ac 55541 Search Results


ac 55541 hy14350  (MedChemExpress)
90
MedChemExpress ac 55541 hy14350
Ac 55541 Hy14350, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ac 55541  (R&D Systems)
92
R&D Systems ac 55541
Ac 55541, 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
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ac 55541  (Tocris)
90
Tocris ac 55541
Ac 55541, supplied by Tocris, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
ac 55541 - by Bioz Stars, 2026-05
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selective par 2 activator ac55541  (Santa Cruz Biotechnology)
90
Santa Cruz Biotechnology selective par 2 activator ac55541
FIG. 3. Effect of FSLLRY-NH2 on neurocognitive functions after ACA. Effects of FSLLRY-NH2 on neurological functions were assessed by (A) NDS at 24 and 48 h, (B) number of seizures at 24 and 48 h, and (C) T-maze test at 7 days after ACA. ACA significantly worsened performance while treatment with FSLLRY- NH2 at a dose of 50 mg significantly improved neurological functions in all tests following ACA. FSLLRY-NH2 treatment at a dose of 100 mg was not effective in NDS at 24 h and T-maze test. <t>AC55541</t> significantly deteriorated neurobehavioral outcome at all time points compared to the vehicle treated ACA group. Data are expressed as mean SD. n ¼ 6/group. ANOVA, Tukey. **P < 0.001 vs. Sham group, *P < 0.05 vs. Sham group, #P < 0.05 vs. ACA þ vehicle group. ACA indicates asphyxial cardiac arrest; d, days; h, hours.
Selective Par 2 Activator Ac55541, supplied by Santa Cruz Biotechnology, 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/selective par 2 activator ac55541/product/Santa Cruz Biotechnology
Average 90 stars, based on 1 article reviews
selective par 2 activator ac55541 - by Bioz Stars, 2026-05
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ac-55541  (ACADIA Pharmaceuticals)
90
ACADIA Pharmaceuticals ac-55541
FIG. 3. Effect of FSLLRY-NH2 on neurocognitive functions after ACA. Effects of FSLLRY-NH2 on neurological functions were assessed by (A) NDS at 24 and 48 h, (B) number of seizures at 24 and 48 h, and (C) T-maze test at 7 days after ACA. ACA significantly worsened performance while treatment with FSLLRY- NH2 at a dose of 50 mg significantly improved neurological functions in all tests following ACA. FSLLRY-NH2 treatment at a dose of 100 mg was not effective in NDS at 24 h and T-maze test. <t>AC55541</t> significantly deteriorated neurobehavioral outcome at all time points compared to the vehicle treated ACA group. Data are expressed as mean SD. n ¼ 6/group. ANOVA, Tukey. **P < 0.001 vs. Sham group, *P < 0.05 vs. Sham group, #P < 0.05 vs. ACA þ vehicle group. ACA indicates asphyxial cardiac arrest; d, days; h, hours.
Ac 55541, supplied by ACADIA Pharmaceuticals, 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/ac-55541/product/ACADIA Pharmaceuticals
Average 90 stars, based on 1 article reviews
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ac 55541  (Cayman Chemical)
N/A
AC 55541 is a proteinase activated receptor 2 PAR2 agonist that displays no activity at other PAR subtypes or at over 30 other receptors involved in nociception and inflammation It stimulates cell proliferation phosphatidylinositol hydrolysis
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ac-55541  (BOC Sciences)
N/A
AC-55541 is a novel small-molecule protease-activated receptor 2(PAR2) agonist which displays no activity at other PAR subtypes or at over 30 other receptors involved in nociception and inflammation. It activated PAR2 signaling in cellular proliferation
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ac-55541  (TargetMol)
N/A
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ac 55541  (Aladdin Scientific Corporation)
N/A
Shipped at 4°C. Store at -20°C. Store In the Dark. Store under desiccating conditions.
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Image Search Results


