The Experts below are selected from a list of 81 Experts worldwide ranked by ideXlab platform
Prateek Gaur - One of the best experts on this subject based on the ideXlab platform.
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A novel method for spectrophotometric determination of pregabalin in pure form and in capsules
Chemistry Central Journal, 2011Co-Authors: Alka Bali, Prateek GaurAbstract:Background Pregabalin, a γ-amino-n-Butyric Acid Derivative, is an antiepileptic drug not yet official in any pharmacopeia and development of analytical procedures for this drug in bulk/formulation forms is a necessity. We herein, report a new, simple, extraction free, cost effective, sensitive and reproducible spectrophotometric method for the determination of the pregabalin. Results Pregabalin, as a primary amine was reacted with ninhydrin in phosphate buffer pH 7.4 to form blue violet colored chromogen which could be measured spectrophotometrically at λ_max 402.6 nm. The method was validated with respect to linearity, accuracy, precision and robustness. The method showed linearity in a wide concentration range of 50-1000 μg mL^-1 with good correlation coefficient (0.992). The limits of assays detection was found to be 6.0 μg mL^-1 and quantitation limit was 20.0 μg mL^-1. The suggested method was applied to the determination of the drug in capsules. No interference could be observed from the additives in the capsules. The percentage recovery was found to be 100.43 ± 1.24. Conclusion The developed method was successfully validated and applied to the determination of pregabalin in bulk and pharmaceutical formulations without any interference from common excipients. Hence, this method can be potentially useful for routine laboratory analysis of pregabalin.
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A novel method for spectrophotometric determination of pregabalin in pure form and in capsules.
Chemistry Central journal, 2011Co-Authors: Alka Bali, Prateek GaurAbstract:Pregabalin, a γ-amino-n-Butyric Acid Derivative, is an antiepileptic drug not yet official in any pharmacopeia and development of analytical procedures for this drug in bulk/formulation forms is a necessity. We herein, report a new, simple, extraction free, cost effective, sensitive and reproducible spectrophotometric method for the determination of the pregabalin. Pregabalin, as a primary amine was reacted with ninhydrin in phosphate buffer pH 7.4 to form blue violet colored chromogen which could be measured spectrophotometrically at λmax 402.6 nm. The method was validated with respect to linearity, accuracy, precision and robustness. The method showed linearity in a wide concentration range of 50-1000 μg mL-1 with good correlation coefficient (0.992). The limits of assays detection was found to be 6.0 μg mL-1 and quantitation limit was 20.0 μg mL-1. The suggested method was applied to the determination of the drug in capsules. No interference could be observed from the additives in the capsules. The percentage recovery was found to be 100.43 ± 1.24. The developed method was successfully validated and applied to the determination of pregabalin in bulk and pharmaceutical formulations without any interference from common excipients. Hence, this method can be potentially useful for routine laboratory analysis of pregabalin.
Ada Rephaeli - One of the best experts on this subject based on the ideXlab platform.
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In vivo efficacy of a novel histone deacetylase inhibitor in combination with radiation for the treatment of gliomas.
Neuro-oncology, 2007Co-Authors: Michal Entin-meer, Ada Rephaeli, Abraham Nudelman, Xiaodong Yang, Scott R. Vandenberg, Kathleen R. Lamborn, Daphne A. Haas-koganAbstract:Histone modification has emerged as a promising approach to cancer therapy. We explored the in vivo efficacy of a Butyric Acid Derivative, pivaloyloxymethyl butyrate (AN-9), for the treatment of gliomas. Relative to control and single-modality treatments, the combination of AN-9 and radiation significantly inhibited tumor growth and prolonged time to failure in mice bearing glioma xenografts. The enhanced response to radiation was accompanied by inhibition of cellular proliferation and by increased phosphorylation of H2AX, implicating DNA double-strand breaks in the antineoplastic effects of AN-9 and radiation. The data suggest that AN-9 in combination with radiation may be an effective therapy for malignant gliomas.
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Butyric Acid and pivaloyloxymethyl butyrate, AN-9, a novel Butyric Acid Derivative, induce apoptosis in HL-60 cells
Journal of Cancer Research and Clinical Oncology, 1997Co-Authors: Yael Zimra, Lea Maron, Abraham Nudelman, Mati Shaklai, Lina Wasserman, Ada RephaeliAbstract:A novel Butyric Acid Derivative, pivaloyloxymethyl butyrate, AN-9, was previously shown to be a potent differentiating agent. AN-9 exerts a significant anticancer activity in vitro and in vivo. In all the activities examined, AN-9 was more potent than Butyric Acid. Here we show that AN-9 and Butyric Acid induce cell death by apoptosis. Exposure of HL-60 cells to Butyric Acid and AN-9 decreased cell numbers and induced cell differentiation and the appearance of typical apoptotic features. Induction of apoptosis and/or differentiation by AN-9 and Butyric Acid was dependent on the concentration and the time of exposure to the drugs. The advantage of AN- 9 over Butyric Acid was further confirmed. Apoptosis induced by AN-9 occurred after a shorter exposure and at lower drug concentrations than that induced by Butyric Acid. Apoptosis by AN-9 was accompanied by reduction in Bcl-2 expression. Preincubation with antioxidants did not protect HL-60 cells from apoptosis induced by AN-9. HL-60 cells that were induced to differentiate by preincubation with retinoic Acid or low AN-9 concentrations were more resistant to apoptosis, induced later by high concentrations of AN-9, than were undifferentiated cells.
