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inos-specific inhibitor n-[3-(aminomethyl)benzyl]acetamidine (1400w)  (Cayman Chemical)


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    Structured Review

    Cayman Chemical inos-specific inhibitor n-[3-(aminomethyl)benzyl]acetamidine (1400w)
    Viability loss of glioblastoma cells after a photodynamic challenge. (a) ALA-treated U87 cells were exposed to the indicated light fluences in the absence (○) or presence of 25 μM 1400W (□) or 25 μM cPTIO (△). After irradiation, cells were switched to serum-containing medium, and after 20 h of dark incubation, examined for viability by MTT assay. (b) U251 cells were sensitized identically to U87 cells, irradiated in the absence (○) vs. presence of 25 μM 1400W (□) or 1 mM <t>L-NAME</t> (△), and then examined for viability after 20 h in the dark. Also represented in (a) and (b) are ALA-only or light-only controls (x). Plotted values in (a) and (b) are means ± SEM (n=3); W, cP, and N denote 1400W, cPTIO, and L-NAME, respectively.
    Inos Specific Inhibitor N [3 (Aminomethyl)benzyl]Acetamidine (1400w), 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/product/inos+specific+inhibitor+1400w/1400w/pmc05161550-41-5-32
    Average 90 stars, based on 1 article reviews
    inos-specific inhibitor n-[3-(aminomethyl)benzyl]acetamidine (1400w) - by Bioz Stars, 2026-09
    90/100 stars

    Images

    1) Product Images from "Antagonistic Effects of Endogenous Nitric Oxide in a Glioblastoma Photodynamic Therapy Model"

    Article Title: Antagonistic Effects of Endogenous Nitric Oxide in a Glioblastoma Photodynamic Therapy Model

    Journal: Photochemistry and photobiology

    doi: 10.1111/php.12636

    Viability loss of glioblastoma cells after a photodynamic challenge. (a) ALA-treated U87 cells were exposed to the indicated light fluences in the absence (○) or presence of 25 μM 1400W (□) or 25 μM cPTIO (△). After irradiation, cells were switched to serum-containing medium, and after 20 h of dark incubation, examined for viability by MTT assay. (b) U251 cells were sensitized identically to U87 cells, irradiated in the absence (○) vs. presence of 25 μM 1400W (□) or 1 mM L-NAME (△), and then examined for viability after 20 h in the dark. Also represented in (a) and (b) are ALA-only or light-only controls (x). Plotted values in (a) and (b) are means ± SEM (n=3); W, cP, and N denote 1400W, cPTIO, and L-NAME, respectively.
    Figure Legend Snippet: Viability loss of glioblastoma cells after a photodynamic challenge. (a) ALA-treated U87 cells were exposed to the indicated light fluences in the absence (○) or presence of 25 μM 1400W (□) or 25 μM cPTIO (△). After irradiation, cells were switched to serum-containing medium, and after 20 h of dark incubation, examined for viability by MTT assay. (b) U251 cells were sensitized identically to U87 cells, irradiated in the absence (○) vs. presence of 25 μM 1400W (□) or 1 mM L-NAME (△), and then examined for viability after 20 h in the dark. Also represented in (a) and (b) are ALA-only or light-only controls (x). Plotted values in (a) and (b) are means ± SEM (n=3); W, cP, and N denote 1400W, cPTIO, and L-NAME, respectively.

    Techniques Used: Irradiation, Incubation, MTT Assay

    Apoptotic photokilling of U87 cells and effects of NOS inhibitors. U87 cells at 40–45% confluence were treated with 1 mM ALA without or with a NOS inhibitor (25 μM 1400W or 1 mM L-NAME), and then irradiated (1 J/cm2). After 4 h of follow-up dark incubation, the cells were treated with Annexin V-FITC and Propidium Iodide (PI) according to supplier recommendations. Camptothecin (CPT, 25 μM) served as a maximum apoptosis standard. Extent of staining was quantified using a plate reater with excitation/emission wavelengths of 485/535 nm for Annexin V-FITC and 560/595 nm for PI. Less than 5% PI staining was detected for any of the treatment conditions.
    Figure Legend Snippet: Apoptotic photokilling of U87 cells and effects of NOS inhibitors. U87 cells at 40–45% confluence were treated with 1 mM ALA without or with a NOS inhibitor (25 μM 1400W or 1 mM L-NAME), and then irradiated (1 J/cm2). After 4 h of follow-up dark incubation, the cells were treated with Annexin V-FITC and Propidium Iodide (PI) according to supplier recommendations. Camptothecin (CPT, 25 μM) served as a maximum apoptosis standard. Extent of staining was quantified using a plate reater with excitation/emission wavelengths of 485/535 nm for Annexin V-FITC and 560/595 nm for PI. Less than 5% PI staining was detected for any of the treatment conditions.

