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pimozide  (MedChemExpress)


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    Structured Review

    MedChemExpress pimozide
    A , <t>Pimozide</t> decreased the survival of the rats during 3‐day follow‐up <t>after</t> <t>empagliflozin</t> treatment. (n = 15). B , Pimozide decreased the NDSs of the rats at 72 hours after empagliflozin treatment. C , Pimozide decreased the brain TNF‐α levels of the rats at 72 hours after empagliflozin treatment. D , pimozide decreased the brain IL‐1β levels of the rats at 72 hours after empagliflozin treatment. E , PMZ increased neuronal injury at 72 hours after empagliflozin treatment. MAP2 immunofluorescence staining (left) showed neuronal injury in the hippocampal neurons at 72 hours after CA. Quantification of MAP2 immunofluorescence staining (right) levels of hippocampal neurons. F , pimozide decreased the brain ATP levels of the rats at 72 hours after empagliflozin treatment. G , PMZ decreased the brain succinate levels of the rats at 72 hours after empagliflozin treatment. H , pimozide decreased the protein expression of OXCT1 and BDH1 in the brain at 72 hours after empagliflozin treatment. I , Quantification of brain OXCT1 and BDH1 protein expression by western blot band intensity measurement. Data are shown as mean ± SD, n = 3 or 6. ATP indicates adenosine triphosphate; BDH1, β‐hydroxybutyrate dehydrogenase 1; BHB, β‐hydroxybutyrate; CA, cardiac arrest; EMP, empaglifloxin; IL‐1β, interleukin‐1β; MAP2, microtubule‐associated protein 2; NDS, neurologic deficit scores; OXCT1, succinyl‐CoA:3‐ketoacid CoA transferase‐1; PMZ, pimozide; and TNF‐α, tumor necrosis factor alpha.
    Pimozide, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pimozide/Pimozide/pmc13055723-23-2-3
    Average 94 stars, based on 11 article reviews
    pimozide - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "Empagliflozin Attenuates Global Cerebral Ischemic Injury After Cardiac Arrest Through Enhancing Ketone Body Oxidative Metabolism in Rats"

    Article Title: Empagliflozin Attenuates Global Cerebral Ischemic Injury After Cardiac Arrest Through Enhancing Ketone Body Oxidative Metabolism in Rats

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    doi: 10.1161/JAHA.125.043523

    A , Pimozide decreased the survival of the rats during 3‐day follow‐up after empagliflozin treatment. (n = 15). B , Pimozide decreased the NDSs of the rats at 72 hours after empagliflozin treatment. C , Pimozide decreased the brain TNF‐α levels of the rats at 72 hours after empagliflozin treatment. D , pimozide decreased the brain IL‐1β levels of the rats at 72 hours after empagliflozin treatment. E , PMZ increased neuronal injury at 72 hours after empagliflozin treatment. MAP2 immunofluorescence staining (left) showed neuronal injury in the hippocampal neurons at 72 hours after CA. Quantification of MAP2 immunofluorescence staining (right) levels of hippocampal neurons. F , pimozide decreased the brain ATP levels of the rats at 72 hours after empagliflozin treatment. G , PMZ decreased the brain succinate levels of the rats at 72 hours after empagliflozin treatment. H , pimozide decreased the protein expression of OXCT1 and BDH1 in the brain at 72 hours after empagliflozin treatment. I , Quantification of brain OXCT1 and BDH1 protein expression by western blot band intensity measurement. Data are shown as mean ± SD, n = 3 or 6. ATP indicates adenosine triphosphate; BDH1, β‐hydroxybutyrate dehydrogenase 1; BHB, β‐hydroxybutyrate; CA, cardiac arrest; EMP, empaglifloxin; IL‐1β, interleukin‐1β; MAP2, microtubule‐associated protein 2; NDS, neurologic deficit scores; OXCT1, succinyl‐CoA:3‐ketoacid CoA transferase‐1; PMZ, pimozide; and TNF‐α, tumor necrosis factor alpha.
    Figure Legend Snippet: A , Pimozide decreased the survival of the rats during 3‐day follow‐up after empagliflozin treatment. (n = 15). B , Pimozide decreased the NDSs of the rats at 72 hours after empagliflozin treatment. C , Pimozide decreased the brain TNF‐α levels of the rats at 72 hours after empagliflozin treatment. D , pimozide decreased the brain IL‐1β levels of the rats at 72 hours after empagliflozin treatment. E , PMZ increased neuronal injury at 72 hours after empagliflozin treatment. MAP2 immunofluorescence staining (left) showed neuronal injury in the hippocampal neurons at 72 hours after CA. Quantification of MAP2 immunofluorescence staining (right) levels of hippocampal neurons. F , pimozide decreased the brain ATP levels of the rats at 72 hours after empagliflozin treatment. G , PMZ decreased the brain succinate levels of the rats at 72 hours after empagliflozin treatment. H , pimozide decreased the protein expression of OXCT1 and BDH1 in the brain at 72 hours after empagliflozin treatment. I , Quantification of brain OXCT1 and BDH1 protein expression by western blot band intensity measurement. Data are shown as mean ± SD, n = 3 or 6. ATP indicates adenosine triphosphate; BDH1, β‐hydroxybutyrate dehydrogenase 1; BHB, β‐hydroxybutyrate; CA, cardiac arrest; EMP, empaglifloxin; IL‐1β, interleukin‐1β; MAP2, microtubule‐associated protein 2; NDS, neurologic deficit scores; OXCT1, succinyl‐CoA:3‐ketoacid CoA transferase‐1; PMZ, pimozide; and TNF‐α, tumor necrosis factor alpha.

