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pol7200 inhibition  (R&D Systems)


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    R&D Systems pol7200 inhibition
    A. Effects of FPR-1 antagonists on fMLF-induced PMN Ca2+depletion from ER. PMN were prepared from six healthy volunteers and stimulated with 100 nM fMLF. fMLF-induced Ca2+ store depletion was studied using Fura-2AM. Responses were assessed as the area under the intracellular Ca2+ concentration ([Ca2+]i) curve for 60 sec after stimulation (AUC60 – see Supplemental Digital Content 1). Dose-dependent inhibition of fMLF-induced Ca2+ depletion was seen in the presence of all three compounds, <t>POL7200,</t> POL7178, and CsH. Effect size was determined by comparing AUC60 for Ca2+ depletion in the presence of antagonists with vehicle (DMSO) assigned as 100%. Values are shown as mean ± SE.
    Pol7200 Inhibition, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 34 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pol7200 inhibition/product/R&D Systems
    Average 92 stars, based on 34 article reviews
    pol7200 inhibition - by Bioz Stars, 2026-03
    92/100 stars

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    1) Product Images from "FPR1 blockade prevents receptor regulation by mitochondrial DAMPs and preserves neutrophil function after trauma"

    Article Title: FPR1 blockade prevents receptor regulation by mitochondrial DAMPs and preserves neutrophil function after trauma

    Journal: Critical care medicine

    doi: 10.1097/CCM.0000000000004094

    A. Effects of FPR-1 antagonists on fMLF-induced PMN Ca2+depletion from ER. PMN were prepared from six healthy volunteers and stimulated with 100 nM fMLF. fMLF-induced Ca2+ store depletion was studied using Fura-2AM. Responses were assessed as the area under the intracellular Ca2+ concentration ([Ca2+]i) curve for 60 sec after stimulation (AUC60 – see Supplemental Digital Content 1). Dose-dependent inhibition of fMLF-induced Ca2+ depletion was seen in the presence of all three compounds, POL7200, POL7178, and CsH. Effect size was determined by comparing AUC60 for Ca2+ depletion in the presence of antagonists with vehicle (DMSO) assigned as 100%. Values are shown as mean ± SE.
    Figure Legend Snippet: A. Effects of FPR-1 antagonists on fMLF-induced PMN Ca2+depletion from ER. PMN were prepared from six healthy volunteers and stimulated with 100 nM fMLF. fMLF-induced Ca2+ store depletion was studied using Fura-2AM. Responses were assessed as the area under the intracellular Ca2+ concentration ([Ca2+]i) curve for 60 sec after stimulation (AUC60 – see Supplemental Digital Content 1). Dose-dependent inhibition of fMLF-induced Ca2+ depletion was seen in the presence of all three compounds, POL7200, POL7178, and CsH. Effect size was determined by comparing AUC60 for Ca2+ depletion in the presence of antagonists with vehicle (DMSO) assigned as 100%. Values are shown as mean ± SE.

    Techniques Used: Concentration Assay, Inhibition

    A. Inhibition of fMLF/mtDAMPs-induced PMN CTX. PMN isolated from blood of healthy volunteers (n=6) were pretreated with DMSO (vehicle), POL7200 (1 μM) or anti-FPR1-antibody (3 μg/mL) for 15 min at room temperature and 30 min at 37°C, respectively. PMN were applied to the upper chambers and either fMLF (100 nM) or mtDAMPs (150 μg/mL) were placed in the bottom chambers of transwells. PMN migration was evaluated after 60 min as above. Chemotaxis of DMSO-treated PMN was established as 100%. Mean ± SE are shown.
    Figure Legend Snippet: A. Inhibition of fMLF/mtDAMPs-induced PMN CTX. PMN isolated from blood of healthy volunteers (n=6) were pretreated with DMSO (vehicle), POL7200 (1 μM) or anti-FPR1-antibody (3 μg/mL) for 15 min at room temperature and 30 min at 37°C, respectively. PMN were applied to the upper chambers and either fMLF (100 nM) or mtDAMPs (150 μg/mL) were placed in the bottom chambers of transwells. PMN migration was evaluated after 60 min as above. Chemotaxis of DMSO-treated PMN was established as 100%. Mean ± SE are shown.

