Cell Based Assay: Ca2+ signaling studies were performed using a FLIPR TETRA system (Molecular Devices, Sunnyvale, Calif., USA) in the 384-format. This is a high-throughput instrument for cell-based assays to monitor Ca2+ signaling associated with GPCRs and ion channels. Cells were seeded at a density of 5×104 cells/well in BioCoat poly-D-lysine coated, black wall, clear bottom 384-well plates (BD Biosciences, Franklin lakes, NJ, USA) and allowed to attach overnight in an incubator at 37° C. The cells were then washed twice with HBSS-HEPES buffer (Hanks' balanced salt solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using an ELx405 Select CW Microplate Washer (BioTek, Winooski, Vt., USA). After 60 min of dye-loading in the dark using the Ca2+-sensitive dye Fluo-4AM (Invitrogen, Carlsbad, Calif., USA), at a final concentration of 2×10^−6M, the plates were washed 4 times with HBSS-HEPES buffer to remove excess dye and leaving 50 μl of buffer in each well. The plates were then placed in the FLIPR TETRA instrument and allowed to equilibrate at 37° C. AGN-211377 was added in a 25 μl volume to each well to give final concentrations of 0.1 μM, 0.3 μM, 1 μM, 3 μM, 10 μM, and 30 μM; or 0.067 μM, 0.1 μM, 0.2 μM, 0.3 μM, 0.67 μM, and 1 μM for cells over-expressing TP receptors. After 4.5 minutes, a 7-point serial dilution of the standard agonist for the corresponding receptor, in a 25 μl volume was injected at the final concentrations from 10^−11M to 10^−5M in 10-fold serial dilution increments for cells expressing human recombinant DP1, EP1, EP2, EP3, EP4, FP, and IP receptors. The dose range for the standard agonist for human recombinant TP receptors was from 10^−12M to 10^−6M. HBSS-HEPES buffer was used as the negative control for the standard agonists. Cells were excited with LED (light emitting diode) excitation at 470-495 nm and emission was measured through an emission filter at 515-575 nm. Assay plates were read for 3.5 minutes using the FLIPRTETRA.Cell Based Assay: Ca2+ signaling studies were performed using a FLIPR TETRA system (Molecular Devices, Sunnyvale, Calif., USA) in the 384-format. This is a high-throughput instrument for cell-based assays to monitor Ca2+ signaling associated with GPCRs and ion channels. Cells were seeded at a density of 5×104 cells/well in BioCoat poly-D-lysine coated, black wall, clear bottom 384-well plates (BD Biosciences, Franklin lakes, NJ, USA) and allowed to attach overnight in an incubator at 37° C. The cells were then washed twice with HBSS-HEPES buffer (Hanks' balanced salt solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using an ELx405 Select CW Microplate Washer (BioTek, Winooski, Vt., USA). After 60 min of dye-loading in the dark using the Ca2+-sensitive dye Fluo-4AM (Invitrogen, Carlsbad, Calif., USA), at a final concentration of 2×10^−6M, the plates were washed 4 times with HBSS-HEPES buffer to remove excess dye and leaving 50 μl of buffer in each well. The plates were then placed in the FLIPR TETRA instrument and allowed to equilibrate at 37° C. AGN-211377 was added in a 25 μl volume to each well to give final concentrations of 0.1 μM, 0.3 μM, 1 μM, 3 μM, 10 μM, and 30 μM; or 0.067 μM, 0.1 μM, 0.2 μM, 0.3 μM, 0.67 μM, and 1 μM for cells over-expressing TP receptors. After 4.5 minutes, a 7-point serial dilution of the standard agonist for the corresponding receptor, in a 25 μl volume was injected at the final concentrations from 10^−11M to 10^−5M in 10-fold serial dilution increments for cells expressing human recombinant DP1, EP1, EP2, EP3, EP4, FP, and IP receptors. The dose range for the standard agonist for human recombinant TP receptors was from 10^−12M to 10^−6M. HBSS-HEPES buffer was used as the negative control for the standard agonists. Cells were excited with LED (light emitting diode) excitation at 470-495 nm and emission was measured through an emission filter at 515-575 nm. Assay plates were read for 3.5 minutes using the FLIPRTETRA.

