Review

cb2 antagonist sr 144528 (Cayman Chemical)

Cayman Chemical is a verified supplier

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Cayman Chemical cb2 antagonist sr 144528

Figure 4. Comparative analysis of the effects of intranasal and oral administration of <t>CB2</t> agonist on cold hypersensitivity in IONC mice. The area under the curve was determined from the acetone test data following either intranasal (i.n.) or oral (p.o.) repeated administration of HU-308 (HU, 30 nmole, 10 µL) and compared. Individual data and mean ± SEM are shown. N = 5; * p < 0.05, ** p < 0.01 (two-way ANOVA followed by Tukey’s multiple comparisons test).

Cb2 Antagonist Sr 144528, supplied by Cayman Chemical, 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/cb2 antagonist sr 144528/product/Cayman Chemical
Average 94 stars, based on 1 article reviews

cb2 antagonist sr 144528 - by Bioz Stars, 2026-05

94/100 stars

Images

1) Product Images from "Intranasal Treatment with Cannabinoid 2 Receptor Agonist HU-308 Ameliorates Cold Sensitivity in Mice with Traumatic Trigeminal Neuropathic Pain."

Article Title: Intranasal Treatment with Cannabinoid 2 Receptor Agonist HU-308 Ameliorates Cold Sensitivity in Mice with Traumatic Trigeminal Neuropathic Pain.

Journal: Cells

doi: 10.3390/cells13231943

Figure 4. Comparative analysis of the effects of intranasal and oral administration of CB2 agonist on cold hypersensitivity in IONC mice. The area under the curve was determined from the acetone test data following either intranasal (i.n.) or oral (p.o.) repeated administration of HU-308 (HU, 30 nmole, 10 µL) and compared. Individual data and mean ± SEM are shown. N = 5; * p < 0.05, ** p < 0.01 (two-way ANOVA followed by Tukey’s multiple comparisons test).

Figure Legend Snippet: Figure 4. Comparative analysis of the effects of intranasal and oral administration of CB2 agonist on cold hypersensitivity in IONC mice. The area under the curve was determined from the acetone test data following either intranasal (i.n.) or oral (p.o.) repeated administration of HU-308 (HU, 30 nmole, 10 µL) and compared. Individual data and mean ± SEM are shown. N = 5; * p < 0.05, ** p < 0.01 (two-way ANOVA followed by Tukey’s multiple comparisons test).

Techniques Used:

Image Search Results

Journal: Cells

Article Title: Intranasal Treatment with Cannabinoid 2 Receptor Agonist HU-308 Ameliorates Cold Sensitivity in Mice with Traumatic Trigeminal Neuropathic Pain.

doi: 10.3390/cells13231943

Figure Lengend Snippet: Figure 4. Comparative analysis of the effects of intranasal and oral administration of CB2 agonist on cold hypersensitivity in IONC mice. The area under the curve was determined from the acetone test data following either intranasal (i.n.) or oral (p.o.) repeated administration of HU-308 (HU, 30 nmole, 10 µL) and compared. Individual data and mean ± SEM are shown. N = 5; * p < 0.05, ** p < 0.01 (two-way ANOVA followed by Tukey’s multiple comparisons test).

Article Snippet: Regardless of the administration methods, 30 nmol of CB2 agonist HU-308 (Cat. #: 90086; Cayman Chemical, Ann Arbor, MI, USA) and 100 nmol of CB2 antagonist SR 144528 (Cat. #: 9000491; Cayman Chemical, Ann Arbor, MI, USA) were used in this study.

Techniques:

The synthetic cannabinoid WIN 55,212-2 (WIN) inhibits NE differentiation of LNCaP cells. ( a ) NE differentiation cells was induced by serum deprivation of LNCaP for 6 days. Cell morphology of control LNCaP cells (control, C) and serum-deprived cells (NE cells) was monitored by phase-contrast microscopy (upper panel) and immunofluorescence of class III β Tubulin (βIII Tub, red) counterstained with DAPI (blue) (lower panel). ( b ) Expression of the NE markers neuron-specific enolase (NSE) and βIII Tub in control and NE cells. GADPH was probed as a loading control. ( c ) LNCaP control cells (C) and NE cells were incubated with increasing concentrations of WIN for 48 h and cell viability was monitored by MTT. ( d ) LNCaP control cells and NE cells were treated with vehicle (Vhc), 3 μ M of WIN (WIN) or 1 μ M of the CB1inverse agonist SR1 and 1 μ M of the CB2 inverse agonist SR2 (SR1/SR2) for 6 days. Levels of the NSE and βIII Tub were determined by western blot. GADPH was probed as a loading control. The image is representative of other four experiments. Densitiometric analysis of the western blot bands is shown on the right. The data shown are the means±s.d. of four different experiments (* P< 0.05 and ** P< 0.01 versus control cells, # P< 0.05 and ## P< 0.01 versus NE, compared by the Student's t -test). NE, neuroendocrine.

