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WIN55,212‐2 increases blood pressure in a <t>B1R‐dependent</t> manner. (a) Experimental schematic showing acute intravenous injection of WIN55,212‐2 (400 μg/kg) via the jugular vein, followed by blood pressure measurement and tissue collection. (b) Mean arterial pressure (MAP) response to WIN55,212‐2 in wild‐type (WT) and <t>B1</t> <t>receptor</t> knockout (B1RKO) mice. WIN55,212‐2 significantly increased MAP in WT but not in B1RKO mice, suggesting a B1R‐dependent mechanism. Data are presented as mean ± SD. Repeated measures 2‐way ANOVA, n = 3–6 mice/group.

B1r, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/b1r/Anti-B1+Bradykinin+Receptor+(BDKRB1)+Antibody/pmc12450756-70-7-10
Average 93 stars, based on 23 article reviews

b1r - by Bioz Stars, 2026-09

93/100 stars

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1) Product Images from "Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice"

Article Title: Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice

Journal: Physiological Reports

doi: 10.14814/phy2.70579

WIN55,212‐2 increases blood pressure in a B1R‐dependent manner. (a) Experimental schematic showing acute intravenous injection of WIN55,212‐2 (400 μg/kg) via the jugular vein, followed by blood pressure measurement and tissue collection. (b) Mean arterial pressure (MAP) response to WIN55,212‐2 in wild‐type (WT) and B1 receptor knockout (B1RKO) mice. WIN55,212‐2 significantly increased MAP in WT but not in B1RKO mice, suggesting a B1R‐dependent mechanism. Data are presented as mean ± SD. Repeated measures 2‐way ANOVA, n = 3–6 mice/group.

Figure Legend Snippet: WIN55,212‐2 increases blood pressure in a B1R‐dependent manner. (a) Experimental schematic showing acute intravenous injection of WIN55,212‐2 (400 μg/kg) via the jugular vein, followed by blood pressure measurement and tissue collection. (b) Mean arterial pressure (MAP) response to WIN55,212‐2 in wild‐type (WT) and B1 receptor knockout (B1RKO) mice. WIN55,212‐2 significantly increased MAP in WT but not in B1RKO mice, suggesting a B1R‐dependent mechanism. Data are presented as mean ± SD. Repeated measures 2‐way ANOVA, n = 3–6 mice/group.

Techniques Used: Injection, Knock-Out

Brain and cardiac expression of B1R, CB1R, and oxidative stress following WIN55,212‐2 administration. Representative images and quantification of B1R (a), CB1R (b), and oxidative stress (DHE, c) expression in the paraventricular nucleus (PVN) of the hypothalamus. Images and corresponding expressions of B1R (d), CB1R (e), and oxidative stress (DHE, f) in heart tissue. WIN55,212‐2 increased CB1R expression and oxidative stress in WT but not B1RKO mice in both brain and heart. Data are presented as mean ± SD. n = 3–6 mice/group; 2‐way ANOVA with Tukey's multiple comparisons test.

Figure Legend Snippet: Brain and cardiac expression of B1R, CB1R, and oxidative stress following WIN55,212‐2 administration. Representative images and quantification of B1R (a), CB1R (b), and oxidative stress (DHE, c) expression in the paraventricular nucleus (PVN) of the hypothalamus. Images and corresponding expressions of B1R (d), CB1R (e), and oxidative stress (DHE, f) in heart tissue. WIN55,212‐2 increased CB1R expression and oxidative stress in WT but not B1RKO mice in both brain and heart. Data are presented as mean ± SD. n = 3–6 mice/group; 2‐way ANOVA with Tukey's multiple comparisons test.

Techniques Used: Expressing

Effects of WIN55,212‐2 on oxidative stress and mitochondrial function in H9c2 cardiomyocytes and human cardiac fibroblasts. Quantification of DHE (a), B1R (b), CB1R (c), mitochondrial superoxide (MitoSOX, d), and mitochondrial membrane potential (TMRE, e) in H9c2 cardiomyocytes following WIN55,212‐2 treatment. WIN55,212‐2 in H9c2 cells increased oxidative stress, B1R, and CB1R expression, and decreased mitochondrial membrane potential. Corresponding quantification of DHE (f), B1R (g), CB1R (h), MitoSOX (i), and TMRE (j) in human cardiac fibroblasts. Unlike H9c2 cells, WIN55,212‐2 did not significantly alter TMRE in HCFs, despite increasing oxidative stress and receptor expression. Data are presented as mean ± SD. n = 3–6 independent cultures/group: One‐way ANOVA followed by Tukey's multiple comparisons.