    Techniques Used: Immunofluorescence, Staining, Expressing, Western Blot

    Related Articles

    Solvent:

    Article Title: Empagliflozin Attenuates Global Cerebral Ischemic Injury After Cardiac Arrest Through Enhancing Ketone Body Oxidative Metabolism in Rats
    Article Snippet: .. Empagliflozin and pimozide (MedChem Express, Monmouth Junction) were meticulously dissolved in a solvent mixture comprising 10% dimethyl sulfoxide, 20% Kolliphor (Sigma Aldrich, St. Louis, MO), and 70% phosphate- buffered saline. .. BHB (Sigma Aldrich) was dissolved in phosphate- buffered saline.

    Article Title: Empagliflozin Attenuates Global Cerebral Ischemic Injury After Cardiac Arrest Through Enhancing Ketone Body Oxidative Metabolism in Rats
    Article Snippet: .. Empagliflozin and pimozide (MedChem Express, Monmouth Junction) were meticulously dissolved in a solvent mixture comprising 10% dimethyl sulfoxide, 20% Kolliphor (Sigma Aldrich, St. Louis, MO), and 70% phosphate‐buffered saline. .. BHB (Sigma Aldrich) was dissolved in phosphate‐buffered saline.

    Saline:

    Article Title: Empagliflozin Attenuates Global Cerebral Ischemic Injury After Cardiac Arrest Through Enhancing Ketone Body Oxidative Metabolism in Rats
    Article Snippet: .. Empagliflozin and pimozide (MedChem Express, Monmouth Junction) were meticulously dissolved in a solvent mixture comprising 10% dimethyl sulfoxide, 20% Kolliphor (Sigma Aldrich, St. Louis, MO), and 70% phosphate- buffered saline. .. BHB (Sigma Aldrich) was dissolved in phosphate- buffered saline.

    Article Title: Empagliflozin Attenuates Global Cerebral Ischemic Injury After Cardiac Arrest Through Enhancing Ketone Body Oxidative Metabolism in Rats
    Article Snippet: .. Empagliflozin and pimozide (MedChem Express, Monmouth Junction) were meticulously dissolved in a solvent mixture comprising 10% dimethyl sulfoxide, 20% Kolliphor (Sigma Aldrich, St. Louis, MO), and 70% phosphate‐buffered saline. .. BHB (Sigma Aldrich) was dissolved in phosphate‐buffered saline.

    Incubation:

    Article Title: Real-time visualization of STAT activation in live cells using genetically encoded biosensors.
    Article Snippet: .. For the STAT5 inhibitor study, cells were incubated with 10 μM AC-4-130 (MedChemExpress), SH-4-54 (Cayman Chemical), pimozide (Sigma-Aldrich) or 573108 (Sigma-Aldrich) for 1 h. For the JAK inhibitor studies in HEK-Blue IL-2 and primary CD4+ T cells, cells were incubated with 0.8 μM of JAK inhibitors (MedChemExpress) overnight or for 1 h, respectively. .. Plasmids pLV-STAT5-mNG and pLV-STAT5-mSC-I were synthesized and VSV-G pseudotyped third-generation lentiviral particles were produced by VectorBuilder.

    other:

    Article Title: Dual-cardiotoxicity evaluation of torsadogenic risk drugs using human iPSC-derived cardiomyocytes.
    Article Snippet: TdP risk 28 drugs reported in CiPA, bepridil (MedChemExpress, NJ, USA), vandetanib (MedChemExpress), quinidine (Sigma-Aldrich), dofetilide (Sigma-Aldrich), azimilide (Sigma-Aldrich), disopyramide (MedChemExpress), ibutilide (MedChemExpress), D, L-sotalol (SigmaAldrich), chlorpromazine (Selleckchem), clozapine (MedChemExpress), terfenadine (Sigma-Aldrich), risperidone (Selleckchem), cisapride (Sigma-Aldrich), astemizole (MedChemExpress), clarithromycin (MedChemExpress), pimozide (MedChemExpress), droperidol (MedChemExpress), ondansetron (MedChemExpress), domperidone (MedChemExpress), verapamil (Sigma-Aldrich), diltiazem (Selleckchem), nitrendipine (selleckchem), nifedipine (Sigma-Aldrich), loratadine (MedChemExpress), mexiletine (Sigma-Aldrich), tamoxifen (Selleckchem), metoprolol (MedChemExpress), and ranolazine (SigmaAldrich) were prepared.



