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. 2018 Jun 7;176(8):1059–1078. doi: 10.1111/bph.14335

Figure 2.

Figure 2

The ability of AL‐8810 to antagonize the signal transduction process in rat aortic smooth muscle A7r5 cells mediated by various FP receptor PGAs is shown. (A) and (B) Illustrate the [Ca2+]i mobilization induced by free acids of travoprost (TA) and bimatoprost (BA) in the absence and presence of increasing concentrations of the FP receptor antagonist, AL‐8810. Note the reduction in [Ca2+]i mobilization evoked by the agonists in the presence of AL‐8810. (C) and (D) Show how AL‐8810 also antagonized [Ca2+]i mobilization induced by the commercially available bimatoprost (amide) and the clinically used version of bimatoprost (Lumigan®). (E) The cumulative concentration–response curves showing the inhibitory effects of AL‐8810 on FP receptor PG agonists‐stimulated generation of [Ca2+]i (all adapted and modified from Sharif et al., 2001, 2002d, 2003a,d).