    Techniques Used: Inhibition, Isolation, Migration, Chemotaxis Assay

    A. POL7200 specifically inhibits PMN migration to fMLF but not to CXCL1 or LTB4. PMN pre-treated with vehicle (0.1% DMSO; presented as (–)) or POL7200 (1 μM) were placed in the upper chambers of transwells and allowed to migrate toward 100 nM fMLF, 50 nM CXCL1 or 100 nM LTB4 placed in the lower chambers for 60 min. Chemotaxis of vehicle-treated PMN toward each chemoattractant was designated as 100%. All experiments were done in quadruplicate. Blank values (spontaneous migration /chemokinesis) were used to correct the results. Data are shown as mean ± SE and are representative of at least three different experiments. POL7200 completely inhibits chemotaxis to fMLF (black bars) but has no effect on chemotaxis toward CXCL1 (white bars) or LTB4 (grey bars).
    Figure Legend Snippet: A. POL7200 specifically inhibits PMN migration to fMLF but not to CXCL1 or LTB4. PMN pre-treated with vehicle (0.1% DMSO; presented as (–)) or POL7200 (1 μM) were placed in the upper chambers of transwells and allowed to migrate toward 100 nM fMLF, 50 nM CXCL1 or 100 nM LTB4 placed in the lower chambers for 60 min. Chemotaxis of vehicle-treated PMN toward each chemoattractant was designated as 100%. All experiments were done in quadruplicate. Blank values (spontaneous migration /chemokinesis) were used to correct the results. Data are shown as mean ± SE and are representative of at least three different experiments. POL7200 completely inhibits chemotaxis to fMLF (black bars) but has no effect on chemotaxis toward CXCL1 (white bars) or LTB4 (grey bars).

    Techniques Used: Migration, Chemotaxis Assay

    A: FPR1 role in phagocytosis by PMN. Human PMN were incubated with pHrodo-labeled bacteria (ratio 20:1) for 30 min at 37°C as described in Supplemental Digital Content 1. Control PMN were pretreated with vehicle (1% DMSO). Experimental groups were treated with 10 μg/mL Cytochalasin D, with 1 or 10 μM POL7200, or with 1 or 10 μM CsH. All experiments were repeated using three different PMN preparations. The number of bacteria phagocytosed per PMN was assayed by flow cytometry. Data were normalized to the phagocytosis of bacteria by vehicle-treated PMN (established as 100%). Mean ± SE values are shown. Cytochalasin D was used as a positive control and showed the expected suppression of phagocytosis. FPR1 blocking by POL7200 showed no detectable inhibition of bacterial phagocytosis either at 1 μM (~EC50) or at 10 μM (~EC90)(see Figure 2). 1 μM CsH (~EC20) had no effect on phagocytosis. Unexpectedly, 10 μM CsH (~EC50) significantly decreased phagocytosis. *: p<0.005 vs. all other treatments. #: p<0.0001 vs. all except vs. CytoD (p=0.0412).
    Figure Legend Snippet: A: FPR1 role in phagocytosis by PMN. Human PMN were incubated with pHrodo-labeled bacteria (ratio 20:1) for 30 min at 37°C as described in Supplemental Digital Content 1. Control PMN were pretreated with vehicle (1% DMSO). Experimental groups were treated with 10 μg/mL Cytochalasin D, with 1 or 10 μM POL7200, or with 1 or 10 μM CsH. All experiments were repeated using three different PMN preparations. The number of bacteria phagocytosed per PMN was assayed by flow cytometry. Data were normalized to the phagocytosis of bacteria by vehicle-treated PMN (established as 100%). Mean ± SE values are shown. Cytochalasin D was used as a positive control and showed the expected suppression of phagocytosis. FPR1 blocking by POL7200 showed no detectable inhibition of bacterial phagocytosis either at 1 μM (~EC50) or at 10 μM (~EC90)(see Figure 2). 1 μM CsH (~EC20) had no effect on phagocytosis. Unexpectedly, 10 μM CsH (~EC50) significantly decreased phagocytosis. *: p<0.005 vs. all other treatments. #: p<0.0001 vs. all except vs. CytoD (p=0.0412).

    Techniques Used: Incubation, Labeling, Bacteria, Flow Cytometry, Positive Control, Blocking Assay, Inhibition



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    pol7200 inhibition  (R&D Systems)
    92
    R&D Systems pol7200 inhibition
    A. Effects of FPR-1 antagonists on fMLF-induced PMN Ca2+depletion from ER. PMN were prepared from six healthy volunteers and stimulated with 100 nM fMLF. fMLF-induced Ca2+ store depletion was studied using Fura-2AM. Responses were assessed as the area under the intracellular Ca2+ concentration ([Ca2+]i) curve for 60 sec after stimulation (AUC60 – see Supplemental Digital Content 1). Dose-dependent inhibition of fMLF-induced Ca2+ depletion was seen in the presence of all three compounds, <t>POL7200,</t> POL7178, and CsH. Effect size was determined by comparing AUC60 for Ca2+ depletion in the presence of antagonists with vehicle (DMSO) assigned as 100%. Values are shown as mean ± SE.
    Pol7200 Inhibition, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pol7200 inhibition/product/R&D Systems
    Average 92 stars, based on 1 article reviews
    pol7200 inhibition - by Bioz Stars, 2026-03
    92/100 stars
    		  Buy from Supplier