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    A , <t>Pimozide</t> decreased the survival of the rats during 3‐day follow‐up <t>after</t> <t>empagliflozin</t> treatment. (n = 15). B , Pimozide decreased the NDSs of the rats at 72 hours after empagliflozin treatment. C , Pimozide decreased the brain TNF‐α levels of the rats at 72 hours after empagliflozin treatment. D , pimozide decreased the brain IL‐1β levels of the rats at 72 hours after empagliflozin treatment. E , PMZ increased neuronal injury at 72 hours after empagliflozin treatment. MAP2 immunofluorescence staining (left) showed neuronal injury in the hippocampal neurons at 72 hours after CA. Quantification of MAP2 immunofluorescence staining (right) levels of hippocampal neurons. F , pimozide decreased the brain ATP levels of the rats at 72 hours after empagliflozin treatment. G , PMZ decreased the brain succinate levels of the rats at 72 hours after empagliflozin treatment. H , pimozide decreased the protein expression of OXCT1 and BDH1 in the brain at 72 hours after empagliflozin treatment. I , Quantification of brain OXCT1 and BDH1 protein expression by western blot band intensity measurement. Data are shown as mean ± SD, n = 3 or 6. ATP indicates adenosine triphosphate; BDH1, β‐hydroxybutyrate dehydrogenase 1; BHB, β‐hydroxybutyrate; CA, cardiac arrest; EMP, empaglifloxin; IL‐1β, interleukin‐1β; MAP2, microtubule‐associated protein 2; NDS, neurologic deficit scores; OXCT1, succinyl‐CoA:3‐ketoacid CoA transferase‐1; PMZ, pimozide; and TNF‐α, tumor necrosis factor alpha.
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    A , <t>Pimozide</t> decreased the survival of the rats during 3‐day follow‐up <t>after</t> <t>empagliflozin</t> treatment. (n = 15). B , Pimozide decreased the NDSs of the rats at 72 hours after empagliflozin treatment. C , Pimozide decreased the brain TNF‐α levels of the rats at 72 hours after empagliflozin treatment. D , pimozide decreased the brain IL‐1β levels of the rats at 72 hours after empagliflozin treatment. E , PMZ increased neuronal injury at 72 hours after empagliflozin treatment. MAP2 immunofluorescence staining (left) showed neuronal injury in the hippocampal neurons at 72 hours after CA. Quantification of MAP2 immunofluorescence staining (right) levels of hippocampal neurons. F , pimozide decreased the brain ATP levels of the rats at 72 hours after empagliflozin treatment. G , PMZ decreased the brain succinate levels of the rats at 72 hours after empagliflozin treatment. H , pimozide decreased the protein expression of OXCT1 and BDH1 in the brain at 72 hours after empagliflozin treatment. I , Quantification of brain OXCT1 and BDH1 protein expression by western blot band intensity measurement. Data are shown as mean ± SD, n = 3 or 6. ATP indicates adenosine triphosphate; BDH1, β‐hydroxybutyrate dehydrogenase 1; BHB, β‐hydroxybutyrate; CA, cardiac arrest; EMP, empaglifloxin; IL‐1β, interleukin‐1β; MAP2, microtubule‐associated protein 2; NDS, neurologic deficit scores; OXCT1, succinyl‐CoA:3‐ketoacid CoA transferase‐1; PMZ, pimozide; and TNF‐α, tumor necrosis factor alpha.
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    MedChemExpress clas females
    A , <t>Pimozide</t> decreased the survival of the rats during 3‐day follow‐up <t>after</t> <t>empagliflozin</t> treatment. (n = 15). B , Pimozide decreased the NDSs of the rats at 72 hours after empagliflozin treatment. C , Pimozide decreased the brain TNF‐α levels of the rats at 72 hours after empagliflozin treatment. D , pimozide decreased the brain IL‐1β levels of the rats at 72 hours after empagliflozin treatment. E , PMZ increased neuronal injury at 72 hours after empagliflozin treatment. MAP2 immunofluorescence staining (left) showed neuronal injury in the hippocampal neurons at 72 hours after CA. Quantification of MAP2 immunofluorescence staining (right) levels of hippocampal neurons. F , pimozide decreased the brain ATP levels of the rats at 72 hours after empagliflozin treatment. G , PMZ decreased the brain succinate levels of the rats at 72 hours after empagliflozin treatment. H , pimozide decreased the protein expression of OXCT1 and BDH1 in the brain at 72 hours after empagliflozin treatment. I , Quantification of brain OXCT1 and BDH1 protein expression by western blot band intensity measurement. Data are shown as mean ± SD, n = 3 or 6. ATP indicates adenosine triphosphate; BDH1, β‐hydroxybutyrate dehydrogenase 1; BHB, β‐hydroxybutyrate; CA, cardiac arrest; EMP, empaglifloxin; IL‐1β, interleukin‐1β; MAP2, microtubule‐associated protein 2; NDS, neurologic deficit scores; OXCT1, succinyl‐CoA:3‐ketoacid CoA transferase‐1; PMZ, pimozide; and TNF‐α, tumor necrosis factor alpha.
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    A , Pimozide decreased the survival of the rats during 3‐day follow‐up after empagliflozin treatment. (n = 15). B , Pimozide decreased the NDSs of the rats at 72 hours after empagliflozin treatment. C , Pimozide decreased the brain TNF‐α levels of the rats at 72 hours after empagliflozin treatment. D , pimozide decreased the brain IL‐1β levels of the rats at 72 hours after empagliflozin treatment. E , PMZ increased neuronal injury at 72 hours after empagliflozin treatment. MAP2 immunofluorescence staining (left) showed neuronal injury in the hippocampal neurons at 72 hours after CA. Quantification of MAP2 immunofluorescence staining (right) levels of hippocampal neurons. F , pimozide decreased the brain ATP levels of the rats at 72 hours after empagliflozin treatment. G , PMZ decreased the brain succinate levels of the rats at 72 hours after empagliflozin treatment. H , pimozide decreased the protein expression of OXCT1 and BDH1 in the brain at 72 hours after empagliflozin treatment. I , Quantification of brain OXCT1 and BDH1 protein expression by western blot band intensity measurement. Data are shown as mean ± SD, n = 3 or 6. ATP indicates adenosine triphosphate; BDH1, β‐hydroxybutyrate dehydrogenase 1; BHB, β‐hydroxybutyrate; CA, cardiac arrest; EMP, empaglifloxin; IL‐1β, interleukin‐1β; MAP2, microtubule‐associated protein 2; NDS, neurologic deficit scores; OXCT1, succinyl‐CoA:3‐ketoacid CoA transferase‐1; PMZ, pimozide; and TNF‐α, tumor necrosis factor alpha.

