JNK Activator

Meptyldinocap (2,4-DNOPC) is a fungicide and cytotoxic agent that acts against powdery mildew. Meptyldinocap upregulates the phosphorylation levels of ERK1/2, JNK and p38. Meptyldinocap induces apoptosis and endoplasmic reticulum stress, disrupts calcium homeostasis, inhibits cell proliferation and migration, downregulates the expression of proliferation- and pregnancy-related genes, and triggers mitochondrial dysfunction. Meptyldinocap can be used in studies related to powdery mildew and implantation failure.

6-Methoxydihydrosanguinarine is an alkaloid with activity across multiple cancer cell types. 6-Methoxydihydrosanguinarine activates IRE1/JNK signaling, blocks Akt/mTOR and PI3K/AKT/mTOR pathways, reduces expression of Cdc25C, CyclinB1, Cdc2, YAP/TAZ, Survivin, GPX4, and EGFR, upregulates IRE1 and DR5, and activates JNK and caspases. 6-Methoxydihydrosanguinarine induces apoptosis, G2/M phase arrest, DNA damage, ROS generation, lipid peroxidation, ferroptosis, autophagy, and suppresses cancer cell growth. 6-Methoxydihydrosanguinarine disruptes the biofilm formation of Candida albicans (C. albicans). 6-Methoxydihydrosanguinarine can be used for the research of non-small cell lung cancer, hepatocellular carcinoma, melanoma, colon carcinoma, ovarian cancer and breast cancer.

β-Zearalenol is a zearalenone metabolite and Estrogen receptor binder (K_d = 0.406 nM) that induces apoptosis through activation of p53, JNK, and p38 kinases and the mitochondrial apoptosis pathway, while inhibiting CYP19A1 and inducing autophagy via SIRT1. β-Zearalenol is used in research on cardiotoxicity, mycotoxin-induced reproductive toxicity, and breast cancer.

α-Linolenic acid (Standard) is the analytical standard of α-Linolenic acid. This product is intended for research and analytical applications. α-Linolenic acid, isolated from Perilla frutescens, is an essential fatty acid that cannot be synthesized by humans. α-Linolenic acid can affect the process of thrombotic through the modulation of PI3K/Akt signaling. α-Linolenic acid possess the anti-arrhythmic properties and is related to cardiovascular disease and cancer.

OVA-E1 peptide TFA, is an antagonist variant of SIINFEKL [OVA (257-264). OVA-E1 peptide, activates the p38 and JNK cascades similarly in mutant and wild-type thymocytes.

Actein, a triterpene glycoside, shows an inhibitory effect on cancer cells, which is isolated from the rhizomes of Cimicifuga foetida. Actein suppresses cell proliferation, induces autophagy and apoptosis through promoting ROS/JNK activation, and blunting AKT pathway in bladder cancer. Actein has little toxicity in vivo.

[D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P, a Substance P derivative, is a biased agonist toward neuropeptide and chemokine receptors. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P activates G12. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P binds to IL-8 and GRP receptors. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P inhibits ERK-2 activation, activates JNK activity. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P stimulates an increase in neutrophil migration and Ca²⁺ mobilization. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P is also a bombesin antagonist, and inhibits the growth of small cell lung cancer

Anisomycin (Standard) is the analytical standard of Anisomycin. This product is intended for research and analytical applications. Anisomycin is a potent protein synthesis inhibitor which interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system[1]. Anisomycin is a JNK activator, which increases phospho-JNK[2][3]. Anisomycin is a bacterial antibiotic[4].

Glyoxal (40% w/w in water) is an α-oxoaldehyde that inhibits Aldose Reductase, Glutathione Reductase, and NADPH synthase. Glyoxal (40% w/w in water) exhibits cytotoxicity, triggers oxidative stress, induces ROS accumulation, lipid peroxidation, mitochondrial membrane potential collapse, DNA damage, apoptosis, and massive production of advanced glycation end products (AGEs). Glyoxal (40% w/w in water) depletes glutathione and activates MAPK phosphorylation. It has lower toxicity as a fixative than paraformaldehyde (PFA) and serves as a precursor for the synthesis of oxalates and dietary carcinogens. Glyoxal (40% w/w in water) is suitable for research related to calcium oxalate kidney stones, diabetes, atherosclerosis, cardiovascular diseases, retinopathy, and cataracts.

p-Cresyl sulfate (potassium) (Standard) is the analytical standard of p-Cresyl sulfate (potassium). This product is intended for research and analytical applications. p-Cresyl sulfate (p-Tolyl sulfate) potassium is a uremic toxin, that can cause renal damage and dysfunction. p-Cresyl sulfate potassium shows antiproliferation activity. p-Cresyl sulfate potassium increases the protein expression of HIF-1α and VHL, decreases the protein expression of HIF-2α. p-Cresyl sulfate potassium induces epithelial-mesenchymal transition (EMT). p-Cresyl sulfate potassium activates the JNK and p38 MAPK signaling pathways.