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Esterase inhibitors diminish the modulation of gene expression by Butyric Acid Derivative, pivaloyloxymethyl butyrate (AN-9).
Israel journal of medical sciences, 1996Co-Authors: Esther Rabizadeh, Mati Shaklai, Abraham Nudelman, Lea Eisenbach, Ada RephaeliAbstract:Pivaloyloxymethyl butyrate (AN-9) belongs to the family of acyloxyalkyl ester prodrugs of carboxylic Acids which undergo intracellular hydrolysis to yield Butyric Acid (BA). We have previously shown that AN-9 and BA reduce the level of c-myc and enhance c-jun transcripts in HL-60 cells, and that the differentiation of these cells, induced by AN-9, is dependent on the presence of intracellular esterases. In this study we show that esterase inhibitors abolish the changes induced by AN-9 on c-myc and c-jun expression. In contrast, esterase inhibitors do not change the effects of BA on c-myc or c-jun. Interestingly, these inhibitors affect the modulation induced by both AN-9 and BA on the retinoblastoma tumor suppressor gene. These data suggest that AN-9 is indeed a prodrug of BA and that prior intracellular hydrolysis by esterases is material for AN-9 activity.
Alka Bali - One of the best experts on this subject based on the ideXlab platform.
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A novel method for spectrophotometric determination of pregabalin in pure form and in capsules
Chemistry Central Journal, 2011Co-Authors: Alka Bali, Prateek GaurAbstract:Background Pregabalin, a γ-amino-n-Butyric Acid Derivative, is an antiepileptic drug not yet official in any pharmacopeia and development of analytical procedures for this drug in bulk/formulation forms is a necessity. We herein, report a new, simple, extraction free, cost effective, sensitive and reproducible spectrophotometric method for the determination of the pregabalin. Results Pregabalin, as a primary amine was reacted with ninhydrin in phosphate buffer pH 7.4 to form blue violet colored chromogen which could be measured spectrophotometrically at λ_max 402.6 nm. The method was validated with respect to linearity, accuracy, precision and robustness. The method showed linearity in a wide concentration range of 50-1000 μg mL^-1 with good correlation coefficient (0.992). The limits of assays detection was found to be 6.0 μg mL^-1 and quantitation limit was 20.0 μg mL^-1. The suggested method was applied to the determination of the drug in capsules. No interference could be observed from the additives in the capsules. The percentage recovery was found to be 100.43 ± 1.24. Conclusion The developed method was successfully validated and applied to the determination of pregabalin in bulk and pharmaceutical formulations without any interference from common excipients. Hence, this method can be potentially useful for routine laboratory analysis of pregabalin.
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A novel method for spectrophotometric determination of pregabalin in pure form and in capsules.
Chemistry Central journal, 2011Co-Authors: Alka Bali, Prateek GaurAbstract:Pregabalin, a γ-amino-n-Butyric Acid Derivative, is an antiepileptic drug not yet official in any pharmacopeia and development of analytical procedures for this drug in bulk/formulation forms is a necessity. We herein, report a new, simple, extraction free, cost effective, sensitive and reproducible spectrophotometric method for the determination of the pregabalin. Pregabalin, as a primary amine was reacted with ninhydrin in phosphate buffer pH 7.4 to form blue violet colored chromogen which could be measured spectrophotometrically at λmax 402.6 nm. The method was validated with respect to linearity, accuracy, precision and robustness. The method showed linearity in a wide concentration range of 50-1000 μg mL-1 with good correlation coefficient (0.992). The limits of assays detection was found to be 6.0 μg mL-1 and quantitation limit was 20.0 μg mL-1. The suggested method was applied to the determination of the drug in capsules. No interference could be observed from the additives in the capsules. The percentage recovery was found to be 100.43 ± 1.24. The developed method was successfully validated and applied to the determination of pregabalin in bulk and pharmaceutical formulations without any interference from common excipients. Hence, this method can be potentially useful for routine laboratory analysis of pregabalin.
Abraham Nudelman - One of the best experts on this subject based on the ideXlab platform.
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In vivo efficacy of a novel histone deacetylase inhibitor in combination with radiation for the treatment of gliomas.