Cell Based Assay: Ca2+ signaling studies were performed using a FLIPR TETRA system (Molecular Devices, Sunnyvale, Calif., USA) in the 384-format. This is a high-throughput instrument for cell-based assays to monitor Ca2+ signaling associated with GPCRs and ion channels. Cells were seeded at a density of 5×104 cells/well in BioCoat poly-D-lysine coated, black wall, clear bottom 384-well plates (BD Biosciences, Franklin lakes, NJ, USA) and allowed to attach overnight in an incubator at 37° C. The cells were then washed twice with HBSS-HEPES buffer (Hanks' balanced salt solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using an ELx405 Select CW Microplate Washer (BioTek, Winooski, Vt., USA). After 60 min of dye-loading in the dark using the Ca2+-sensitive dye Fluo-4AM (Invitrogen, Carlsbad, Calif., USA), at a final concentration of 2×10^−6M, the plates were washed 4 times with HBSS-HEPES buffer to remove excess dye and leaving 50 μl of buffer in each well. The plates were then placed in the FLIPR TETRA instrument and allowed to equilibrate at 37° C. AGN-211377 was added in a 25 μl volume to each well to give final concentrations of 0.1 μM, 0.3 μM, 1 μM, 3 μM, 10 μM, and 30 μM; or 0.067 μM, 0.1 μM, 0.2 μM, 0.3 μM, 0.67 μM, and 1 μM for cells over-expressing TP receptors. After 4.5 minutes, a 7-point serial dilution of the standard agonist for the corresponding receptor, in a 25 μl volume was injected at the final concentrations from 10^−11M to 10^−5M in 10-fold serial dilution increments for cells expressing human recombinant DP1, EP1, EP2, EP3, EP4, FP, and IP receptors. The dose range for the standard agonist for human recombinant TP receptors was from 10^−12M to 10^−6M. HBSS-HEPES buffer was used as the negative control for the standard agonists. Cells were excited with LED (light emitting diode) excitation at 470-495 nm and emission was measured through an emission filter at 515-575 nm. Assay plates were read for 3.5 minutes using the FLIPRTETRA.Cell Based Assay: Ca2+ signaling studies were performed using a FLIPR TETRA system (Molecular Devices, Sunnyvale, Calif., USA) in the 384-format. This is a high-throughput instrument for cell-based assays to monitor Ca2+ signaling associated with GPCRs and ion channels. Cells were seeded at a density of 5×104 cells/well in BioCoat poly-D-lysine coated, black wall, clear bottom 384-well plates (BD Biosciences, Franklin lakes, NJ, USA) and allowed to attach overnight in an incubator at 37° C. The cells were then washed twice with HBSS-HEPES buffer (Hanks' balanced salt solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using an ELx405 Select CW Microplate Washer (BioTek, Winooski, Vt., USA). After 60 min of dye-loading in the dark using the Ca2+-sensitive dye Fluo-4AM (Invitrogen, Carlsbad, Calif., USA), at a final concentration of 2×10^−6M, the plates were washed 4 times with HBSS-HEPES buffer to remove excess dye and leaving 50 μl of buffer in each well. The plates were then placed in the FLIPR TETRA instrument and allowed to equilibrate at 37° C. AGN-211377 was added in a 25 μl volume to each well to give final concentrations of 0.1 μM, 0.3 μM, 1 μM, 3 μM, 10 μM, and 30 μM; or 0.067 μM, 0.1 μM, 0.2 μM, 0.3 μM, 0.67 μM, and 1 μM for cells over-expressing TP receptors. After 4.5 minutes, a 7-point serial dilution of the standard agonist for the corresponding receptor, in a 25 μl volume was injected at the final concentrations from 10^−11M to 10^−5M in 10-fold serial dilution increments for cells expressing human recombinant DP1, EP1, EP2, EP3, EP4, FP, and IP receptors. The dose range for the standard agonist for human recombinant TP receptors was from 10^−12M to 10^−6M. HBSS-HEPES buffer was used as the negative control for the standard agonists. Cells were excited with LED (light emitting diode) excitation at 470-495 nm and emission was measured through an emission filter at 515-575 nm. Assay plates were read for 3.5 minutes using the FLIPRTETRA.

