Dimethyl Sulfoxide
Apexbio Technology LLC ASC-J9(Synonyms: Dimethylcurcumin, GO-Y025, AR degrader enhancer ASC-J9), 10mM (in 1mL DMSO), CAS: 52328-98-0.
ASC-J9 (CAS 52328-98-0) is a small-molecule degrader targeting androgen receptor (AR) By promoting degradation of full-length AR and splice variants such as AR3/fAR ASC-J9 inhibits androgen receptor signaling pathways involved in castration-resistant prostate cancer (CRPC) progression and metastatic behavior ASC-J9 interferes with AR-dependent transcriptional modulation and AR-independent signaling pathways notably inhibiting STAT3 phosphorylation and CCL2 chemokine secretion thus reducing macrophage infiltration and prostate cancer invasiveness Research indicates ASC-J9 may represent an alternative therapeutic strategy for CRPC treatment and metastasis prevention
Apexbio Technology LLC AM095 1345614-59-6 10mM (in 1mL DMSO)
AM095 (CAS 1345614-59-6) is an orally bioavailable antagonist targeting the lysophosphatidic acid receptor 1 (LPA1) It selectively inhibits recombinant human and mouse LPA1 receptors with IC50 values of 0 98 M and 0 73 M respectively In cell-based assays AM095 suppresses LPA1-mediated chemotaxis in mouse LPA1/CHO and human melanoma A2058 cells (IC50 values 0 78 M and 0 23 M respectively) In vivo studies demonstrate its ability to prevent LPA-triggered histamine release reduce collagen and protein accumulation and limit inflammatory cell infiltration in mouse pulmonary models AM095 serves as a valuable tool for investigating LPA1-associated pathologies
Apexbio Technology LLC JNK-IN-8 1410880-22-6 10mM (in 1mL DMSO)
JNK-IN-8 (CAS 1410880-22-6) is a potent and specific inhibitor of c-Jun N-terminal kinase (JNK) isoforms JNK1 JNK2 and JNK3 It functions by forming a covalent bond with a conserved cysteine residue in JNKs inducing conformational alteration in the kinase activation loop consequently impairing substrate binding Its IC50 values for JNK1 JNK2 and JNK3 are 4 67 nM 18 7 nM and 0 98 nM respectively In cellular assays JNK-IN-8 prevention of c-Jun phosphorylation demonstrates robust selectivity towards the JNK signaling pathway thus making it valuable as a research tool in studying stress-related cellular responses and apoptosis