psb603 Search Results


chlorophenyl piperazide 1 sulfonyl phenyl 1 propylxanthine psb 603  (Tocris)
95
Tocris chlorophenyl piperazide 1 sulfonyl phenyl 1 propylxanthine psb 603
Chlorophenyl Piperazide 1 Sulfonyl Phenyl 1 Propylxanthine Psb 603, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/chlorophenyl piperazide 1 sulfonyl phenyl 1 propylxanthine psb 603/product/Tocris
Average 95 stars, based on 1 article reviews
chlorophenyl piperazide 1 sulfonyl phenyl 1 propylxanthine psb 603 - by Bioz Stars, 2026-03
95/100 stars
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psb 603  (MedChemExpress)
92
MedChemExpress psb 603
Psb 603, supplied by MedChemExpress, 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/psb 603/product/MedChemExpress
Average 92 stars, based on 1 article reviews
psb 603 - by Bioz Stars, 2026-03
92/100 stars
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psb603  (Tocris)
93
Tocris psb603
Psb603, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/psb603/product/Tocris
Average 93 stars, based on 1 article reviews
psb603 - by Bioz Stars, 2026-03
93/100 stars
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psb-603  (Biomol GmbH)
90
Biomol GmbH psb-603
Influence of EA 575 ® ( A , B ) or the antagonists <t>PSB-603</t> and SCH 442416 ( C ) on the CRE activation in transiently transfected HEK cells mediated by stimulation with adenosine ( A , C ) or BAY 60-6583 ( B ). Pre-incubation with 40–240 µg/mL EA 575 ® was conducted for 16 h ( A , B ) or with 0.1–10 µM of the antagonists for 2 h ( C ) before cells were stimulated by adding 100 µM adenosine ( A , C ) or 10 µM BAY 60-6583 ( B ). The non-specifically mediated CRE activation was significantly inhibited by pre-incubation with 80–240 µg/mL EA 575 ® ( A ) or 1 µM PSB-603 ( C ), compared to stimulated control cells not pre-incubated with EA 575 ® (SC). SCH 442416 also significantly reduced the CRE activation at a concentration of 10 µM, whereas this effect could not be observed at lower concentrations of both antagonists. Instead, 0.1 µM SCH 442416 slightly increased the CRE activation ( C ). The inhibition of the specific A 2B AR-mediated CRE activation was achieved by pre-incubation with 80–240 µg/mL EA 575 ® ( B ). Influence of the A 2A AR agonist CGS 21680 and, in comparison, BAY 60-6583 and adenosine on the CRE activation in transiently transfected HEK cells ( D ). Stimulation was performed with 1–10 µM CGS 21680, 10 µM BAY 60-6583, or 100 µM adenosine. The A 2A AR-mediated CRE activation was significantly increased by 10 µM CGS 21680 compared with completely untreated control cells (UTC), but to a lesser extent than that mediated by A 2B AR or non-specifically using adenosine ( D ). Data are shown as AUC of the fold change (FC) after stimulation normalised to stimulated control cells not pre-incubated with EA 575 ® (SC) ( A – C ) or completely untreated control cells (UTC) ( D ). Results represent the mean and SEM ( n = 3 independent experiments performed in triplicate, * p < 0.05).
Psb 603, supplied by Biomol GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/psb-603/product/Biomol GmbH
Average 90 stars, based on 1 article reviews
psb-603 - by Bioz Stars, 2026-03
90/100 stars
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3 h]psb-603  (Pharmaron Inc)
90
Pharmaron Inc 3 h]psb-603
Influence of EA 575 ® ( A , B ) or the antagonists <t>PSB-603</t> and SCH 442416 ( C ) on the CRE activation in transiently transfected HEK cells mediated by stimulation with adenosine ( A , C ) or BAY 60-6583 ( B ). Pre-incubation with 40–240 µg/mL EA 575 ® was conducted for 16 h ( A , B ) or with 0.1–10 µM of the antagonists for 2 h ( C ) before cells were stimulated by adding 100 µM adenosine ( A , C ) or 10 µM BAY 60-6583 ( B ). The non-specifically mediated CRE activation was significantly inhibited by pre-incubation with 80–240 µg/mL EA 575 ® ( A ) or 1 µM PSB-603 ( C ), compared to stimulated control cells not pre-incubated with EA 575 ® (SC). SCH 442416 also significantly reduced the CRE activation at a concentration of 10 µM, whereas this effect could not be observed at lower concentrations of both antagonists. Instead, 0.1 µM SCH 442416 slightly increased the CRE activation ( C ). The inhibition of the specific A 2B AR-mediated CRE activation was achieved by pre-incubation with 80–240 µg/mL EA 575 ® ( B ). Influence of the A 2A AR agonist CGS 21680 and, in comparison, BAY 60-6583 and adenosine on the CRE activation in transiently transfected HEK cells ( D ). Stimulation was performed with 1–10 µM CGS 21680, 10 µM BAY 60-6583, or 100 µM adenosine. The A 2A AR-mediated CRE activation was significantly increased by 10 µM CGS 21680 compared with completely untreated control cells (UTC), but to a lesser extent than that mediated by A 2B AR or non-specifically using adenosine ( D ). Data are shown as AUC of the fold change (FC) after stimulation normalised to stimulated control cells not pre-incubated with EA 575 ® (SC) ( A – C ) or completely untreated control cells (UTC) ( D ). Results represent the mean and SEM ( n = 3 independent experiments performed in triplicate, * p < 0.05).
3 H]Psb 603, supplied by Pharmaron Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/3 h]psb-603/product/Pharmaron Inc
Average 90 stars, based on 1 article reviews
3 h]psb-603 - by Bioz Stars, 2026-03
90/100 stars
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8-(4-(4-(4-chlorophenyl) piperazide1-sulfonyl) phenyl)-1-propylxanthine (psb-603)  (Merck KGaA)
90
Merck KGaA 8-(4-(4-(4-chlorophenyl) piperazide1-sulfonyl) phenyl)-1-propylxanthine (psb-603)