Figure Legend Snippet: Effects of WIN55,212‐2 on oxidative stress and mitochondrial function in H9c2 cardiomyocytes and human cardiac fibroblasts. Quantification of DHE (a), B1R (b), CB1R (c), mitochondrial superoxide (MitoSOX, d), and mitochondrial membrane potential (TMRE, e) in H9c2 cardiomyocytes following WIN55,212‐2 treatment. WIN55,212‐2 in H9c2 cells increased oxidative stress, B1R, and CB1R expression, and decreased mitochondrial membrane potential. Corresponding quantification of DHE (f), B1R (g), CB1R (h), MitoSOX (i), and TMRE (j) in human cardiac fibroblasts. Unlike H9c2 cells, WIN55,212‐2 did not significantly alter TMRE in HCFs, despite increasing oxidative stress and receptor expression. Data are presented as mean ± SD. n = 3–6 independent cultures/group: One‐way ANOVA followed by Tukey's multiple comparisons.

Techniques Used: Membrane, Expressing

WIN55,212‐2‐induced effects in primary neurons are mediated in part by B1R. Quantification of CB1R (a), DHE (b), and B1R (c) expression following WIN55,212‐2 with or without B1R antagonist pretreatment. WIN55,212‐2 increased CB1R, B1R and oxidative stress, and was attenuated by pharmacological inhibition of B1R. Mitochondrial superoxide (MitoSOX, d) and membrane potential (TMRE, e) showed impaired mitochondrial function with WIN55,212‐2, partially rescued by B1R antagonism. Data are presented as mean ± SD. n = 5–8 independent cultures/group: One‐way ANOVA followed by Tukey's multiple comparisons.

Figure Legend Snippet: WIN55,212‐2‐induced effects in primary neurons are mediated in part by B1R. Quantification of CB1R (a), DHE (b), and B1R (c) expression following WIN55,212‐2 with or without B1R antagonist pretreatment. WIN55,212‐2 increased CB1R, B1R and oxidative stress, and was attenuated by pharmacological inhibition of B1R. Mitochondrial superoxide (MitoSOX, d) and membrane potential (TMRE, e) showed impaired mitochondrial function with WIN55,212‐2, partially rescued by B1R antagonism. Data are presented as mean ± SD. n = 5–8 independent cultures/group: One‐way ANOVA followed by Tukey's multiple comparisons.

Techniques Used: Expressing, Inhibition, Membrane

Incubation:

Article Title: Inhibition of kinin B1 receptor alleviates SARS-CoV-2 induced long-lasting cardiovascular complications
Article Snippet: .. Then, sections were incubated with antibodies against SARS-CoV-2 (BEI, NR-10361, 1:500), B1R (Alomone, ABR-011, 1:250), wheat germ agglutin (WGA, Invitrogen, W11261 , 5ug/ml), alpha-smooth muscle actin (α-SMA; Novus, NB300–978, 1:500), Ki67 (Abcam, AB15580, 1:100), TUNEL (Invitrogen, C10619 ), CD3 (Invitrogen, 14–0032-82, 1:500), CD20 (Invitrogen, PA5–16701, 1:500), CD68 (Abcam, AB31630, 1:500), connexin 43 (CX43; Sigma-Aldrich, C6219, 1:500), CXCR4 (Invitrogen, PA3305, 1:500), IL-1B (Abcam, ab2105, 1:500), or caspase-1 (Invitrogen, MA5–16215, 1:500) at 4°C overnight. .. The next day, sections were washed with PBS + 0.2% Tween-20 and incubated with appropriate Alexa fluor conjugated secondary antibodies (ThermoFisher, 1:1000 dilution) for 1h at room temperature.