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    Article Title: Empagliflozin Attenuates Global Cerebral Ischemic Injury After Cardiac Arrest Through Enhancing Ketone Body Oxidative Metabolism in Rats

    doi: 10.1161/JAHA.125.043523

    Figure Lengend Snippet: A , Pimozide decreased the survival of the rats during 3‐day follow‐up after empagliflozin treatment. (n = 15). B , Pimozide decreased the NDSs of the rats at 72 hours after empagliflozin treatment. C , Pimozide decreased the brain TNF‐α levels of the rats at 72 hours after empagliflozin treatment. D , pimozide decreased the brain IL‐1β levels of the rats at 72 hours after empagliflozin treatment. E , PMZ increased neuronal injury at 72 hours after empagliflozin treatment. MAP2 immunofluorescence staining (left) showed neuronal injury in the hippocampal neurons at 72 hours after CA. Quantification of MAP2 immunofluorescence staining (right) levels of hippocampal neurons. F , pimozide decreased the brain ATP levels of the rats at 72 hours after empagliflozin treatment. G , PMZ decreased the brain succinate levels of the rats at 72 hours after empagliflozin treatment. H , pimozide decreased the protein expression of OXCT1 and BDH1 in the brain at 72 hours after empagliflozin treatment. I , Quantification of brain OXCT1 and BDH1 protein expression by western blot band intensity measurement. Data are shown as mean ± SD, n = 3 or 6. ATP indicates adenosine triphosphate; BDH1, β‐hydroxybutyrate dehydrogenase 1; BHB, β‐hydroxybutyrate; CA, cardiac arrest; EMP, empaglifloxin; IL‐1β, interleukin‐1β; MAP2, microtubule‐associated protein 2; NDS, neurologic deficit scores; OXCT1, succinyl‐CoA:3‐ketoacid CoA transferase‐1; PMZ, pimozide; and TNF‐α, tumor necrosis factor alpha.

    Article Snippet: Empagliflozin and pimozide (MedChem Express, Monmouth Junction) were meticulously dissolved in a solvent mixture comprising 10% dimethyl sulfoxide, 20% Kolliphor (Sigma Aldrich, St. Louis, MO), and 70% phosphate‐buffered saline.

    Techniques: Immunofluorescence, Staining, Expressing, Western Blot