Influence of EA 575 ® ( A , B ) or the antagonists <t>PSB-603</t> and SCH 442416 ( C ) on the CRE activation in transiently transfected HEK cells mediated by stimulation with adenosine ( A , C ) or BAY 60-6583 ( B ). Pre-incubation with 40–240 µg/mL EA 575 ® was conducted for 16 h ( A , B ) or with 0.1–10 µM of the antagonists for 2 h ( C ) before cells were stimulated by adding 100 µM adenosine ( A , C ) or 10 µM BAY 60-6583 ( B ). The non-specifically mediated CRE activation was significantly inhibited by pre-incubation with 80–240 µg/mL EA 575 ® ( A ) or 1 µM PSB-603 ( C ), compared to stimulated control cells not pre-incubated with EA 575 ® (SC). SCH 442416 also significantly reduced the CRE activation at a concentration of 10 µM, whereas this effect could not be observed at lower concentrations of both antagonists. Instead, 0.1 µM SCH 442416 slightly increased the CRE activation ( C ). The inhibition of the specific A 2B AR-mediated CRE activation was achieved by pre-incubation with 80–240 µg/mL EA 575 ® ( B ). Influence of the A 2A AR agonist CGS 21680 and, in comparison, BAY 60-6583 and adenosine on the CRE activation in transiently transfected HEK cells ( D ). Stimulation was performed with 1–10 µM CGS 21680, 10 µM BAY 60-6583, or 100 µM adenosine. The A 2A AR-mediated CRE activation was significantly increased by 10 µM CGS 21680 compared with completely untreated control cells (UTC), but to a lesser extent than that mediated by A 2B AR or non-specifically using adenosine ( D ). Data are shown as AUC of the fold change (FC) after stimulation normalised to stimulated control cells not pre-incubated with EA 575 ® (SC) ( A – C ) or completely untreated control cells (UTC) ( D ). Results represent the mean and SEM ( n = 3 independent experiments performed in triplicate, * p < 0.05).
8 (4 (4 (4 Chlorophenyl) Piperazide1 Sulfonyl) Phenyl) 1 Propylxanthine (Psb 603), supplied by Merck KGaA, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/8-(4-(4-(4-chlorophenyl) piperazide1-sulfonyl) phenyl)-1-propylxanthine (psb-603)/product/Merck KGaA
Average 90 stars, based on 1 article reviews
8-(4-(4-(4-chlorophenyl) piperazide1-sulfonyl) phenyl)-1-propylxanthine (psb-603) - by Bioz Stars, 2026-03
90/100 stars
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psb 603  (TargetMol)
94
TargetMol psb 603
Influence of EA 575 ® ( A , B ) or the antagonists <t>PSB-603</t> and SCH 442416 ( C ) on the CRE activation in transiently transfected HEK cells mediated by stimulation with adenosine ( A , C ) or BAY 60-6583 ( B ). Pre-incubation with 40–240 µg/mL EA 575 ® was conducted for 16 h ( A , B ) or with 0.1–10 µM of the antagonists for 2 h ( C ) before cells were stimulated by adding 100 µM adenosine ( A , C ) or 10 µM BAY 60-6583 ( B ). The non-specifically mediated CRE activation was significantly inhibited by pre-incubation with 80–240 µg/mL EA 575 ® ( A ) or 1 µM PSB-603 ( C ), compared to stimulated control cells not pre-incubated with EA 575 ® (SC). SCH 442416 also significantly reduced the CRE activation at a concentration of 10 µM, whereas this effect could not be observed at lower concentrations of both antagonists. Instead, 0.1 µM SCH 442416 slightly increased the CRE activation ( C ). The inhibition of the specific A 2B AR-mediated CRE activation was achieved by pre-incubation with 80–240 µg/mL EA 575 ® ( B ). Influence of the A 2A AR agonist CGS 21680 and, in comparison, BAY 60-6583 and adenosine on the CRE activation in transiently transfected HEK cells ( D ). Stimulation was performed with 1–10 µM CGS 21680, 10 µM BAY 60-6583, or 100 µM adenosine. The A 2A AR-mediated CRE activation was significantly increased by 10 µM CGS 21680 compared with completely untreated control cells (UTC), but to a lesser extent than that mediated by A 2B AR or non-specifically using adenosine ( D ). Data are shown as AUC of the fold change (FC) after stimulation normalised to stimulated control cells not pre-incubated with EA 575 ® (SC) ( A – C ) or completely untreated control cells (UTC) ( D ). Results represent the mean and SEM ( n = 3 independent experiments performed in triplicate, * p < 0.05).
Psb 603, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/psb 603/product/TargetMol
Average 94 stars, based on 1 article reviews
psb 603 - by Bioz Stars, 2026-03
94/100 stars
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psb-603  (Cayman Chemical)
90
Cayman Chemical psb-603
Influence of EA 575 ® ( A , B ) or the antagonists <t>PSB-603</t> and SCH 442416 ( C ) on the CRE activation in transiently transfected HEK cells mediated by stimulation with adenosine ( A , C ) or BAY 60-6583 ( B ). Pre-incubation with 40–240 µg/mL EA 575 ® was conducted for 16 h ( A , B ) or with 0.1–10 µM of the antagonists for 2 h ( C ) before cells were stimulated by adding 100 µM adenosine ( A , C ) or 10 µM BAY 60-6583 ( B ). The non-specifically mediated CRE activation was significantly inhibited by pre-incubation with 80–240 µg/mL EA 575 ® ( A ) or 1 µM PSB-603 ( C ), compared to stimulated control cells not pre-incubated with EA 575 ® (SC). SCH 442416 also significantly reduced the CRE activation at a concentration of 10 µM, whereas this effect could not be observed at lower concentrations of both antagonists. Instead, 0.1 µM SCH 442416 slightly increased the CRE activation ( C ). The inhibition of the specific A 2B AR-mediated CRE activation was achieved by pre-incubation with 80–240 µg/mL EA 575 ® ( B ). Influence of the A 2A AR agonist CGS 21680 and, in comparison, BAY 60-6583 and adenosine on the CRE activation in transiently transfected HEK cells ( D ). Stimulation was performed with 1–10 µM CGS 21680, 10 µM BAY 60-6583, or 100 µM adenosine. The A 2A AR-mediated CRE activation was significantly increased by 10 µM CGS 21680 compared with completely untreated control cells (UTC), but to a lesser extent than that mediated by A 2B AR or non-specifically using adenosine ( D ). Data are shown as AUC of the fold change (FC) after stimulation normalised to stimulated control cells not pre-incubated with EA 575 ® (SC) ( A – C ) or completely untreated control cells (UTC) ( D ). Results represent the mean and SEM ( n = 3 independent experiments performed in triplicate, * p < 0.05).
Psb 603, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/psb-603/product/Cayman Chemical
Average 90 stars, based on 1 article reviews
psb-603 - by Bioz Stars, 2026-03
90/100 stars
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Image Search Results