Journal: Prostate Cancer and Prostatic Diseases

Article Title: The cannabinoid WIN 55,212-2 prevents neuroendocrine differentiation of LNCaP prostate cancer cells

doi: 10.1038/pcan.2016.19

Figure Lengend Snippet: The synthetic cannabinoid WIN 55,212-2 (WIN) inhibits NE differentiation of LNCaP cells. ( a ) NE differentiation cells was induced by serum deprivation of LNCaP for 6 days. Cell morphology of control LNCaP cells (control, C) and serum-deprived cells (NE cells) was monitored by phase-contrast microscopy (upper panel) and immunofluorescence of class III β Tubulin (βIII Tub, red) counterstained with DAPI (blue) (lower panel). ( b ) Expression of the NE markers neuron-specific enolase (NSE) and βIII Tub in control and NE cells. GADPH was probed as a loading control. ( c ) LNCaP control cells (C) and NE cells were incubated with increasing concentrations of WIN for 48 h and cell viability was monitored by MTT. ( d ) LNCaP control cells and NE cells were treated with vehicle (Vhc), 3 μ M of WIN (WIN) or 1 μ M of the CB1inverse agonist SR1 and 1 μ M of the CB2 inverse agonist SR2 (SR1/SR2) for 6 days. Levels of the NSE and βIII Tub were determined by western blot. GADPH was probed as a loading control. The image is representative of other four experiments. Densitiometric analysis of the western blot bands is shown on the right. The data shown are the means±s.d. of four different experiments (* P< 0.05 and ** P< 0.01 versus control cells, # P< 0.05 and ## P< 0.01 versus NE, compared by the Student's t -test). NE, neuroendocrine.

Article Snippet: The CB1 antagonist SR-141716 and the CB2 antagonist SR-144528 were kindly provided from Sanofi-Synthelabo (Montpellier, France).

Techniques: Control, Microscopy, Immunofluorescence, Expressing, Incubation, Western Blot

Inhibition of NE differentiation by WIN 55,212-2 (WIN) in IL-6 long treated LNCaP cells and in PC-3 cells. ( a ) NE differentiation of LNCaP cells was induced by incubation with IL-6 (20 ng ml 1 ) -supplemented medium for 6 days. Cells were treated with vehicle (Vhc), 3 μ M of WIN (WIN) or 1 μ M of the CB1inverse agonist SR1 and 1 μ M of the CB2 inverse agonist SR2 (SR1/SR2) for 6 days. Levels of the NE markers neuron-specific enolase (NSE) and βIII tubulin (βIII Tub) were determined by western blot. ( b ) NE markers NSE and βIII Tub in PC-3 cells treated as above. The image is representative of other three experiments. GADPH was probed as a loading control. Densitiometric analysis of the western blot bands is shown on the right. The data shown are the means±s.d. of three different experiments (* P< 0.05 versus control cells, compared by the Student's t -test). ( c ) Effect of WIN on PC-3 growth and βIII Tub expression in vivo . PC-3 xenografts were generated by subcutaneously. injection in athymic mice ( n =8). When tumors reached 100 mm 3 volume, mice were randomly divided into two groups and treated with 0.5 mg kg 1 WIN or vehicle. Graph represents tumor growth from the first day of treatment and results are expressed as the mean±s.e.m. of the size of the tumor. A representative image of the tumor at the end of the treatment is shown on the right. Down, levels of βIII Tub in the dissected tumors. IL, interleukin; NE, neuroendocrine.

Journal: Prostate Cancer and Prostatic Diseases

Article Title: The cannabinoid WIN 55,212-2 prevents neuroendocrine differentiation of LNCaP prostate cancer cells

doi: 10.1038/pcan.2016.19

Figure Lengend Snippet: Inhibition of NE differentiation by WIN 55,212-2 (WIN) in IL-6 long treated LNCaP cells and in PC-3 cells. ( a ) NE differentiation of LNCaP cells was induced by incubation with IL-6 (20 ng ml 1 ) -supplemented medium for 6 days. Cells were treated with vehicle (Vhc), 3 μ M of WIN (WIN) or 1 μ M of the CB1inverse agonist SR1 and 1 μ M of the CB2 inverse agonist SR2 (SR1/SR2) for 6 days. Levels of the NE markers neuron-specific enolase (NSE) and βIII tubulin (βIII Tub) were determined by western blot. ( b ) NE markers NSE and βIII Tub in PC-3 cells treated as above. The image is representative of other three experiments. GADPH was probed as a loading control. Densitiometric analysis of the western blot bands is shown on the right. The data shown are the means±s.d. of three different experiments (* P< 0.05 versus control cells, compared by the Student's t -test). ( c ) Effect of WIN on PC-3 growth and βIII Tub expression in vivo . PC-3 xenografts were generated by subcutaneously. injection in athymic mice ( n =8). When tumors reached 100 mm 3 volume, mice were randomly divided into two groups and treated with 0.5 mg kg 1 WIN or vehicle. Graph represents tumor growth from the first day of treatment and results are expressed as the mean±s.e.m. of the size of the tumor. A representative image of the tumor at the end of the treatment is shown on the right. Down, levels of βIII Tub in the dissected tumors. IL, interleukin; NE, neuroendocrine.