Article Title: Targeting Kinin B1R Attenuates Hypertension Through AT1R-Dependent Mechanisms
Article Snippet: .. Then sections were incubated with B1R (Alomone ABR-011 or LSBio LS-C54590, 1:250), AT1R (Alomone AAR-011, 1:250), vGLUT2 (Abcam ab216463, 1:500), cFOS (Cell signaling 2250S, 1:500), NeuN (Sigma MAB377, 1:500), TMEM119 (Synaptic Systems 400- 002, 1:500), PSD-95 (Invitrogen MA1-046, 1:500), Tyrosine hydroxylase (Sigma AB152, 1:500), GFAP (Thermo 14-9892-82), homer1 (synaptic systems 160-003, 1:500), synaptophysin1 (Synaptic systems 101-011, 1:500), IBA1 (Wako 011-27991, 1:1000), and HuC/HuD (Invitrogen A21271, 1:500) antibodies at 4°C overnight in 1xPBS containing 1% normal donkey serum and 0.1% Tween20. ..

Article Title: Emerging Role of Kinin B1 Receptor in Persistent Neuroinflammation and Neuropsychiatric Symptoms in Mice Following Recovery from SARS-CoV-2 Infection
Article Snippet: .. Free-floating brain sections were washed with PBS and blocked with 5% donkey serum in 1 × PBS containing 0.2% Tween-20 for 1 h. They were then incubated with appropriate primary antibodies: B1R (#ABR-011, lot An-01, Alomone labs, Jerusalem, Israel; 1:500 dilution), IL-6 (12912S, lot 2, Cell Signaling Technologies, Beverly, MA, USA; 1:500) TNF (11948S, lot 5, Cell Signaling Technologies, Beverly, MA, USA; 1:500), AT1R (#AAR-011, lot AAR011AN2002, Alomone labs, Jerusalem, Israel; 1:500), NeuN (MAB377, lot 3808682, Millipore Sigma, Burlington, MA, USA; 1:500), SARS-CoV antiserum (NR-10362, BEI resources, Manassas, VA, USA; 1:500), and dsRNA (Ab01299-23.0, absolute antibody, Boston, MA, USA; 1:500). .. The next day, sections were washed with PBS + 0.2% Tween-20 and incubated with appropriate Alexa flour conjugated secondary antibodies (ThermoFisher, Hanover Park, IL, USA; 1:1000 dilution) for 1 h at room temperature, followed by DAPI nuclear stain.

Article Title: Emerging Role of Kinin B1 Receptor in Persistent Neuroinflammation and Neuropsychiatric Symptoms in Mice Following Recovery from SARS-CoV-2 Infection.
Article Snippet: .. Free-floating brain sections were washed with PBS and blocked with 5% donkey serum in 1×PBS containing 0.2% Tween-20 for 1 h. They were then incubated with appropriate primary antibodies: B1R (#ABR-011, lot An-01, Alomone labs, Jerusalem, Israel; 1:500 dilution), IL-6 (12912S, lot 2, Cell Signaling Technologies, Beverly, MA, USA; 1:500) TNF (11948S, lot 5, Cell Signaling Technologies, Beverly, MA, USA; 1:500), AT1R (#AAR-011, lot AAR011AN2002, Alomone labs, Jerusalem, Israel; 1:500), NeuN (MAB377, lot 3808682, Millipore Sigma, Burlington, MA, USA; 1:500), SARS-CoV antiserum (NR10362, BEI resources, Manassas, VA, USA; 1:500), and dsRNA (Ab01299-23.0, absolute antibody, Boston, MA, USA; 1:500). .. The next day, sections were washed with PBS + 0.2% Tween-20 and incubated with appropriate Alexa flour conjugated secondary antibodies (ThermoFisher, Hanover Park, IL, USA; 1:1000 dilution) for 1 h at room temperature, followed by DAPI nuclear stain.

Article Title: Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice
Article Snippet: Samples were washed 3 times with 1×PBS and blocked with 2% normal donkey serum (017‐000‐121, Jackson ImmunoResearch), 0.05% Tween 20 (P9416, Sigma), 50 mM glycine (G8898, Sigma), 0.1% Triton‐X 100 (X100, Sigma), and 0.01% BSA (A9647, Sigma) in 1×PBS for 60 min at room temperature. .. Samples were incubated at 4°C overnight in B1R (1:250, ABR‐011, Alomone Labs), CB1R (1:200, custom), or MAP2 (1:500, NBP3‐05552, Novus Biologicals). ..

