|1.||Yang, Jinyan: 1 article (08/2014)|
|2.||Pan, Xiaoxia: 1 article (08/2014)|
|3.||Pan, Shitian: 1 article (08/2014)|
|4.||Zhang, Changhong: 1 article (08/2014)|
|5.||Xu, Xiangting: 1 article (08/2014)|
|6.||Leung, George Pakheng: 1 article (08/2014)|
|7.||Yang, Cui: 1 article (08/2014)|
|8.||Yan, Sanmei: 1 article (08/2014)|
|9.||Paul, Arun George: 1 article (06/2013)|
|10.||Chandran, Bala: 1 article (06/2013)|
08/01/2012 - "The pharmacological inhibition study revealed that exposure of HUVEC to NS398 and AH6809 under hypoxia impaired the biological responses of ECs to hypoxia. "
01/01/2013 - "However, AH6809 (3 µM), an antagonist of EP1, EP2, EP3 and DP1 receptors, exerted no effect on KPSS or hypoxia induced vessel contraction. "
08/01/2012 - "Then we treated HUVECs with COX-2 selective inhibitor NS398, EP1/2 combined antagonist AH6809 and exogenous PGE(2) to investigate the role of COX-2/PGE(2) signalling in the angiogenic response of ECs to hypoxia. "
12/15/2009 - "Interestingly, treatment with EP2 antagonist AH-6809 resulted in suppression of hypoxia induced EP2, IL-1beta and iNOS mRNA and protein expression, TNF-alpha protein expression and intracellular cAMP level in BV-2 cells. "
|3.||Non-Hodgkin Lymphoma (Lymphosarcoma)
06/01/2013 - "Our study demonstrated that (1) EP1-4 receptor protein levels vary among the various non-Hodgkin's lymphoma (NHL) cell lines tested (BCBL-1:KSHV+/EBV-;BC-3: KSHV+/EBV-; Akata/EBV+: KSHV-/EBV+; and JSC-1 cells: KSHV+/EBV + cells); (2) 5.0 μM of EP1 antagonist (SC-51322) had a significant antiproliferative effect on BCBL-1, BC-3, Akata/EBV+, and JSC-1 cells; (3) 50.0 μM of EP2 antagonist (AH6809) was required to induce a significant antiproliferative effect on BCBL-1, Akata/EBV+, and JSC-1 cells; (4) 5.0 μM of EP4 antagonist (GW 627368X) had a significant antiproliferative effect on BC-3, Akata/EBV+, and JSC-1 cells; (5) COX-2 selective inhibitor celecoxib (5.0 μM) had significant antiproliferative effects on BCBL-1, BC-3, Akata/EBV+, and JSC-1 cells; and (6) a combination of 1.0 μM each of celecoxib, SC-51322 and GW 627368X could potentiate the proapoptotic properties of celecoxib or vice-versa. "
10/01/2010 - "Using a murine model of metastatic breast cancer, we now show that pharmacologic antagonism of EP1 with SC19220 or AH6809 promoted lung colonization of mammary tumor cells by 3.7- to 5.4-fold. "
01/21/2011 - "Blocking PGE(2) synthesis by NS398 or through the use of PGE(2) receptor antagonists AH-6809 (EP2 antagonist) and AH-23848 (EP4 antagonist) completely reversed the inhibitory effect of tumor-conditioned medium (TCM) on LPS-induced CCL5 expression. "
01/01/2005 - "Examples of the "hit" compounds involved in cancer therapy, namely DMXAA, psorospermin, mangiferin, norathyriol, mangostins, and AH6809, a prostanoid receptor antagonist, are also mentioned. "
05/01/1995 - "On the other hand, AH6809 blocked the PGE2-induced hyperalgesia at the highest dose examined (50 micrograms kg-1) but had no effect on the PGE2-induced allodynia. "
02/26/1990 - "Conversely, prostaglandin E2-induced hyperalgesia was blocked by AH6809 (greater than or equal to 500 ng) but not by the substance P antagonist. "
|1.||N- (2- cyclohexyloxy- 4- nitrophenyl)methanesulfonamide
|4.||Prostaglandins E (PGE)
|5.||Sodium Selenite (Selenite)
|6.||Cyclic AMP-Dependent Protein Kinases (cAMP-Dependent Protein Kinase)
|7.||Conditioned Culture Media
|10.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)