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=50%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=50%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=50%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=50%)

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=95%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=100%)

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.FLIPR Assay: Calciium Signal Studies of the Flipr. Cells were seeded at a density of 5×104 cells per well in Biocoati® Poly-D-lysine-coated black-wall, clear-bottom 96-well plates (Becton-Dickinson) and allowed to attach overnight in an incubator at 37° C. Cells were then washed two times with HBSS-HEPES buffer (Hanks Balanced Salt Solution without bicarbonate and phenol red, 20 mM HEPES, pH 7.4) using a Denley Cellwash plate washer (Labsystems). After 45 minutes of dye-loading in the dark, using the calcium-sensitive dye Fluo-4 AM at a final concentration of 2 μM, plates were washed four times with HBSS-HEPES buffer to remove excess dye leaving 100 μl in each well. Plates were re-equilibrated to 37° C. for a few minutes. Cells were excited with an Argon laser at 488 nm, and emission was measured through a 510-570 nm bandwidth emission filter (FLIPR, Molecular Devices, Sunnyvale, Calif.). Drug solution was added in a 50 μl volume to each well to give the desired final concentration.

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=90%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=90%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=90%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=90%)

Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=90%)Functional activity in RAT-1cells, transiently-transfected with human TP-receptor (% of control ligand, [3H]-U-46,619=90%)

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Agonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assayAgonist activity at human recombinant TP receptor expressed in HEK293 cells assessed as effect on calcium accumulation by Fluo-4 AM dye based FLIPR assay

Antagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assayAntagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assay

Antagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assayAntagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assay

Antagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assayAntagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assay

Antagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assayAntagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assay

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Antagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assayAntagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assay

Antagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assayAntagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assay

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasmaIn vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasma

In vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasmaIn vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasma

In vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasmaIn vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasma

In vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasmaIn vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasma

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

Antagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

In vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human plateletsIn vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human platelets

In vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human plateletsIn vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human platelets

Antagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

Antagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assayAntagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assay

Antagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assayAntagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assay

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

In vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasmaIn vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasma

In vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasmaIn vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasma

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Inhibition of human TP receptor expressed in QBI-HEK 293A cells assessed as IP3 metabolite level after 1 hr by HTRF assayInhibition of human TP receptor expressed in QBI-HEK 293A cells assessed as IP3 metabolite level after 1 hr by HTRF assay

Inhibition of human TP receptor expressed in QBI-HEK 293A cells assessed as IP3 metabolite level after 1 hr by HTRF assayInhibition of human TP receptor expressed in QBI-HEK 293A cells assessed as IP3 metabolite level after 1 hr by HTRF assay

In vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human plateletsIn vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human platelets

In vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human plateletsIn vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human platelets

In vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human plateletsIn vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human platelets

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Antagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assayAntagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assay

Antagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assayAntagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assay

Activity at TPalpha (short isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilizationActivity at TPalpha (short isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilization

Activity at TPalpha (short isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilizationActivity at TPalpha (short isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilization

In vitro thromboxane receptor antagonist against U-46619 induced aggregation of washed human plateletsIn vitro thromboxane receptor antagonist against U-46619 induced aggregation of washed human platelets

In vitro thromboxane receptor antagonist against U-46619 induced aggregation of washed human plateletsIn vitro thromboxane receptor antagonist against U-46619 induced aggregation of washed human platelets

Activity at TPbeta (long isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilizationActivity at TPbeta (long isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilization

Activity at TPbeta (long isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilizationActivity at TPbeta (long isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilization

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasmaIn vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasma

In vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasmaIn vitro inhibition of arachidonic acid induced platelet aggregation in human platelet-rich plasma