FIG. 3. Effect of FSLLRY-NH2 on neurocognitive functions after ACA. Effects of FSLLRY-NH2 on neurological functions were assessed by (A) NDS at 24 and 48 h, (B) number of seizures at 24 and 48 h, and (C) T-maze test at 7 days after ACA. ACA significantly worsened performance while treatment with FSLLRY- NH2 at a dose of 50 mg significantly improved neurological functions in all tests following ACA. FSLLRY-NH2 treatment at a dose of 100 mg was not effective in NDS at 24 h and T-maze test. AC55541 significantly deteriorated neurobehavioral outcome at all time points compared to the vehicle treated ACA group. Data are expressed as mean SD. n ¼ 6/group. ANOVA, Tukey. **P < 0.001 vs. Sham group, *P < 0.05 vs. Sham group, #P < 0.05 vs. ACA þ vehicle group. ACA indicates asphyxial cardiac arrest; d, days; h, hours.

Journal: Shock

Article Title: Inhibition of PAR-2 Attenuates Neuroinflammation and Improves Short-Term Neurocognitive Functions Via ERK1/2 Signaling Following Asphyxia-Induced Cardiac Arrest in Rats

doi: 10.1097/shk.0000000000001516

Figure Lengend Snippet: FIG. 3. Effect of FSLLRY-NH2 on neurocognitive functions after ACA. Effects of FSLLRY-NH2 on neurological functions were assessed by (A) NDS at 24 and 48 h, (B) number of seizures at 24 and 48 h, and (C) T-maze test at 7 days after ACA. ACA significantly worsened performance while treatment with FSLLRY- NH2 at a dose of 50 mg significantly improved neurological functions in all tests following ACA. FSLLRY-NH2 treatment at a dose of 100 mg was not effective in NDS at 24 h and T-maze test. AC55541 significantly deteriorated neurobehavioral outcome at all time points compared to the vehicle treated ACA group. Data are expressed as mean SD. n ¼ 6/group. ANOVA, Tukey. **P < 0.001 vs. Sham group, *P < 0.05 vs. Sham group, #P < 0.05 vs. ACA þ vehicle group. ACA indicates asphyxial cardiac arrest; d, days; h, hours.

Article Snippet: Selective PAR-2 activator AC55541 (30 mg/rat) and ERK1/2 inhibitor PD98059 (Santa Cruz Biotechnology, Dallas, Tex; 2 mL of 2 mmol/L) were used for intervention (25).

Techniques:

FIG. 4. Effect of FSLLRY-NH2 on neuronal degeneration after ACA. Representative microphotographs (A) and quantitative analyses (B) of FJC-positive cells revealed significant neuronal degeneration in hippocampal CA1 region at 7 days after ACA. AC55541 further exacerbated the number of FJC-positive cells in rats subjected to ACA while FSLLRY-NH2 at doses of 50 mg and 150 mg markedly reduced hippocampal neuronal degeneration. Data are expressed as mean SD. n ¼ 6/group. ANOVA, Tukey. Scale bar ¼ 100 mm. **P < 0.001 vs. Sham group, ##P < 0.001 vs. ACA þ vehicle group, #P < 0.05 vs. ACA þ vehicle group. ACA indicates asphyxial cardiac arrest.

Journal: Shock

Article Title: Inhibition of PAR-2 Attenuates Neuroinflammation and Improves Short-Term Neurocognitive Functions Via ERK1/2 Signaling Following Asphyxia-Induced Cardiac Arrest in Rats

doi: 10.1097/shk.0000000000001516

Figure Lengend Snippet: FIG. 4. Effect of FSLLRY-NH2 on neuronal degeneration after ACA. Representative microphotographs (A) and quantitative analyses (B) of FJC-positive cells revealed significant neuronal degeneration in hippocampal CA1 region at 7 days after ACA. AC55541 further exacerbated the number of FJC-positive cells in rats subjected to ACA while FSLLRY-NH2 at doses of 50 mg and 150 mg markedly reduced hippocampal neuronal degeneration. Data are expressed as mean SD. n ¼ 6/group. ANOVA, Tukey. Scale bar ¼ 100 mm. **P < 0.001 vs. Sham group, ##P < 0.001 vs. ACA þ vehicle group, #P < 0.05 vs. ACA þ vehicle group. ACA indicates asphyxial cardiac arrest.

