apoptosis in cells NPC-39 and HONE-1 through the upregulation of ERK1/2, p38, and JNK1/2 pathway.

GO-Y078 is a curcumin (HY-N0005) analog. GO-Y078 activates p38/JNK1/2. GO-Y078 activates the MAPK pathway, Caspase 3/8/9, PARP, AP-1, DR5, and TP53, while inhibiting cIAP-1, XIAP, and NF-κB. GO-Y078 induces sub-G₁/G₂/M phase arrest and Apoptosis. GO-Y078 impairs angiogenesis. GO-Y078 can be used in research related to osteosarcoma, cervical cancer, oral squamous cell carcinoma, and peritoneal metastasis of gastric cancer.

3-AP-Me is a dimethyl derivative of the nucleotide reductase inhibitor 3-AP (SML0568). 3-AP-Me can activate the endoplasmic reticulum (ER) stress pathway by promoting the phosphorylation of eIF2α and increasing the gene expression of transcription factors ATF4 and ATF6, leading to cell apoptosis. Additionally, 3-AP-Me can activate the stress kinases c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases. 3-AP-Me also leads to the upregulation of the spliced mRNA variant XBP1, can be used in cancer research.

Myrothecine A is a trichothecene mycotoxin found in M. roridum. Myrothecine A induces apoptosis, promotes the cytochrome c release, PARP-cleavage and phosphorylation of JNK, increases Bax and cleaved caspase-3, -5, and -8 levels. Myrothecine A has anticancer activities and promotes the maturation of DC cells in the microenvironment. Myrothecine A inhibits proliferation of A549, MCF-7, HepG2, and SMMC-7721 cancer cells with IC₅₀s of 95, 70, 60, and 25 µM, respectively.

CeY-B1 is a ceramide analog. CeY-B1 inhibits the proliferation, migration and invasion of cervical cancer cells, induces apoptosis and cell cycle arrest. CeY-B1 upregulates ASK1, promotes the phosphorylation of JNK, downregulates Bcl‑2, and inhibits the PI3K/AKT pathway. CeY-B1 suppresses tumor growth in cervical cancer xenograft mouse models. CeY-B1 can be used for relevant research on cervical cancer.

RKS262 is an orally active cyclin/CDK inhibitor. RKS262 is also an apoptosis inducer and cell cycle regulator, exhibiting cytotoxic activity against cancer cells. RKS262 induces caspase-3 cleavage, ROS generation, SAPK/JNK activation, and upregulates the expression of p53, Bid, Bad, Bok, and p27. RKS262 inhibits the expression of Bcl-2, Mcl-1, Bcl-xL, p21, cyclin D1, cyclin B1, cdc-2, cyclin D4, and DNA-pk KU-80 subunit. RKS262 suppresses the phosphorylation of the IGF-1R/PI3K/PKC pathway, ras oncogene activity, and Cdk-6, while increasing total Akt expression. RKS262 induces G₂/M or S phase cell cycle arrest, disrupts mitochondrial transmembrane potential, and reduces tumor burden in xenograft models. RKS262 is used in research on neuroblastoma and ovarian cancer.

Vanillylamine is an immediate precursor for capsaicinoids. Vanillylamine is a derivative of Vanillin (HY-N0098) is synthesized through a transaminase reaction in the phenylpropanoid pathway of capsaicinoid synthesis. Vanillylamine significantly alleviates myelosuppression caused by abdominal and pelvic tumor chemotherapy.

Phaeosphaeride A is a STAT3 inhibitor with an IC₅₀ of 0.61 mM against human STAT3. It exhibits higher selectivity for STAT3 over STAT1 and STAT5. Phaeosphaeride A inhibits the binding of STAT3 to DNA, STAT3-dependent transcriptional activity, as well as IL-6-induced phosphorylation and signaling of STAT3. Phaeosphaeride A activates the JNK, p38, Akt, CREB and STAT5A/B signaling pathways. Phaeosphaeride A induces oxidative stress (ROS), exerts antiproliferative and growth-inhibitory effects in cancer cells, and shows low cytotoxicity toward non-cancerous cells. Phaeosphaeride A is a phytotoxin and a weak animal toxin, with no antimicrobial activity against tested bacteria and fungi. Phaeosphaeride A can be used in research related to conditions such as cervical cancer and multiple myeloma, as well as weed infestations.