    Image Search Results


    A. Effects of FPR-1 antagonists on fMLF-induced PMN Ca2+depletion from ER. PMN were prepared from six healthy volunteers and stimulated with 100 nM fMLF. fMLF-induced Ca2+ store depletion was studied using Fura-2AM. Responses were assessed as the area under the intracellular Ca2+ concentration ([Ca2+]i) curve for 60 sec after stimulation (AUC60 – see Supplemental Digital Content 1). Dose-dependent inhibition of fMLF-induced Ca2+ depletion was seen in the presence of all three compounds, POL7200, POL7178, and CsH. Effect size was determined by comparing AUC60 for Ca2+ depletion in the presence of antagonists with vehicle (DMSO) assigned as 100%. Values are shown as mean ± SE.

    Journal: Critical care medicine

    Article Title: FPR1 blockade prevents receptor regulation by mitochondrial DAMPs and preserves neutrophil function after trauma

    doi: 10.1097/CCM.0000000000004094

    Figure Lengend Snippet: A. Effects of FPR-1 antagonists on fMLF-induced PMN Ca2+depletion from ER. PMN were prepared from six healthy volunteers and stimulated with 100 nM fMLF. fMLF-induced Ca2+ store depletion was studied using Fura-2AM. Responses were assessed as the area under the intracellular Ca2+ concentration ([Ca2+]i) curve for 60 sec after stimulation (AUC60 – see Supplemental Digital Content 1). Dose-dependent inhibition of fMLF-induced Ca2+ depletion was seen in the presence of all three compounds, POL7200, POL7178, and CsH. Effect size was determined by comparing AUC60 for Ca2+ depletion in the presence of antagonists with vehicle (DMSO) assigned as 100%. Values are shown as mean ± SE.

    Article Snippet: POL7200 inhibition was as effective as anti-FPR1 antibody (MAB3744, R&D Systems) ( 5 ) in blocking migration towards sonicated mitochondria (MTD) and was more effective than anti-FPR1 antibody in blocking migration towards fMLF ( ).

    Techniques: Concentration Assay, Inhibition

    A. Inhibition of fMLF/mtDAMPs-induced PMN CTX. PMN isolated from blood of healthy volunteers (n=6) were pretreated with DMSO (vehicle), POL7200 (1 μM) or anti-FPR1-antibody (3 μg/mL) for 15 min at room temperature and 30 min at 37°C, respectively. PMN were applied to the upper chambers and either fMLF (100 nM) or mtDAMPs (150 μg/mL) were placed in the bottom chambers of transwells. PMN migration was evaluated after 60 min as above. Chemotaxis of DMSO-treated PMN was established as 100%. Mean ± SE are shown.

    Journal: Critical care medicine

    Article Title: FPR1 blockade prevents receptor regulation by mitochondrial DAMPs and preserves neutrophil function after trauma

    doi: 10.1097/CCM.0000000000004094

    Figure Lengend Snippet: A. Inhibition of fMLF/mtDAMPs-induced PMN CTX. PMN isolated from blood of healthy volunteers (n=6) were pretreated with DMSO (vehicle), POL7200 (1 μM) or anti-FPR1-antibody (3 μg/mL) for 15 min at room temperature and 30 min at 37°C, respectively. PMN were applied to the upper chambers and either fMLF (100 nM) or mtDAMPs (150 μg/mL) were placed in the bottom chambers of transwells. PMN migration was evaluated after 60 min as above. Chemotaxis of DMSO-treated PMN was established as 100%. Mean ± SE are shown.

    Article Snippet: POL7200 inhibition was as effective as anti-FPR1 antibody (MAB3744, R&D Systems) ( 5 ) in blocking migration towards sonicated mitochondria (MTD) and was more effective than anti-FPR1 antibody in blocking migration towards fMLF ( ).

    Techniques: Inhibition, Isolation, Migration, Chemotaxis Assay

    A. POL7200 specifically inhibits PMN migration to fMLF but not to CXCL1 or LTB4. PMN pre-treated with vehicle (0.1% DMSO; presented as (–)) or POL7200 (1 μM) were placed in the upper chambers of transwells and allowed to migrate toward 100 nM fMLF, 50 nM CXCL1 or 100 nM LTB4 placed in the lower chambers for 60 min. Chemotaxis of vehicle-treated PMN toward each chemoattractant was designated as 100%. All experiments were done in quadruplicate. Blank values (spontaneous migration /chemokinesis) were used to correct the results. Data are shown as mean ± SE and are representative of at least three different experiments. POL7200 completely inhibits chemotaxis to fMLF (black bars) but has no effect on chemotaxis toward CXCL1 (white bars) or LTB4 (grey bars).