Article Title: Kinin B1 Receptor Mediates Bidirectional Interaction between Neuroinflammation and Oxidative Stress
Article Snippet: .. Cells were blocked with 2.5% donkey serum in 1 X PBS containing 0.2% Tween20 for 1 h before being incubated overnight at 4 °C with appropriate primary antibodies that have been validated in knockout mouse tissues, MAP2 antibody (NBP3-05552, lot 16278-011222, Novus Biologicals, 1:500), or B1R (#ABR-011, lot An-01, Alomone labs, 1:500 dilution) [ ]. .. Following this, the cells were rinsed with 1 X PBS + 0.2% Tween20 three times then incubated with appropriate Alexa Fluor conjugated secondary antibodies (Life Technologies, 1:1000 dilution) for 1 h at room temperature.

Whole Genome Amplification:

TUNEL Assay:

Blocking Assay:

Article Title: Electroacupuncture alleviates diabetes-induced mechanical allodynia and downregulates bradykinin B1 receptor expression in spinal cord dorsal horn
Article Snippet: Objective Diabetic neuropathic pain (DNP) is one of the most prevalent symptoms of diabetes.. The alteration of proteins in the spinal cord dorsal horn (SCDH) plays a significant role in the genesis and the development of DNP.. Our previous study has shown electroacupuncture could effectively relieve DNP.

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Journal: Physiological Reports

Article Title: Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice

doi: 10.14814/phy2.70579

Figure Lengend Snippet: WIN55,212‐2 increases blood pressure in a B1R‐dependent manner. (a) Experimental schematic showing acute intravenous injection of WIN55,212‐2 (400 μg/kg) via the jugular vein, followed by blood pressure measurement and tissue collection. (b) Mean arterial pressure (MAP) response to WIN55,212‐2 in wild‐type (WT) and B1 receptor knockout (B1RKO) mice. WIN55,212‐2 significantly increased MAP in WT but not in B1RKO mice, suggesting a B1R‐dependent mechanism. Data are presented as mean ± SD. Repeated measures 2‐way ANOVA, n = 3–6 mice/group.

Article Snippet: Samples were incubated at 4°C overnight in B1R (1:250, ABR‐011, Alomone Labs), CB1R (1:200, custom), or MAP2 (1:500, NBP3‐05552, Novus Biologicals).

Techniques: Injection, Knock-Out

Journal: Physiological Reports

Article Title: Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice

doi: 10.14814/phy2.70579

Figure Lengend Snippet: Brain and cardiac expression of B1R, CB1R, and oxidative stress following WIN55,212‐2 administration. Representative images and quantification of B1R (a), CB1R (b), and oxidative stress (DHE, c) expression in the paraventricular nucleus (PVN) of the hypothalamus. Images and corresponding expressions of B1R (d), CB1R (e), and oxidative stress (DHE, f) in heart tissue. WIN55,212‐2 increased CB1R expression and oxidative stress in WT but not B1RKO mice in both brain and heart. Data are presented as mean ± SD. n = 3–6 mice/group; 2‐way ANOVA with Tukey's multiple comparisons test.

Article Snippet: Samples were incubated at 4°C overnight in B1R (1:250, ABR‐011, Alomone Labs), CB1R (1:200, custom), or MAP2 (1:500, NBP3‐05552, Novus Biologicals).

Techniques: Expressing

Journal: Physiological Reports

Article Title: Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice

doi: 10.14814/phy2.70579

Figure Lengend Snippet: Effects of WIN55,212‐2 on oxidative stress and mitochondrial function in H9c2 cardiomyocytes and human cardiac fibroblasts. Quantification of DHE (a), B1R (b), CB1R (c), mitochondrial superoxide (MitoSOX, d), and mitochondrial membrane potential (TMRE, e) in H9c2 cardiomyocytes following WIN55,212‐2 treatment. WIN55,212‐2 in H9c2 cells increased oxidative stress, B1R, and CB1R expression, and decreased mitochondrial membrane potential. Corresponding quantification of DHE (f), B1R (g), CB1R (h), MitoSOX (i), and TMRE (j) in human cardiac fibroblasts. Unlike H9c2 cells, WIN55,212‐2 did not significantly alter TMRE in HCFs, despite increasing oxidative stress and receptor expression. Data are presented as mean ± SD. n = 3–6 independent cultures/group: One‐way ANOVA followed by Tukey's multiple comparisons.