Article Snippet: The CB1 antagonist SR-141716 and the CB2 antagonist SR-144528 were kindly provided from Sanofi-Synthelabo (Montpellier, France).

Techniques: Inhibition, Incubation, Western Blot, Control, Expressing, In Vivo, Generated, Injection

Journal: Prostate Cancer and Prostatic Diseases

Article Title: The cannabinoid WIN 55,212-2 prevents neuroendocrine differentiation of LNCaP prostate cancer cells

doi: 10.1038/pcan.2016.19

Figure Lengend Snippet: The synthetic cannabinoid WIN 55,212-2 (WIN) blocks the PI3K/Akt/mTOR axe activation produced in NE differentiation of LNCaP cells. ( a ) Phosphorylation profile of key proteins of the PI3K/Akt pathway in LNCaP cells (control, C) and in NE cells (NE). Expression of neuron-specific enolase (NSE) and βIII tubulin (βIII Tub) were monitored as a NE differentiation control. GADPH was probed as a loading control. ( b ) LNCaP control and NE cells were treated with vehicle (Vhc), 3 μ M of WIN, or 1 μ M of the CB1inverse agonist SR1 and 1 μ M of the CB2 inverse agonist SR2 (SR1/SR2) for 6 days. Levels of the phosphorylated and total forms of Akt, mTOR and S6 proteins were determined by western blot. GADPH was probed as a loading control. The image is representative of other three experiments. Densitiometric analyses of the western blot bands are shown on the right of the WB. The data shown are the means±s.d. of three different experiments. (* P< 0.05 and ** P< 0.01 versus control cells, # P< 0.05 and ## P< 0.01 versus NE cells, compared by the Student's t -test). NE, neuroendocrine.

Article Snippet: The CB1 antagonist SR-141716 and the CB2 antagonist SR-144528 were kindly provided from Sanofi-Synthelabo (Montpellier, France).

Techniques: Activation Assay, Produced, Phospho-proteomics, Control, Expressing, Western Blot

Effect of WIN 55,212-2 on IL-6-induced NE differentiation. NE differentiation of LNCaP cells was induced by incubation with IL-6 (20 ng ml 1 ) -supplemented medium for 6 days. Cells were treated with vehicle (Vhc), 3 μ M of WIN (WIN) or 1 μ M of the CB1inverse agonist SR1 and 1 μ M of the CB2 inverse agonist SR2 (SR1/SR2) for 6 days. Levels of the phosphorylated and total forms of Akt, AMPK and acetyl CoA carboxylase (ACC) proteins were determined by western blot. GADPH was probed as a loading control. The image is representative of other three experiments. IL, interleukin; NE, neuroendocrine.

Journal: Prostate Cancer and Prostatic Diseases

Article Title: The cannabinoid WIN 55,212-2 prevents neuroendocrine differentiation of LNCaP prostate cancer cells

doi: 10.1038/pcan.2016.19

Figure Lengend Snippet: Effect of WIN 55,212-2 on IL-6-induced NE differentiation. NE differentiation of LNCaP cells was induced by incubation with IL-6 (20 ng ml 1 ) -supplemented medium for 6 days. Cells were treated with vehicle (Vhc), 3 μ M of WIN (WIN) or 1 μ M of the CB1inverse agonist SR1 and 1 μ M of the CB2 inverse agonist SR2 (SR1/SR2) for 6 days. Levels of the phosphorylated and total forms of Akt, AMPK and acetyl CoA carboxylase (ACC) proteins were determined by western blot. GADPH was probed as a loading control. The image is representative of other three experiments. IL, interleukin; NE, neuroendocrine.

Article Snippet: The CB1 antagonist SR-141716 and the CB2 antagonist SR-144528 were kindly provided from Sanofi-Synthelabo (Montpellier, France).