    Techniques Used: Irradiation, Incubation, Staining

    Images of NO accumulation in U87 cells after a photodynamic challenge. ALA-treated U87 cells were irradiated in the absence vs. presence of a NOS inhibitor as specified in Fig. 2. An ALA-only dark control without or with L-NAME (1 mM) was included. At the indicated post-irradiation times, the cells were treated with DAF-2DA (20 μM) for 20 min in the dark, and then examined by fluorescence microscopy using 488 nm excitation and 650 nm emission. Image intensities were quantified using ImageJ software. Means ± SEM of values from three separate experiments are shown.
    Figure Legend Snippet: Images of NO accumulation in U87 cells after a photodynamic challenge. ALA-treated U87 cells were irradiated in the absence vs. presence of a NOS inhibitor as specified in Fig. 2. An ALA-only dark control without or with L-NAME (1 mM) was included. At the indicated post-irradiation times, the cells were treated with DAF-2DA (20 μM) for 20 min in the dark, and then examined by fluorescence microscopy using 488 nm excitation and 650 nm emission. Image intensities were quantified using ImageJ software. Means ± SEM of values from three separate experiments are shown.

    Techniques Used: Irradiation, Control, Fluorescence, Microscopy, Software

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    Article Title: Hypoxia potentiates tumor necrosis factor-α induced expression of inducible nitric oxide synthase and cyclooxygenase-2 in white and brown adipocytes.
    Article Snippet: Adipocytes kept in normoxia or hypoxia incubators were treated with or without TNF-a (10 ng/ml) for 24 h. The cells were pre-treated either with iNOS specific inhibitor 1400W (10 mM; Cayman chemical) or COX-2 specific inhibitor NS398 (10 mM; Enzo Life Sciences, Lausen, Switzerland).

    Article Title: Nitric Oxide Interacts with Caveolin-1 to Facilitate Autophagy-Lysosome-Mediated Claudin-5 Degradation in Oxygen-Glucose Deprivation-Treated Endothelial Cells
    Article Snippet: Right after the addition of 1 mM Fe(MGD) 2 , bEND3 cells (2×10 6 ) were exposed to OGD or normoxia for 2 h at 37 °C with or without the presence of the iNOS specific inhibitor 1400W (1 μM, Cayman).



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    Viability loss of glioblastoma cells after a photodynamic challenge. (a) ALA-treated U87 cells were exposed to the indicated light fluences in the absence (○) or presence of 25 μM 1400W (□) or 25 μM cPTIO (△). After irradiation, cells were switched to serum-containing medium, and after 20 h of dark incubation, examined for viability by MTT assay. (b) U251 cells were sensitized identically to U87 cells, irradiated in the absence (○) vs. presence of 25 μM 1400W (□) or 1 mM <t>L-NAME</t> (△), and then examined for viability after 20 h in the dark. Also represented in (a) and (b) are ALA-only or light-only controls (x). Plotted values in (a) and (b) are means ± SEM (n=3); W, cP, and N denote 1400W, cPTIO, and L-NAME, respectively.
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    Viability loss of glioblastoma cells after a photodynamic challenge. (a) ALA-treated U87 cells were exposed to the indicated light fluences in the absence (○) or presence of 25 μM 1400W (□) or 25 μM cPTIO (△). After irradiation, cells were switched to serum-containing medium, and after 20 h of dark incubation, examined for viability by MTT assay. (b) U251 cells were sensitized identically to U87 cells, irradiated in the absence (○) vs. presence of 25 μM 1400W (□) or 1 mM <t>L-NAME</t> (△), and then examined for viability after 20 h in the dark. Also represented in (a) and (b) are ALA-only or light-only controls (x). Plotted values in (a) and (b) are means ± SEM (n=3); W, cP, and N denote 1400W, cPTIO, and L-NAME, respectively.
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    Viability loss of glioblastoma cells after a photodynamic challenge. (a) ALA-treated U87 cells were exposed to the indicated light fluences in the absence (○) or presence of 25 μM 1400W (□) or 25 μM cPTIO (△). After irradiation, cells were switched to serum-containing medium, and after 20 h of dark incubation, examined for viability by MTT assay. (b) U251 cells were sensitized identically to U87 cells, irradiated in the absence (○) vs. presence of 25 μM 1400W (□) or 1 mM <t>L-NAME</t> (△), and then examined for viability after 20 h in the dark. Also represented in (a) and (b) are ALA-only or light-only controls (x). Plotted values in (a) and (b) are means ± SEM (n=3); W, cP, and N denote 1400W, cPTIO, and L-NAME, respectively.
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    Image Search Results