Article Snippet: Samples were incubated at 4°C overnight in B1R (1:250, ABR‐011, Alomone Labs), CB1R (1:200, custom), or MAP2 (1:500, NBP3‐05552, Novus Biologicals).

Techniques: Membrane, Expressing

Journal: Physiological Reports

Article Title: Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice

doi: 10.14814/phy2.70579

Figure Lengend Snippet: WIN55,212‐2‐induced effects in primary neurons are mediated in part by B1R. Quantification of CB1R (a), DHE (b), and B1R (c) expression following WIN55,212‐2 with or without B1R antagonist pretreatment. WIN55,212‐2 increased CB1R, B1R and oxidative stress, and was attenuated by pharmacological inhibition of B1R. Mitochondrial superoxide (MitoSOX, d) and membrane potential (TMRE, e) showed impaired mitochondrial function with WIN55,212‐2, partially rescued by B1R antagonism. Data are presented as mean ± SD. n = 5–8 independent cultures/group: One‐way ANOVA followed by Tukey's multiple comparisons.

Article Snippet: Samples were incubated at 4°C overnight in B1R (1:250, ABR‐011, Alomone Labs), CB1R (1:200, custom), or MAP2 (1:500, NBP3‐05552, Novus Biologicals).

Techniques: Expressing, Inhibition, Membrane

( A ) Expression of B1R in human PCa cell lines assessed by qPCR ( n = 2–3). ( B ) B1R gene expression analysis of the human PCa cell line-derived xenografts (CDX) in Nu/Nu mice (four CDX models from Charles River). Affymetrix data are presented as log2 (GCRMA), with higher values indicating increased B1R expression. ( C ) B1R expression in clinical human PCa tissue samples (tumor and matched normal-adjacent; n = 14) analyzed by qPCR. * Indicates p -value < 0.05 according to paired Student t -test. ( D ) Representative pictures taken from cores of normal, PIN, and Gleason 3–4–5 foci, and of metastatic PCa in peripancreatic ganglia. Magnification 20×, scale bar represents 100 µm. Semi-quantitative immunoscores (as per scoring scale shown in ) of normal ( n = 95), PIN ( n = 71), Gleason 3 ( n = 126), 4 ( n = 64), 5 ( n = 18), * indicates p -value < 0.05 and *** <0.001 according to a one-way ANOVA with Tukey’s multiple comparison tests. ( E ) Histogram views and Pearson r correlation coefficients of hB1R gene expression according to tumor Gleason score from The Cancer Genome Atlas (TCGA) firehose legacy and the Memorial Sloan Kettering Cancer Center (MSKCC) 2010 datasets, both retrieved using cBioportal tool. ** Indicates p -value < 0.01 according to Tukey’s multiple comparison tests. ( F ) Kaplan–Meier survival curves according to prostate cancer B1R (BDKRB1) mRNA expression levels for MSKCC Cancer Cell 2010 dataset (high and low, respectively > or <z-score 2.25 compared to normal tissues) and TCGA Firehose Legacy (high and low, respectively > or <z-score 1.75 vs. diploids) accessed by cBioportal. Log-rank test p -values are indicated within each graph.

Journal: Pharmaceutics

Article Title: Theranostic Potential of a New 64 Cu-Labeled NOTA-R954 Peptide Conjugate for Kinin B1R Expressing Prostate Cancer