In vitro evaluation for arachidonic acid induced platelet aggregation of human platelet-rich plasmaIn vitro evaluation for arachidonic acid induced platelet aggregation of human platelet-rich plasma

In vitro evaluation for arachidonic acid induced platelet aggregation of human platelet-rich plasmaIn vitro evaluation for arachidonic acid induced platelet aggregation of human platelet-rich plasma

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

Antagonist activity at human prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence methodAntagonist activity at human prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence method

Antagonist activity at human prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence methodAntagonist activity at human prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence method

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

Antagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assay

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Activity at TPalpha (short isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilizationActivity at TPalpha (short isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilization

Activity at TPalpha (short isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilizationActivity at TPalpha (short isoform) receptor expressed in HEK293 cells assessed as ability to antagonize U46619-mediated calcium ion mobilization

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Activity at human TP receptor in platelet rich plasma assessed as inhibition U44619-induced platelet aggregationActivity at human TP receptor in platelet rich plasma assessed as inhibition U44619-induced platelet aggregation

Activity at human TP receptor in platelet rich plasma assessed as inhibition U44619-induced platelet aggregationActivity at human TP receptor in platelet rich plasma assessed as inhibition U44619-induced platelet aggregation

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

In vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aortaIn vitro thromboxane A2 antagonistic activity on U-46619 (0.1 uM) induced contraction of rat aorta

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence methodAntagonist activity at human prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence method

Antagonist activity at human prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence methodAntagonist activity at human prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence method

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor alpha over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization by fluorescence assay

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

Antagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assayAntagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assay

Antagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assayAntagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assay

Antagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assayAntagonist activity against human thromboxane A2 receptor alpha expressed in QBI-HEK293A cells assessed as reduction in I-BOP-induced inositol monophosphate production incubated for 15 to 60 mins before I-BOP addition by HTRF assay

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

Antagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assayAntagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assay

Antagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assayAntagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assay

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform alpha expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

Antagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilizationAntagonist activity at human thromboxane A2 receptor isoform beta expressed in HEK293 cells assessed as inhibition of U46619-induced calcium mobilization

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619Ability to inhibit blood platelet aggregation of human platelet-rich plasma induced by TP-receptor agonist U 46619

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)Compound was evaluated for the inhibition of platelet aggregation, assessed turbidimetrically in citreated human platelet rich plasma (PRP)

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

Inhibition of U-46,619-induced inositol phosphate accumulation at human Thromboxane A2 receptorInhibition of U-46,619-induced inositol phosphate accumulation at human Thromboxane A2 receptor

Inhibition of U-46,619-induced inositol phosphate accumulation at human Thromboxane A2 receptorInhibition of U-46,619-induced inositol phosphate accumulation at human Thromboxane A2 receptor

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

TXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human plateletsTXA2 receptor antagonism, measured by the displacement of [3H]SQ29,548 from the PGH-2/TXA-2 receptor on human platelets

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)Tested for antagonistic activity on isolated rat thoracic aorta (thromboxane A2 receptor) precontracted by U-46619 (3 x 10 e-8 M)

Antagonist activity at human prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence methodAntagonist activity at human prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence method

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

Antagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assayAntagonist activity at human thromboxane A2 receptor beta over-expressed in HEK293 cells assessed as inhibition of U-46619-induced intracellular calcium mobilization mobilization by fluorescence assay

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)In vitro thromboxane A2 antagonistic activity on aggregation of rabbit platelets induced by U-46,619 (4 uM)

Antagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assayAntagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assay

Antagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assayAntagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assay

Antagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assayAntagonist activity at mouse prostanoid TP receptor expressed in QBI-HEK 293A cells assessed as inhibition of 1-BOP-induced increase in inositol monophosphate after 1 hr by time-resolved fluorescence assay

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.In vitro activity on thromboxane A2 receptor antagonism in gel filtered human platelets.

In vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human plateletsIn vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human platelets

In vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human plateletsIn vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human platelets

In vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human plateletsIn vitro thromboxane receptor antagonist activity was determined by inhibition of U-46619 induced aggregation of washed human platelets