Influence of EA 575 ® ( A , B ) or the antagonists PSB-603 and SCH 442416 ( C ) on the CRE activation in transiently transfected HEK cells mediated by stimulation with adenosine ( A , C ) or BAY 60-6583 ( B ). Pre-incubation with 40–240 µg/mL EA 575 ® was conducted for 16 h ( A , B ) or with 0.1–10 µM of the antagonists for 2 h ( C ) before cells were stimulated by adding 100 µM adenosine ( A , C ) or 10 µM BAY 60-6583 ( B ). The non-specifically mediated CRE activation was significantly inhibited by pre-incubation with 80–240 µg/mL EA 575 ® ( A ) or 1 µM PSB-603 ( C ), compared to stimulated control cells not pre-incubated with EA 575 ® (SC). SCH 442416 also significantly reduced the CRE activation at a concentration of 10 µM, whereas this effect could not be observed at lower concentrations of both antagonists. Instead, 0.1 µM SCH 442416 slightly increased the CRE activation ( C ). The inhibition of the specific A 2B AR-mediated CRE activation was achieved by pre-incubation with 80–240 µg/mL EA 575 ® ( B ). Influence of the A 2A AR agonist CGS 21680 and, in comparison, BAY 60-6583 and adenosine on the CRE activation in transiently transfected HEK cells ( D ). Stimulation was performed with 1–10 µM CGS 21680, 10 µM BAY 60-6583, or 100 µM adenosine. The A 2A AR-mediated CRE activation was significantly increased by 10 µM CGS 21680 compared with completely untreated control cells (UTC), but to a lesser extent than that mediated by A 2B AR or non-specifically using adenosine ( D ). Data are shown as AUC of the fold change (FC) after stimulation normalised to stimulated control cells not pre-incubated with EA 575 ® (SC) ( A – C ) or completely untreated control cells (UTC) ( D ). Results represent the mean and SEM ( n = 3 independent experiments performed in triplicate, * p < 0.05).

