JNJ-pan-AR

JNJ-pan-AR (compound 4) potently and selectively binds to wild-type androgen receptor with an IC₅₀ of 19 nM and a K_i of 8.4 nM, and has minimal affinity for glucocorticoid receptor^[1].
JNJ-pan-AR acted as a complete antagonist in HepG2, LNCaP, and VCaP cells expressing wild-type and mutant androgen receptors such as F877L, L702H, T878A, W742C, and W875L, with no agonistic activity. Its IC₅₀ values ​​against HepG2 cells, LNCaP F877 cells, LNCaP AR cs cells, and wild-type AR VCaP cells transiently transfected with VP16-AR F877L were 127 nM, 98 nM, 191 nM, and 92 nM, respectively. It also effectively antagonized the transcriptional activity of various androgen receptor ligand-binding domain mutants in HepG2 cells^[1].
JNJ-pan-AR potently blocks nuclear translocation of AR^F877L mutant androgen receptor and inhibits PSA expression in LNCaP F877L cells, regardless of androgen stimulation^[1].
JNJ-pan-AR inhibits androgen-stimulated nuclear translocation of wild-type androgen receptor in LNCaP cells^[1].
JNJ-pan-AR (0.01-10 μM; 24 h) potently inhibits androgen-mediated KLK2 and KLK3 mRNA expression in LNCaP prostate cancer cells^[2].
JNJ-pan-AR (0.062-1 μM; 14 day) inhibits androgen-driven colony formation in LNCaP prostate cancer cells^[2].
JNJ-pan-AR (10 μM; >3 months chronic exposure, continuous maintenance) generates LNCaP JNJR prostate cancer cells with acquired resistance to JNJ-pan-AR, characterized by altered morphology and reduced growth rate^[2].
JNJ-pan-AR (0.1-10 μM; 14 day) shows that exogenous AKR1C3 expression induces partial resistance to JNJ-pan-AR in LNCaP prostate cancer cells^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.