JNK Activator

Dehydrocrenatidine, a β-carboline alkaloid that can be isolated from Picrasma quassioides. Dehydrocrenatidine induces cell apoptosis by activates ERK and JNK. Dehydrocrenatidine inhibits invasion and migration of cancer cells, it also suppresses neuronal excitability to exert analgesic effects.

Chloramphenicol/BSA is the antigen-adjuvant conjugate formed by the coupling of Chloramphenicol (HY-B0239) with Bovine Serum Albumin (BSA). By conjugating the antigen with a protein adjuvant, the production of antigen-specific antibodies in vaccine models can be enhanced. The conjugate does not affect protein folding or disrupt major epitopes, and it can enhance cross-presentation and the generation of antigen-specific T cells.

Actein (Standard) is the analytical standard of Actein. This product is intended for research and analytical applications. 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.

Buforin IIb TFA (BF2-B TFA) is an anticancer peptide, as well as an Antibacterial and Antifungal agent. Buforin IIb TFA is derived from histone H2A. Buforin IIb TFA activates SAPK/JNK and p38 MAPK. Buforin IIb TFA induces mitochondria-dependent Apoptosis. Buforin IIb TFA achieves selective targeting by interacting with gangliosides on the surface of cancer cells, and can penetrate cancer cell membranes without causing damage. Buforin IIb TFA exhibits antibacterial activity against Gram-negative bacteria, Gram-positive bacteria and fungi. Buforin IIb TFA can be used in the research of cervical cancer, as well as cancers including leukemia, central nervous system cancer, ovarian cancer, breast cancer, melanoma, colon cancer, non-small cell lung cancer, renal cancer and prostate cancer.

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.

αMβ2 integrin agonist-1 (Compound 8) is a highly selective αMβ2 integrin agonist with anti-inflammatory activity (EC₅₀=1.4 nM). αMβ2 integrin agonist-1 activates integrin-mediated cell adhesion and JNK/ERK signaling. αMβ2 integrin agonist-1 induces tumor-associated macrophage repolarization and enhances antitumor T-cell immune responses. αMβ2 integrin agonist-1 is promising for research of cancers and chronic inflammatory diseases (e.g., pancreatic cancer, rheumatoid arthritis).

MAPK-IN-3 (Compound 4a) is an anti-proliferative agent that shows particularly strong inhibitory effects on KYSE 30, HCT 116, and HGC 27, with IC₅₀ values of 0.57 μM, 3.27 μM, and 2.28 μM, respectively. MAPK-IN-3 blocks the cell cycle via a p53-dependent mechanism and induces cell apoptosis through a p53-independent mechanism. MAPK-IN-3 downregulates the expression of cell cycle-related proteins like Cyclin D1 and cyclin B1, upregulates pro-apoptotic proteins such as cleaved PARP, cleaved caspase-7, and cleaved caspase-9, and reduces the expression of anti-apoptotic proteins like Bcl-2. Additionally, MAPK-IN-3 increases the intracellular level of ROS in KYSE 30 cells and upregulates the expression of members of the MAPK signaling pathway associated with ROS, such as p-ERK, p-p38 and p-JNK.

PTC-IN-1 is a human ribosomal peptidyl transferase center (PTC) inhibitor. PTC-IN-1 forms stable interactions with 28S rRNA and undergoes steric-hindrance electrostatic interactions with nascent polypeptide chains, thereby inducing context-dependent translation arrest. PTC-IN-1 activates the ribotoxic stress response through phosphorylation of p46 and p54 JNK, triggers ribosome collisions, and activates the integrated stress response via phosphorylation of eIF2α. PTC-IN-1 inhibits the proliferation of cancer cells. PTC-IN-1 can be used in the research of triple-negative breast cancer, prostate cancer, colorectal cancer.

Nur77 antagonist 2 (Compound 12b) is an orally active Nur77 antagonist with a K_D value of 0.42 μM. Nur77 antagonist 2 exhibits proliferative activity on liver cancer cells. Nur77 antagonist 2 stabilizes Nur77 by inhibiting its ubiquitin-proteasomal degradation, leading to Nur77-dependent apoptosis via the ASK1-JNK/p38 pathway. Nur77 antagonist 2 inhibits tumor growth in the HCCLM3 xenograft model. Nur77 antagonist 2 can be used for the study of hepatocellular carcinoma (HCC).

MT-21 is an Apoptosis inducer and adenine nucleotide translocase inhibitor. MT-21 induces Apoptosis by activating JNK via the Krs/MST protein. MT-21 activates caspase-3 via caspase-9. MT-21 induces the release of cytochrome c. MT-21 can be used in the research of tumors.