    Presented bargraphs showcase the impact of 1400W, a potent inhibitor of inducible NOS (iNOS) on PE-induced contraction in aortic rings isolated from male and female MFS/ Cav1KO mice. Data clearly shows that pre-treatment of aortic rings with 1400W (1 µM) has no effects on PE- induced aortic contraction in age-matched male and female mice, indicating that the excessive increase in aortic endogenous NO production in the absence of Cav1 is not mediated by iNOS activation (Means ± SE, N = 6-8 mic/group, Two Way ANOVA followed by Tukey’s pairwise comparison, P ≤ 0.05).

    Journal: bioRxiv

    Article Title: Genetic Manipulation of Caveolin-1 in the Mouse Model of Marfan Syndrome Associated Aortic Root Aneurysm: Effects on Endothelial and Smooth Muscle Function

    doi: 10.1101/2024.07.29.605631

    Figure Lengend Snippet: Presented bargraphs showcase the impact of 1400W, a potent inhibitor of inducible NOS (iNOS) on PE-induced contraction in aortic rings isolated from male and female MFS/ Cav1KO mice. Data clearly shows that pre-treatment of aortic rings with 1400W (1 µM) has no effects on PE- induced aortic contraction in age-matched male and female mice, indicating that the excessive increase in aortic endogenous NO production in the absence of Cav1 is not mediated by iNOS activation (Means ± SE, N = 6-8 mic/group, Two Way ANOVA followed by Tukey’s pairwise comparison, P ≤ 0.05).

    Article Snippet: All pharmacological agonists and blockers including vasoconstricting agent phenylephrine (PE), vasodilatory agent acetylcholine (ACh), non-specific and reversible nitric oxide synthase (NOS) inhibitor L-N G -Nitro arginine methyl ester (L-NAME), and specific and potent inhibitor of inducible nitic oxide synthase (iNOS) 1400W dihydrochloride, were purchased from Sigma Millipore (Sigma Millipore, St. Louis, MO).

    Techniques: Isolation, Activation Assay, Comparison

    Viability loss of glioblastoma cells after a photodynamic challenge. (a) ALA-treated U87 cells were exposed to the indicated light fluences in the absence (○) or presence of 25 μM 1400W (□) or 25 μM cPTIO (△). After irradiation, cells were switched to serum-containing medium, and after 20 h of dark incubation, examined for viability by MTT assay. (b) U251 cells were sensitized identically to U87 cells, irradiated in the absence (○) vs. presence of 25 μM 1400W (□) or 1 mM L-NAME (△), and then examined for viability after 20 h in the dark. Also represented in (a) and (b) are ALA-only or light-only controls (x). Plotted values in (a) and (b) are means ± SEM (n=3); W, cP, and N denote 1400W, cPTIO, and L-NAME, respectively.

    Journal: Photochemistry and photobiology

    Article Title: Antagonistic Effects of Endogenous Nitric Oxide in a Glioblastoma Photodynamic Therapy Model

    doi: 10.1111/php.12636

    Figure Lengend Snippet: Viability loss of glioblastoma cells after a photodynamic challenge. (a) ALA-treated U87 cells were exposed to the indicated light fluences in the absence (○) or presence of 25 μM 1400W (□) or 25 μM cPTIO (△). After irradiation, cells were switched to serum-containing medium, and after 20 h of dark incubation, examined for viability by MTT assay. (b) U251 cells were sensitized identically to U87 cells, irradiated in the absence (○) vs. presence of 25 μM 1400W (□) or 1 mM L-NAME (△), and then examined for viability after 20 h in the dark. Also represented in (a) and (b) are ALA-only or light-only controls (x). Plotted values in (a) and (b) are means ± SEM (n=3); W, cP, and N denote 1400W, cPTIO, and L-NAME, respectively.