Journal: International Journal of Molecular Sciences

Article Title: Ivy Leaf Dry Extract EA 575 ® Has an Inhibitory Effect on the Signalling Cascade of Adenosine Receptor A 2B

doi: 10.3390/ijms241512373

Figure Lengend Snippet: Influence of EA 575 ® ( A , B ) or the antagonists PSB-603 and SCH 442416 ( C ) on the CRE activation in transiently transfected HEK cells mediated by stimulation with adenosine ( A , C ) or BAY 60-6583 ( B ). Pre-incubation with 40–240 µg/mL EA 575 ® was conducted for 16 h ( A , B ) or with 0.1–10 µM of the antagonists for 2 h ( C ) before cells were stimulated by adding 100 µM adenosine ( A , C ) or 10 µM BAY 60-6583 ( B ). The non-specifically mediated CRE activation was significantly inhibited by pre-incubation with 80–240 µg/mL EA 575 ® ( A ) or 1 µM PSB-603 ( C ), compared to stimulated control cells not pre-incubated with EA 575 ® (SC). SCH 442416 also significantly reduced the CRE activation at a concentration of 10 µM, whereas this effect could not be observed at lower concentrations of both antagonists. Instead, 0.1 µM SCH 442416 slightly increased the CRE activation ( C ). The inhibition of the specific A 2B AR-mediated CRE activation was achieved by pre-incubation with 80–240 µg/mL EA 575 ® ( B ). Influence of the A 2A AR agonist CGS 21680 and, in comparison, BAY 60-6583 and adenosine on the CRE activation in transiently transfected HEK cells ( D ). Stimulation was performed with 1–10 µM CGS 21680, 10 µM BAY 60-6583, or 100 µM adenosine. The A 2A AR-mediated CRE activation was significantly increased by 10 µM CGS 21680 compared with completely untreated control cells (UTC), but to a lesser extent than that mediated by A 2B AR or non-specifically using adenosine ( D ). Data are shown as AUC of the fold change (FC) after stimulation normalised to stimulated control cells not pre-incubated with EA 575 ® (SC) ( A – C ) or completely untreated control cells (UTC) ( D ). Results represent the mean and SEM ( n = 3 independent experiments performed in triplicate, * p < 0.05).

