CAY10526

CAY10526 is an inhibitor of Y-box binding protein 1 (YB-1) and microsomal prostaglandin E2 synthase 1 (mPGES1). CAY10526 inhibits the production of PGE₂ by suppressing YB-1 and mPGES1. CAY10526 induces cell apoptosis (apoptosis) and inhibits the JAK/STAT, TGF-β/Smad3 and PI3K/AKT signaling pathways. CAY10526 can be used in research related to melanoma, prostate cancer, esophageal adenocarcinoma, T-cell lymphoma, etc^{[1][2][3][4][5]}. In Vitro:CAY10526 (5 μM; 1 h) potently inhibits NO donor-induced PGE₂ production in human melanoma cell lines A375 and SB2^[1].
CAY10526 (0-20 μM; 72 h) potently reduces the viability of human melanoma cell lines A375, SB2 and WM793 with high mPGES1 expression, with an IC₅₀ < 5 μM; whereas in human melanoma cell lines SK-MEL-28, WM1361A with low mPGES1 expression and BJ fibroblasts, the activity of this compound is significantly attenuated (IC₅₀ >10 μM)^[1].
CAY10526 (5 μM; 48 h) regulates 69 proteins associated with cell death and survival, including reducing the phosphorylation level of YB-1, cyclin B1, and the anti-apoptotic proteins BCL-2/BCL-XL, while upregulating p21, the pro-apoptotic proteins BAX/BAK, and activated caspase-3 in A375 and SB2 human melanoma cells^[1].
CAY10526 (1-50 μM; 12 h) inhibits the proliferation of DU-145 prostate cancer cells in a concentration-dependent manner. A significant reduction in cell viability is observed at concentrations of 10 μM and 20 μM, and the inhibitory effect reaches a plateau when the concentration exceeds 20 μM^[2].
CAY10526 (10-20 μM; 12 h) downregulates mPGES-1 expression in DU-145 prostate cancer cells in a concentration-dependent manner in vitro; at a concentration of 10 μM, it maintains high expression levels of Beclin-1 compared with the complete medium control group, while at 20 μM, it significantly reduces the expression of both mPGES-1 and Beclin-1^[2].
CAY10526 (1-50 μM; 18 h) potently inhibits leptin-induced PGE₂ production in OE33 esophageal adenocarcinoma cells, achieving complete inhibition at concentrations of 10 μM and 50 μM^[4].
CAY10526 (10 μM; 18 h) inhibits leptin-induced mPGES-1 protein expression in OE33 esophageal adenocarcinoma cells without altering COX-2 expression^[4].
CAY10526 (1-50 μM; 24 h) inhibits leptin-induced proliferation in OE33 esophageal adenocarcinoma cells in a concentration-dependent manner, reaching maximum inhibitory activity at 10 μM and 50 μM, which is comparable to the activity of active COX-2 inhibitors at corresponding concentrations^[4].
CAY10526 (1-50 μM; 48 h) reduces the number of viable serum-cultured OE33 esophageal adenocarcinoma cells in a concentration-dependent manner, with maximal activity observed at 10 μM^[4].
CAY10526 (1-50 μM; 25 h) inhibits leptin-induced increase in the number of viable OE33 esophageal adenocarcinoma cells in a concentration-dependent manner, with its maximal activity achieved at 10 μM^[4].
CAY10526 (10 μM; 25 h) inhibits leptin-induced proliferation in OE33 esophageal adenocarcinoma cells by targeting the upstream pathway of PGE₂ production, while exogenous PGE₂ restores this proliferative effect^[4].
CAY10526 (10 μM; 25 h) inhibits IL-1β-induced PGE₂ production and promotes PGI₂ production in HUVECs, without affecting endothelial prostacyclin synthesis^[4].
CAY10526 (25 h) inhibits thrombin-induced PGE₂ production and promotes PGI₂ production in human umbilical vein endothelial cells (HUVECs), without affecting endothelial prostacyclin synthesis^[4].
CAY10526 (10-80 μM; 24-72 h) inhibits the proliferation of human T-cell lymphoma Hut78 cells, with an IC₅₀ of 27.64 μM at 24 h, and suppresses cell viability in a dose-dependent manner after 72 h of incubation^[5].
CAY10526 (10-80 μM; 24 h) reduces the expression of mPGES-1 protein in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and exerts significant inhibitory effects at concentrations of 40 μM and 80 μM after 24 h^[5].
CAY10526 (10-80 μM; 24 h) inhibits PGE₂ synthesis in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and exerts significant inhibitory effects at concentrations of 10, 20, 40 and 80 μM after 24 h^[5].
CAY10526 (20-40 μM; 24 h) induces apoptosis in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and the apoptosis rates at concentrations of 20 μM and 40 μM increase significantly after 24 h^[5].
CAY10526 (20-40 μM; 24 h) upregulates the expression of activated caspase-3 in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and the expression levels at 20 μM and 40 μM increase significantly after 24 h^[5].
CAY10526 (20-40 μM; 24 h) dose-dependently inhibits the JAK/STAT signaling pathway in human T-cell lymphoma Hut78 cells by reducing the expression of JAK1, JAK2 and p-STAT3; after 24 h, the inhibitory effect is significant at concentrations of 20 μM and 40 μM, while the total STAT3 level remains unchanged^[5].
CAY10526 (20-40 μM; 24 h) dose-dependently inhibits the PI3K/AKT signaling pathway in human T-cell lymphoma Hut78 cells by reducing the expression of PI3Kp110, PI3Kp85 and p-AKT; after 24 h of treatment, the inhibitory effect is significant at concentrations of 20 μM and 40 μM, while the total AKT level remains unchanged^[5].
CAY10526 (20-40 μM; 24 h) inhibits the TGF-β/Smad3 signaling pathway in human T-cell lymphoma Hut78 cells in a dose-dependent manner by reducing the expression of TGF-β and p-Smad3; after 24 h of treatment, the inhibitory effect is significant at concentrations of 20 μM and 40 μM, while the total Smad3 level remains unchanged^[5].
CAY10526 (20-40 μM; 24 h) reduces CyclinD1 expression in human T-cell lymphoma Hut78 cells in a dose-dependent manner, and exerts significant inhibitory effects at concentrations of 20 μM and 40 μM after 24 h^[5]. In Vivo:CAY10526 (25-50 mg/kg; i.p.; daily; 15 days) reduces melanoma xenograft tumor volume by 43% and tumor weight by 48%, while decreasing p-YB-1 levels and increasing cleaved caspase 3 levels in tumor tissue^[1].
CAY10526 (2.5 mg/kg; i.p.; daily; 7 days) either during obstruction or starting at obstruction release normalizes PGE₂ levels and improves or restores colon motility and smooth muscle contractility in post-BO rats^[3].