IDB-003 is an orally active inhibitor of the human ribosomal peptidyl transferase center (PTC). IDB-003 exhibits antiproliferative activity against MYC-dependent cancer cells. IDB-003 binds to PTC, maintains ribosomal RNA interactions, blocks translation via context-dependent nascent polypeptide chain interactions, depletes MYC and CCND1, activates JNK phosphorylation through ribosomal collision, and downregulates the MYC target pathway. IDB-003 inhibits the growth of triple-negative breast cancer xenografts in mice. IDB-003 can be used for the research of triple-negative breast cancer.

Estrogen receptor-IN-2 is a potent estrogen receptor inhibitor formed by the conjugation of Tam (HY-13757)-NHC and gold (I). Estrogen receptor-IN-2 significantly downregulates estrogen receptor (ER) levels, inhibits ER-mediated downstream signaling pathways, and induces immunogenic cell death (ICD) mediated by damage-associated molecular patterns (DAMPs). Estrogen receptor-IN-2 can overcome drug resistance in MCF-7^Y537S mutant cells via the RAMP3/CALCR signaling pathway. It is suitable for research on endocrine-resistant breast cancer.

Buforin IIb (BF2-B) is an anticancer peptide, as well as an Antibacterial and Antifungal agent. Buforin IIb is derived from histone H2A. Buforin IIb activates SAPK/JNK and p38 MAPK. Buforin IIb induces mitochondria-dependent Apoptosis. Buforin IIb achieves selective targeting by interacting with gangliosides on the surface of cancer cells, and can penetrate cancer cell membranes without causing damage. Buforin IIb exhibits antibacterial activity against Gram-negative bacteria, Gram-positive bacteria and fungi. Buforin IIb can be used in the research of cervical cancer, as well as cancers including leukemia, central nervous system cancer, ovarian cancer, breast cancer, melanoma, colon cancer, non-small cell lung cancer, renal cancer and prostate cancer.

d-T101 peptide, a human hormone-peptide, is a T1/ST2 receptor ligand. d-T101 peptide binds to the T1/ST2 receptor and activates caspases 8, 9 and 3 mediated apoptosis, together with activation of JNKinase and p38 MAPKinase. d-T101 peptide also changes Golgi structural with function loss and downregulation of the endoplasmic reticulum (ER) stress repair mechanism. d-T101 peptide has immunostimulatory and anticancer activity, selectively induces apoptosis in proliferating cancer cells and increases IL-2 and IFN-γ expression as well as the recruitment of NK cells and M1 macrophages to the tumor site.

OVA-E1 peptide, 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.

BSO-07 is a ROS/JNK activator with significant anticancer effects, having an IC₅₀ value of 24.81 μM against human breast cancer (BC) cells. BSO-07 induces apoptosis (Apoptosis) and paraptosis by activating JNK and increasing ROS levels, including enhancing the expression of apoptosis-associated proteins such as PARP, Bax, phosphorylated p53, ATF4, and CHOP, while decreasing the levels of anti-apoptotic proteins like Bcl-2, Bcl-xL, and Survivin. BSO-07 holds promise for research in the field of breast cancer.

Polyphyllin I (Standard) is the analytical standard of Polyphyllin I. This product is intended for research and analytical applications. Polyphyllin I is a bioactive constituent extracted from Paris polyphylla, has strong anti-tumor activity. Polyphyllin I is an activator of the JNK signaling pathway and is an inhibitor of PDK1/Akt/mTOR signaling. Polyphyllin I induces autophagy, G2/M phase arrest and apoptosis.

Lonchocarpin (Lonchocarpine) is a Wnt/β-catenin signaling pathway inhibitor. The IC₅₀ of Lonchocarpin in SW480 pBAR/Renilla cells is 4 μM. Acting downstream of β-catenin stabilization, Lonchocarpin inhibits β-catenin nuclear localization and TCF-mediated transcription, as well as the proliferation and migration of colorectal cancer cells. Lonchocarpin enhances Nrf2/ARE-mediated antioxidant responses in primary astrocytes via AMPK and JNK-related signaling, reduces H₂O₂-induced ROS production, and increases the expression of HO-1, NQO1 and MnSOD. Lonchocarpin can be used in research on colorectal cancer and oxidative stress.

Cernuumolide J (TMJ-105) is an JAK2/STAT3 inhibitor. Cernuumolide J induces G2/M phase arrest and apoptosis in HEL leukemia cells by downregulating the phosphorylation of JAK2, STAT3, and Erk, and activating the phosphorylation of JNK and p38 MAPK. Cernuumolide J inhibits HEL leukemia cell growth in a time- and concentration-dependent manner, with an IC₅₀ value of 1.79 μM. Cernuumolide J can be used for research in the field of anti-cancer therapy.

Desipramine is a first-generation tricyclic antidepressant. Desipramine selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine can be used for the research of hepatocellular cancer, inflammation, and neurological diseases.