    Journal: Critical care medicine

    Article Title: FPR1 blockade prevents receptor regulation by mitochondrial DAMPs and preserves neutrophil function after trauma

    doi: 10.1097/CCM.0000000000004094

    Figure Lengend Snippet: A. POL7200 specifically inhibits PMN migration to fMLF but not to CXCL1 or LTB4. PMN pre-treated with vehicle (0.1% DMSO; presented as (–)) or POL7200 (1 μM) were placed in the upper chambers of transwells and allowed to migrate toward 100 nM fMLF, 50 nM CXCL1 or 100 nM LTB4 placed in the lower chambers for 60 min. Chemotaxis of vehicle-treated PMN toward each chemoattractant was designated as 100%. All experiments were done in quadruplicate. Blank values (spontaneous migration /chemokinesis) were used to correct the results. Data are shown as mean ± SE and are representative of at least three different experiments. POL7200 completely inhibits chemotaxis to fMLF (black bars) but has no effect on chemotaxis toward CXCL1 (white bars) or LTB4 (grey bars).

    Article Snippet: POL7200 inhibition was as effective as anti-FPR1 antibody (MAB3744, R&D Systems) ( 5 ) in blocking migration towards sonicated mitochondria (MTD) and was more effective than anti-FPR1 antibody in blocking migration towards fMLF ( ).

    Techniques: Migration, Chemotaxis Assay

    A: FPR1 role in phagocytosis by PMN. Human PMN were incubated with pHrodo-labeled bacteria (ratio 20:1) for 30 min at 37°C as described in Supplemental Digital Content 1. Control PMN were pretreated with vehicle (1% DMSO). Experimental groups were treated with 10 μg/mL Cytochalasin D, with 1 or 10 μM POL7200, or with 1 or 10 μM CsH. All experiments were repeated using three different PMN preparations. The number of bacteria phagocytosed per PMN was assayed by flow cytometry. Data were normalized to the phagocytosis of bacteria by vehicle-treated PMN (established as 100%). Mean ± SE values are shown. Cytochalasin D was used as a positive control and showed the expected suppression of phagocytosis. FPR1 blocking by POL7200 showed no detectable inhibition of bacterial phagocytosis either at 1 μM (~EC50) or at 10 μM (~EC90)(see Figure 2). 1 μM CsH (~EC20) had no effect on phagocytosis. Unexpectedly, 10 μM CsH (~EC50) significantly decreased phagocytosis. *: p<0.005 vs. all other treatments. #: p<0.0001 vs. all except vs. CytoD (p=0.0412).

    Journal: Critical care medicine

    Article Title: FPR1 blockade prevents receptor regulation by mitochondrial DAMPs and preserves neutrophil function after trauma

    doi: 10.1097/CCM.0000000000004094

    Figure Lengend Snippet: A: FPR1 role in phagocytosis by PMN. Human PMN were incubated with pHrodo-labeled bacteria (ratio 20:1) for 30 min at 37°C as described in Supplemental Digital Content 1. Control PMN were pretreated with vehicle (1% DMSO). Experimental groups were treated with 10 μg/mL Cytochalasin D, with 1 or 10 μM POL7200, or with 1 or 10 μM CsH. All experiments were repeated using three different PMN preparations. The number of bacteria phagocytosed per PMN was assayed by flow cytometry. Data were normalized to the phagocytosis of bacteria by vehicle-treated PMN (established as 100%). Mean ± SE values are shown. Cytochalasin D was used as a positive control and showed the expected suppression of phagocytosis. FPR1 blocking by POL7200 showed no detectable inhibition of bacterial phagocytosis either at 1 μM (~EC50) or at 10 μM (~EC90)(see Figure 2). 1 μM CsH (~EC20) had no effect on phagocytosis. Unexpectedly, 10 μM CsH (~EC50) significantly decreased phagocytosis. *: p<0.005 vs. all other treatments. #: p<0.0001 vs. all except vs. CytoD (p=0.0412).

    Article Snippet: POL7200 inhibition was as effective as anti-FPR1 antibody (MAB3744, R&D Systems) ( 5 ) in blocking migration towards sonicated mitochondria (MTD) and was more effective than anti-FPR1 antibody in blocking migration towards fMLF ( ).

    Techniques: Incubation, Labeling, Bacteria, Flow Cytometry, Positive Control, Blocking Assay, Inhibition