doi: 10.3390/pharmaceutics17091215

Figure Lengend Snippet: ( A ) Expression of B1R in human PCa cell lines assessed by qPCR ( n = 2–3). ( B ) B1R gene expression analysis of the human PCa cell line-derived xenografts (CDX) in Nu/Nu mice (four CDX models from Charles River). Affymetrix data are presented as log2 (GCRMA), with higher values indicating increased B1R expression. ( C ) B1R expression in clinical human PCa tissue samples (tumor and matched normal-adjacent; n = 14) analyzed by qPCR. * Indicates p -value < 0.05 according to paired Student t -test. ( D ) Representative pictures taken from cores of normal, PIN, and Gleason 3–4–5 foci, and of metastatic PCa in peripancreatic ganglia. Magnification 20×, scale bar represents 100 µm. Semi-quantitative immunoscores (as per scoring scale shown in ) of normal ( n = 95), PIN ( n = 71), Gleason 3 ( n = 126), 4 ( n = 64), 5 ( n = 18), * indicates p -value < 0.05 and *** <0.001 according to a one-way ANOVA with Tukey’s multiple comparison tests. ( E ) Histogram views and Pearson r correlation coefficients of hB1R gene expression according to tumor Gleason score from The Cancer Genome Atlas (TCGA) firehose legacy and the Memorial Sloan Kettering Cancer Center (MSKCC) 2010 datasets, both retrieved using cBioportal tool. ** Indicates p -value < 0.01 according to Tukey’s multiple comparison tests. ( F ) Kaplan–Meier survival curves according to prostate cancer B1R (BDKRB1) mRNA expression levels for MSKCC Cancer Cell 2010 dataset (high and low, respectively > or or

Article Snippet: B1R gene expression analysis of the human PCa cell line-derived xenografts (four CDX models) in Nu/Nu mice was conducted by Charles River custom services (Freiburg, Germany) [ ].

Techniques: Expressing, Gene Expression, Derivative Assay, Comparison

Chemical structure and metabolic stability of the novel B1R-targeting theranostic antagonist, 64 Cu/NOTA-βAla-R954. ( A ) Theranostic peptide sequence. ( B ) Radiolabeling of NOTA-βAla-R954 to 64 Cu. Representative radio-UPLC chromatograms are shown. ( C , D ) Radiolysis evaluation of 64 Cu/NOTA-βAla-R954 at time point 0 and 24 h assessed by radio-UPLC and radio-TLC, respectively. Representative experiments are shown. ( E ) Ex vivo metabolic stability of 64 Cu/NOTA-βAla-R954 following a 24 h incubation at 37 °C in undiluted mouse and human plasma. Representative radio-UPLC chromatograms are shown ( n = 2). ( F ) UPLC radiometric chromatogram illustrating the complete in vivo stability of the 64 Cu/NOTA-βAla-R954 (appearing as an intact form—single peak—in blood and urine extracts) following I.V. injection in normal mice. Blood and urine were collected 90 min after bolus I.V. administration ( n = 2).

Journal: Pharmaceutics

Article Title: Theranostic Potential of a New 64 Cu-Labeled NOTA-R954 Peptide Conjugate for Kinin B1R Expressing Prostate Cancer

doi: 10.3390/pharmaceutics17091215

Figure Lengend Snippet: Chemical structure and metabolic stability of the novel B1R-targeting theranostic antagonist, 64 Cu/NOTA-βAla-R954. ( A ) Theranostic peptide sequence. ( B ) Radiolabeling of NOTA-βAla-R954 to 64 Cu. Representative radio-UPLC chromatograms are shown. ( C , D ) Radiolysis evaluation of 64 Cu/NOTA-βAla-R954 at time point 0 and 24 h assessed by radio-UPLC and radio-TLC, respectively. Representative experiments are shown. ( E ) Ex vivo metabolic stability of 64 Cu/NOTA-βAla-R954 following a 24 h incubation at 37 °C in undiluted mouse and human plasma. Representative radio-UPLC chromatograms are shown ( n = 2). ( F ) UPLC radiometric chromatogram illustrating the complete in vivo stability of the 64 Cu/NOTA-βAla-R954 (appearing as an intact form—single peak—in blood and urine extracts) following I.V. injection in normal mice. Blood and urine were collected 90 min after bolus I.V. administration ( n = 2).

Article Snippet: B1R gene expression analysis of the human PCa cell line-derived xenografts (four CDX models) in Nu/Nu mice was conducted by Charles River custom services (Freiburg, Germany) [ ].