    Article Snippet: Chemicals, Reagents, and Antibodies The non-specific NOS inhibitor L-N G -nitroarginine methyl ester (L-NAME), iNOS-specific inhibitor N-[3-(aminomethyl)benzyl]acetamidine (1400W), NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), and NO fluorophore probe 4,5-diaminofluorescein diacetate (DAF-2DA) were obtained from Cayman Chemicals (Ann Arbor, MI).

    Techniques: Irradiation, Incubation, MTT Assay

    Apoptotic photokilling of U87 cells and effects of NOS inhibitors. U87 cells at 40–45% confluence were treated with 1 mM ALA without or with a NOS inhibitor (25 μM 1400W or 1 mM L-NAME), and then irradiated (1 J/cm2). After 4 h of follow-up dark incubation, the cells were treated with Annexin V-FITC and Propidium Iodide (PI) according to supplier recommendations. Camptothecin (CPT, 25 μM) served as a maximum apoptosis standard. Extent of staining was quantified using a plate reater with excitation/emission wavelengths of 485/535 nm for Annexin V-FITC and 560/595 nm for PI. Less than 5% PI staining was detected for any of the treatment conditions.

    Journal: Photochemistry and photobiology

    Article Title: Antagonistic Effects of Endogenous Nitric Oxide in a Glioblastoma Photodynamic Therapy Model

    doi: 10.1111/php.12636

    Figure Lengend Snippet: Apoptotic photokilling of U87 cells and effects of NOS inhibitors. U87 cells at 40–45% confluence were treated with 1 mM ALA without or with a NOS inhibitor (25 μM 1400W or 1 mM L-NAME), and then irradiated (1 J/cm2). After 4 h of follow-up dark incubation, the cells were treated with Annexin V-FITC and Propidium Iodide (PI) according to supplier recommendations. Camptothecin (CPT, 25 μM) served as a maximum apoptosis standard. Extent of staining was quantified using a plate reater with excitation/emission wavelengths of 485/535 nm for Annexin V-FITC and 560/595 nm for PI. Less than 5% PI staining was detected for any of the treatment conditions.

    Article Snippet: Chemicals, Reagents, and Antibodies The non-specific NOS inhibitor L-N G -nitroarginine methyl ester (L-NAME), iNOS-specific inhibitor N-[3-(aminomethyl)benzyl]acetamidine (1400W), NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), and NO fluorophore probe 4,5-diaminofluorescein diacetate (DAF-2DA) were obtained from Cayman Chemicals (Ann Arbor, MI).

    Techniques: Irradiation, Incubation, Staining

    Images of NO accumulation in U87 cells after a photodynamic challenge. ALA-treated U87 cells were irradiated in the absence vs. presence of a NOS inhibitor as specified in Fig. 2. An ALA-only dark control without or with L-NAME (1 mM) was included. At the indicated post-irradiation times, the cells were treated with DAF-2DA (20 μM) for 20 min in the dark, and then examined by fluorescence microscopy using 488 nm excitation and 650 nm emission. Image intensities were quantified using ImageJ software. Means ± SEM of values from three separate experiments are shown.

    Journal: Photochemistry and photobiology

    Article Title: Antagonistic Effects of Endogenous Nitric Oxide in a Glioblastoma Photodynamic Therapy Model

    doi: 10.1111/php.12636

    Figure Lengend Snippet: Images of NO accumulation in U87 cells after a photodynamic challenge. ALA-treated U87 cells were irradiated in the absence vs. presence of a NOS inhibitor as specified in Fig. 2. An ALA-only dark control without or with L-NAME (1 mM) was included. At the indicated post-irradiation times, the cells were treated with DAF-2DA (20 μM) for 20 min in the dark, and then examined by fluorescence microscopy using 488 nm excitation and 650 nm emission. Image intensities were quantified using ImageJ software. Means ± SEM of values from three separate experiments are shown.

    Article Snippet: Chemicals, Reagents, and Antibodies The non-specific NOS inhibitor L-N G -nitroarginine methyl ester (L-NAME), iNOS-specific inhibitor N-[3-(aminomethyl)benzyl]acetamidine (1400W), NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), and NO fluorophore probe 4,5-diaminofluorescein diacetate (DAF-2DA) were obtained from Cayman Chemicals (Ann Arbor, MI).

    Techniques: Irradiation, Control, Fluorescence, Microscopy, Software