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.

PROTAC HPK1 Degrader-3 is an orally active, PROTAC degrader that selectively targets HPK1, with a DC₅₀ of 21.26 nM. PROTAC HPK1 Degrader-3 induces HPK1 degradation via the ubiquitin-proteasome system and forms a stable ternary complex with HPK1 and CRBN. It inhibits the SLP76 and NF-κB signaling pathways, enhances MAPK signal transduction, reverses the immunosuppressive factor-mediated inhibition of T cell cytokine secretion, and promotes the secretion of T cell immune cytokines. PROTAC HPK1 Degrader-3 suppresses tumor growth and enhances anti-PD-L1-mediated antitumor activity. It can be used in studies related to malignant tumors, such as colorectal cancer.

Fluazinam (Standard) is the analytical standard of Fluazinam (HY-B1839). This product is intended for research and analytical applications. Fluazinam is a broad spectrum pyridinamine fungal inhibitor. Fluazinam is an orally active dinitroaniline fungicide. Fluazinam induces phosphorylation of JNK, activates p38 pathway, decreases Bcl-2, activates caspase-3, decreases complex I activity, increases Autophagy and Apoptosis. Fluazinam has strong antifungal activity against F. fujikuroi and B. maydis. Fluazinam has a negative impact on Brachydanio rerio and worker bees.

β-Zearalanol-d₄ is the deuterated-labeled β-Zearalenol (HY-N6741). β-Zearalenol is a zearalenone metabolite and Estrogen receptor binder (K_d = 0.406 nM) that induces apoptosis through activation of p53, JNK, and p38 kinases and the mitochondrial apoptosis pathway, while inhibiting CYP19A1 and inducing autophagy via SIRT1. β-Zearalenol is used in research on cardiotoxicity, mycotoxin-induced reproductive toxicity, and breast cancer.

(E)-2-Hexadecenal (trans-2-Hexadecenal) is an MLK3 activator that induces cytoskeletal remodeling, leading to cell rounding, detachment, and ultimately apoptosis in human and mouse cells. (E)-2-Hexadecenal activates the MLK3 signaling pathway, phosphorylating MKK4/7 and JNK, subsequently activating downstream targets of JNK, such as c-Jun phosphorylation, cytochrome c release, Bax activation, Bid cleavage, and Bim translocation to mitochondria. (E)-2-Hexadecenal has potential applications in research related to sphingolipid signaling pathways.

Triphenyl phosphate-d₁₅ is the deuterium labeled Triphenyl phosphate. Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.

Oncrasin-60 (NSC-741909) is a compound with antitumor activity that is active against multiple cancer cell lines in vitro and can induce tumor regression in vivo, with its mechanism involving JNK activation and STAT3 inhibition.

IDB-001 is a human ribosomal peptidyl transferase center (PTC) inhibitor that induces conformational changes and blocks translational elongation in specific sequence contexts through complementary interactions with Asp/Glu residues in nascent polypeptides. IDB-001 preferentially stalls ribosomes at positions containing acidic peptide motifs, thereby inhibiting cancer cell proliferation, and activates the integrated stress response via eIF2α phosphorylation at high concentrations. In addition, IDB-001 mildly triggers ribotoxic stress responses through phosphorylation of JNK and p38. IDB-001 has been applied to mechanistic studies of triple-negative breast cancer.

Procyanidin C2 (Procyanidine C2) is a lipid metabolism regulator and antioxidant with free radical scavenging activity. Procyanidin C2 down-regulates ACC, SREBP-1c, FAS, SCD-1 and PPARγ. Procyanidin C2 increases the level of phosphorylated AMPKα and inhibits the level of phosphorylated mTOR. Procyanidin C2 reduces lipid accumulation, alleviates oxidative stress, enhances fatty acid oxidation and improves mitochondrial function. Procyanidin C2 can be used in the research of non-alcoholic fatty liver disease.

Parbendazole-d₃ (SKF 2904-d₃) is the deuterated-labeled Parbendazole (HY-115364). Parbendazole (SKF‑29044) is an orally active benzimidazole carbamate compound with multiple biological activities. Parbendazole 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 upregulates KAL-1 mRNA expression, reduces nerve growth factor levels, and promotes the terminal differentiation of normal human epidermal keratinocytes. Parbendazole induces apoptosis in differentiated acute myeloid leukemia monocytes and exerts antileukemic activity in a mouse xenograft model of acute myeloid leukemia. Parbendazole exhibits broad-spectrum anthelmintic activity against various animal nematodes. Parbendazole is used in research related to acute myeloid leukemia and parasitic infections.