Techniques: Sequencing, Radioactivity, Ex Vivo, Incubation, Clinical Proteomics, In Vivo, Injection

Efficacy of 64 Cu/NOTA-βAla-R954 for detecting PCa by PET imaging. ( A ) Biodistribution of intravenous 64 Cu/NOTA-βAla-R954 (5–10 MBq) in normal male BALB/c mice at 1 and 4 h post-injection (p.i.) ( n = 4 mice per group). ( B ) Representative micro-PET images of PC3 tumor-bearing nude mouse acquired 1 h post-injection of 64 Cu/NOTA-βAla-R954 (7 MBq) using a LabPET8 scanner ( left ). Tumors are indicated by yellow arrows. Histographic representation of calculated ID/g (%) values of intravenous 64 Cu/NOTA-βAla-R954 (6–7 MBq) at 1 h post-injection in PC3 tumor-bearing nude mice pretreated (10 min before) or not with R954 (0.5–1 mg/kg) ( right ). Mean ± SEM are shown; n = 4 tumors from 2 to 3 mice, ** p < 0.01 vs. corresponding blockade group, using unpaired two-tailed Student’s t -test. IHC confirmed high expression of B1R in harvested tumoral tissues of PC3-bearing mice ( upper-right panel ). IHC staining of B1R was performed on 5 µm thick sections of formalin fixed/paraffin-embedded tissues from subcutaneous PC3 human xenograft tumors in athymic nude mice. IHC analysis was performed using the anti-hB1R antiserum AS434 (1:500 dilution). Negative control with rabbit pre-immune serum (1:500) showed no staining. Nuclei were counterstained with hematoxylin. Optical magnification is indicated in the bottom-left corner of each image. ( C ) PC3 tumor-to-normal-organ ratios for 64 Cu/NOTA-βAla-R954 (~6–7 MBq) at 1 h and 20 h post-injections. Mean ± SEM are shown; n = 4 tumors from 2 to 3 mice. * p < 0.05 vs. corresponding ratio at 1 h, using Mann–Whitney U test.

Journal: Pharmaceutics

Article Title: Theranostic Potential of a New 64 Cu-Labeled NOTA-R954 Peptide Conjugate for Kinin B1R Expressing Prostate Cancer

doi: 10.3390/pharmaceutics17091215

Figure Lengend Snippet: Efficacy of 64 Cu/NOTA-βAla-R954 for detecting PCa by PET imaging. ( A ) Biodistribution of intravenous 64 Cu/NOTA-βAla-R954 (5–10 MBq) in normal male BALB/c mice at 1 and 4 h post-injection (p.i.) ( n = 4 mice per group). ( B ) Representative micro-PET images of PC3 tumor-bearing nude mouse acquired 1 h post-injection of 64 Cu/NOTA-βAla-R954 (7 MBq) using a LabPET8 scanner ( left ). Tumors are indicated by yellow arrows. Histographic representation of calculated ID/g (%) values of intravenous 64 Cu/NOTA-βAla-R954 (6–7 MBq) at 1 h post-injection in PC3 tumor-bearing nude mice pretreated (10 min before) or not with R954 (0.5–1 mg/kg) ( right ). Mean ± SEM are shown; n = 4 tumors from 2 to 3 mice, ** p < 0.01 vs. corresponding blockade group, using unpaired two-tailed Student’s t -test. IHC confirmed high expression of B1R in harvested tumoral tissues of PC3-bearing mice ( upper-right panel ). IHC staining of B1R was performed on 5 µm thick sections of formalin fixed/paraffin-embedded tissues from subcutaneous PC3 human xenograft tumors in athymic nude mice. IHC analysis was performed using the anti-hB1R antiserum AS434 (1:500 dilution). Negative control with rabbit pre-immune serum (1:500) showed no staining. Nuclei were counterstained with hematoxylin. Optical magnification is indicated in the bottom-left corner of each image. ( C ) PC3 tumor-to-normal-organ ratios for 64 Cu/NOTA-βAla-R954 (~6–7 MBq) at 1 h and 20 h post-injections. Mean ± SEM are shown; n = 4 tumors from 2 to 3 mice. * p < 0.05 vs. corresponding ratio at 1 h, using Mann–Whitney U test.

Article Snippet: B1R gene expression analysis of the human PCa cell line-derived xenografts (four CDX models) in Nu/Nu mice was conducted by Charles River custom services (Freiburg, Germany) [ ].

Techniques: Imaging, Injection, Micro-PET, Two Tailed Test, Expressing, Immunohistochemistry, Formalin-fixed Paraffin-Embedded, Negative Control, Staining, MANN-WHITNEY

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b1r (Alomone Labs)

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1) Product Images from "Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice"

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