Article Snippet: Selective PAR-2 activator AC55541 (30 mg/rat) and ERK1/2 inhibitor PD98059 (Santa Cruz Biotechnology, Dallas, Tex; 2 mL of 2 mmol/L) were used for intervention (25).

Techniques:

FIG. 5. Inhibition of ERK1/2 abolished the neuroinflammatory effect of PAR-2 activation at 24 h after ACA. Representative Western blot images (A) and quantitative analysis of PAR-2 (B), ERK1/2 (C), p-ERK1/2 (D), IL-6 (E), and TNF- a (F) in the brain revealed increased protein levels at 24 h following ACA except for ERK1/2 compared to the Sham group. Treatment with FSLLRY-NH2 significantly reduced p-ERK1/2 and proinflammatory cytokine levels compared to the ACA þ vehicle group. Further activation of PAR-2 with AC55541 only aggravated the neuroinflammatory response by increasing p-ERK1/2 expression. Potent ERK1/2 inhibitor PD98059 reversed the neuroinflammatory effect of AC55541. Neurologic outcome assessment with NDS at 24 h following ACA (G) revealed that the inhibition of PAR-2 significantly improved neurologic function while AC55541 alone significantly worsened performance compared to the ACA þ vehicle group. This detrimental effect of AC55541 on NDS was reversed by the ERK1/2 inhibitor, PD98059. Data are expressed as mean SD. n ¼ 6/group. ANOVA, Tukey. **P < 0.001 vs. Sham group, *P < 0.05 vs. Sham group, #P < 0.05 vs. ACA þvehicle group, &&P < 0.001 compared to ACA þ AC55541 group, &P < 0.05 compared to ACA þ AC55541 group. ACA indicates asphyxial cardiac arrest.

Journal: Shock

Article Title: Inhibition of PAR-2 Attenuates Neuroinflammation and Improves Short-Term Neurocognitive Functions Via ERK1/2 Signaling Following Asphyxia-Induced Cardiac Arrest in Rats

doi: 10.1097/shk.0000000000001516

Figure Lengend Snippet: FIG. 5. Inhibition of ERK1/2 abolished the neuroinflammatory effect of PAR-2 activation at 24 h after ACA. Representative Western blot images (A) and quantitative analysis of PAR-2 (B), ERK1/2 (C), p-ERK1/2 (D), IL-6 (E), and TNF- a (F) in the brain revealed increased protein levels at 24 h following ACA except for ERK1/2 compared to the Sham group. Treatment with FSLLRY-NH2 significantly reduced p-ERK1/2 and proinflammatory cytokine levels compared to the ACA þ vehicle group. Further activation of PAR-2 with AC55541 only aggravated the neuroinflammatory response by increasing p-ERK1/2 expression. Potent ERK1/2 inhibitor PD98059 reversed the neuroinflammatory effect of AC55541. Neurologic outcome assessment with NDS at 24 h following ACA (G) revealed that the inhibition of PAR-2 significantly improved neurologic function while AC55541 alone significantly worsened performance compared to the ACA þ vehicle group. This detrimental effect of AC55541 on NDS was reversed by the ERK1/2 inhibitor, PD98059. Data are expressed as mean SD. n ¼ 6/group. ANOVA, Tukey. **P < 0.001 vs. Sham group, *P < 0.05 vs. Sham group, #P < 0.05 vs. ACA þvehicle group, &&P < 0.001 compared to ACA þ AC55541 group, &P < 0.05 compared to ACA þ AC55541 group. ACA indicates asphyxial cardiac arrest.

Article Snippet: Selective PAR-2 activator AC55541 (30 mg/rat) and ERK1/2 inhibitor PD98059 (Santa Cruz Biotechnology, Dallas, Tex; 2 mL of 2 mmol/L) were used for intervention (25).

Techniques: Inhibition, Activation Assay, Western Blot, Expressing