Article Snippet: PSB-603 and CGS 21680 were obtained from Biomol (Hamburg, Germany).

Techniques: Activation Assay, Transfection, Incubation, Concentration Assay, Inhibition

Influence of EA 575 ® ( A , B ) or the antagonists PSB-603 and SCH 442416 ( C ) on the IL-6 release of Calu-3 cells mediated by stimulation with adenosine ( A , C ) or BAY 60-6583 ( B ). Pre-incubation with 40–240 µg/mL EA 575 ® was conducted for 16 h ( A , B ) or with 0.1–10 µM of the antagonists for 1 h ( C ) before cells were stimulated by adding 100 µM adenosine ( A , C ) or 10 µM BAY 60-6583 ( B ) for another 24 h. The non-specifically mediated IL-6 release was significantly and dose-dependently inhibited by pre-incubation with 80–240 µg/mL EA 575 ® (A) or 1 µM PSB-603 ( C ), compared to stimulated control cells not pre-incubated with EA 575 ® (SC). SCH 442416, however, increased the concentration of IL-6 even further. ( C ). The inhibition of the specific A 2B AR-mediated IL-6 release was achieved by pre-incubation with 40–240 µg/mL EA 575 ® ( B ). Influence of the A 2A AR agonist CGS 21680 and, in comparison, BAY 60-6583 on the IL-6 release of Calu-3 cells ( D ). Stimulation was performed with 1–10 µM CGS 21680 or 10 µM BAY 60-6583 for 24 h. The A 2A AR-mediated IL-6 release was slightly, but neither significantly nor dose-dependently, increased compared to completely untreated control cells (UTC) ( D ). Results represent the mean normalised to stimulated control cells not pre-incubated with EA 575 ® (SC) ( A – C ) or completely untreated control cells (UTC) ( D ) and SEM ( n = 3 independent experiments performed in triplicate, * p < 0.05).

Journal: International Journal of Molecular Sciences

Article Title: Ivy Leaf Dry Extract EA 575 ® Has an Inhibitory Effect on the Signalling Cascade of Adenosine Receptor A 2B

doi: 10.3390/ijms241512373

Figure Lengend Snippet: Influence of EA 575 ® ( A , B ) or the antagonists PSB-603 and SCH 442416 ( C ) on the IL-6 release of Calu-3 cells mediated by stimulation with adenosine ( A , C ) or BAY 60-6583 ( B ). Pre-incubation with 40–240 µg/mL EA 575 ® was conducted for 16 h ( A , B ) or with 0.1–10 µM of the antagonists for 1 h ( C ) before cells were stimulated by adding 100 µM adenosine ( A , C ) or 10 µM BAY 60-6583 ( B ) for another 24 h. The non-specifically mediated IL-6 release was significantly and dose-dependently inhibited by pre-incubation with 80–240 µg/mL EA 575 ® (A) or 1 µM PSB-603 ( C ), compared to stimulated control cells not pre-incubated with EA 575 ® (SC). SCH 442416, however, increased the concentration of IL-6 even further. ( C ). The inhibition of the specific A 2B AR-mediated IL-6 release was achieved by pre-incubation with 40–240 µg/mL EA 575 ® ( B ). Influence of the A 2A AR agonist CGS 21680 and, in comparison, BAY 60-6583 on the IL-6 release of Calu-3 cells ( D ). Stimulation was performed with 1–10 µM CGS 21680 or 10 µM BAY 60-6583 for 24 h. The A 2A AR-mediated IL-6 release was slightly, but neither significantly nor dose-dependently, increased compared to completely untreated control cells (UTC) ( D ). Results represent the mean normalised to stimulated control cells not pre-incubated with EA 575 ® (SC) ( A – C ) or completely untreated control cells (UTC) ( D ) and SEM ( n = 3 independent experiments performed in triplicate, * p < 0.05).

Article Snippet: PSB-603 and CGS 21680 were obtained from Biomol (Hamburg, Germany).

Techniques: Incubation, Concentration Assay, Inhibition