Techniques: Incubation, Western Blot, Control

NE differentiation of LNCaP cells induces a decrease of cannabinoid receptors CB1 and CB2 expression. ( a ) Cannabinoid receptors CB1 and CB2 mRNAs levels in LNCaP control and NE cells analyzed by quantitative PCR according to the Materials and Methods section. ( b ) LNCaP cells were serum-deprived for 2, 4 and 6 days and levels of the cannabinoid receptor CB2 protein and NE markers neuron-specific enolase (NSE) and βIII tubulin (βIII Tub) were analyzed by western blot. GADPH was probed as a loading control. The image is representative of other three experiments. Densitiometric analysis of the western blot bands of CB2 is shown on the left. ( c ) LNCaP control and NE cells were treated with vehicle (Vhc), 3 μ M of WIN 55-212,2 (WIN) 1 μ M of the cannabinoid receptor inverse agonists SR1 and SR2 (SR1/SR2) or combined together for 6 days. Levels of CB1 and CB2 mRNA were analyzed by quantitative PCR according to the Materials and Methods section. The data shown are the means±s.d. of three different experiments (* P< 0.05; ** P< 0.01 versus control cells and # P< 0.05 versus NE cells, compared by the Student's t -test). NE, neuroendocrine.

Journal: Prostate Cancer and Prostatic Diseases

Article Title: The cannabinoid WIN 55,212-2 prevents neuroendocrine differentiation of LNCaP prostate cancer cells

doi: 10.1038/pcan.2016.19

Figure Lengend Snippet: NE differentiation of LNCaP cells induces a decrease of cannabinoid receptors CB1 and CB2 expression. ( a ) Cannabinoid receptors CB1 and CB2 mRNAs levels in LNCaP control and NE cells analyzed by quantitative PCR according to the Materials and Methods section. ( b ) LNCaP cells were serum-deprived for 2, 4 and 6 days and levels of the cannabinoid receptor CB2 protein and NE markers neuron-specific enolase (NSE) and βIII tubulin (βIII Tub) were analyzed by western blot. GADPH was probed as a loading control. The image is representative of other three experiments. Densitiometric analysis of the western blot bands of CB2 is shown on the left. ( c ) LNCaP control and NE cells were treated with vehicle (Vhc), 3 μ M of WIN 55-212,2 (WIN) 1 μ M of the cannabinoid receptor inverse agonists SR1 and SR2 (SR1/SR2) or combined together for 6 days. Levels of CB1 and CB2 mRNA were analyzed by quantitative PCR according to the Materials and Methods section. The data shown are the means±s.d. of three different experiments (* P< 0.05; ** P< 0.01 versus control cells and # P< 0.05 versus NE cells, compared by the Student's t -test). NE, neuroendocrine.

Article Snippet: The CB1 antagonist SR-141716 and the CB2 antagonist SR-144528 were kindly provided from Sanofi-Synthelabo (Montpellier, France).

Techniques: Expressing, Control, Real-time Polymerase Chain Reaction, Western Blot

Proposed mechanism for WIN-induced inhibition of prostate LNCaP cells NE differentiation. The synthetic cannabinoid agonist WIN 55,212-2 (WIN) preserves the levels of the cannabinoid receptor CB2. This results in inhibition of the PI3K/Akt pathway. Akt signals through two pathways, activation of mTOR and inhibition of AMPK. The inhibition of Akt by the cannabinoid WIN produces inhibition of mTOR and activation of AMPK. Both phenomena cause inhibition of NE differentiation, although mTOR has a minor contribution than AMPK. ACC, acetyl CoA carboxylase; AMPK, AMP-dependent protein kinase; NE, neuroendocrine.

Journal: Prostate Cancer and Prostatic Diseases

Article Title: The cannabinoid WIN 55,212-2 prevents neuroendocrine differentiation of LNCaP prostate cancer cells

doi: 10.1038/pcan.2016.19

Figure Lengend Snippet: Proposed mechanism for WIN-induced inhibition of prostate LNCaP cells NE differentiation. The synthetic cannabinoid agonist WIN 55,212-2 (WIN) preserves the levels of the cannabinoid receptor CB2. This results in inhibition of the PI3K/Akt pathway. Akt signals through two pathways, activation of mTOR and inhibition of AMPK. The inhibition of Akt by the cannabinoid WIN produces inhibition of mTOR and activation of AMPK. Both phenomena cause inhibition of NE differentiation, although mTOR has a minor contribution than AMPK. ACC, acetyl CoA carboxylase; AMPK, AMP-dependent protein kinase; NE, neuroendocrine.

Article Snippet: The CB1 antagonist SR-141716 and the CB2 antagonist SR-144528 were kindly provided from Sanofi-Synthelabo (Montpellier, France).

Techniques: Inhibition, Activation Assay

Review

Structured Review

Images

1) Product Images from "Intranasal Treatment with Cannabinoid 2 Receptor Agonist HU-308 Ameliorates Cold Sensitivity in Mice with Traumatic Trigeminal Neuropathic Pain."

Similar Products

Image Search Results