Neuro-oncology, 2007Co-Authors: Michal Entin-meer, Ada Rephaeli, Abraham Nudelman, Xiaodong Yang, Scott R. Vandenberg, Kathleen R. Lamborn, Daphne A. Haas-koganAbstract:Histone modification has emerged as a promising approach to cancer therapy. We explored the in vivo efficacy of a Butyric Acid Derivative, pivaloyloxymethyl butyrate (AN-9), for the treatment of gliomas. Relative to control and single-modality treatments, the combination of AN-9 and radiation significantly inhibited tumor growth and prolonged time to failure in mice bearing glioma xenografts. The enhanced response to radiation was accompanied by inhibition of cellular proliferation and by increased phosphorylation of H2AX, implicating DNA double-strand breaks in the antineoplastic effects of AN-9 and radiation. The data suggest that AN-9 in combination with radiation may be an effective therapy for malignant gliomas.
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Butyric Acid and pivaloyloxymethyl butyrate, AN-9, a novel Butyric Acid Derivative, induce apoptosis in HL-60 cells
Journal of Cancer Research and Clinical Oncology, 1997Co-Authors: Yael Zimra, Lea Maron, Abraham Nudelman, Mati Shaklai, Lina Wasserman, Ada RephaeliAbstract:A novel Butyric Acid Derivative, pivaloyloxymethyl butyrate, AN-9, was previously shown to be a potent differentiating agent. AN-9 exerts a significant anticancer activity in vitro and in vivo. In all the activities examined, AN-9 was more potent than Butyric Acid. Here we show that AN-9 and Butyric Acid induce cell death by apoptosis. Exposure of HL-60 cells to Butyric Acid and AN-9 decreased cell numbers and induced cell differentiation and the appearance of typical apoptotic features. Induction of apoptosis and/or differentiation by AN-9 and Butyric Acid was dependent on the concentration and the time of exposure to the drugs. The advantage of AN- 9 over Butyric Acid was further confirmed. Apoptosis induced by AN-9 occurred after a shorter exposure and at lower drug concentrations than that induced by Butyric Acid. Apoptosis by AN-9 was accompanied by reduction in Bcl-2 expression. Preincubation with antioxidants did not protect HL-60 cells from apoptosis induced by AN-9. HL-60 cells that were induced to differentiate by preincubation with retinoic Acid or low AN-9 concentrations were more resistant to apoptosis, induced later by high concentrations of AN-9, than were undifferentiated cells.
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Esterase inhibitors diminish the modulation of gene expression by Butyric Acid Derivative, pivaloyloxymethyl butyrate (AN-9).
Israel journal of medical sciences, 1996Co-Authors: Esther Rabizadeh, Mati Shaklai, Abraham Nudelman, Lea Eisenbach, Ada RephaeliAbstract:Pivaloyloxymethyl butyrate (AN-9) belongs to the family of acyloxyalkyl ester prodrugs of carboxylic Acids which undergo intracellular hydrolysis to yield Butyric Acid (BA). We have previously shown that AN-9 and BA reduce the level of c-myc and enhance c-jun transcripts in HL-60 cells, and that the differentiation of these cells, induced by AN-9, is dependent on the presence of intracellular esterases. In this study we show that esterase inhibitors abolish the changes induced by AN-9 on c-myc and c-jun expression. In contrast, esterase inhibitors do not change the effects of BA on c-myc or c-jun. Interestingly, these inhibitors affect the modulation induced by both AN-9 and BA on the retinoblastoma tumor suppressor gene. These data suggest that AN-9 is indeed a prodrug of BA and that prior intracellular hydrolysis by esterases is material for AN-9 activity.
Yael Zimra - One of the best experts on this subject based on the ideXlab platform.
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Doxorubicin and a Butyric Acid Derivative effectively reduce levels of BCL-2 protein in the cells of chronic lymphocytic leukemia patient
European journal of haematology, 2001Co-Authors: Esther Rabizadeh, Mati Shaklai, Osnat Bairey, Adina Aviram, I. Ben‐dror, Yael ZimraAbstract:: B-chronic lymphocytic leukemia (B-CLL) is a disease caused primarily by defects in the apoptosis mechanism. AN-9, a Butyric Acid (BA) Derivative, is a potent differentiating and an anti-cancer drug that induces apoptosis in HL-60 cells. Herein we show the affect of AN-9, alone and in combination with doxorubicin, on cell cultures from B-CLL patients. Cells from 17 patients were cultured and tested for viability, apoptosis, bcl-2 and bax protein expression. Exposure of B-CLL cell cultures to AN-9 was accompanied by apoptosis and a marked viability loss (up to 46%, p=0.0017). AN-9 reduced up to 51% (p=0.0017) the levels of bcl-2 in 57% of the cultures that express bcl-2. The combination of low concentrations of AN-9 and doxorubicin more than additively enhanced apoptosis and reduced bcl-2 levels in B-CLL cultures which were resistant to AN-9. AN-9 enhanced bax expression up to 58%(p=0.008) in cultures from 53% of the patients, but had no effect on bax levels when combined with doxorubicin. In conclusion, AN-9 alone reduced bcl-2 and enhanced bax expression in cultures from B-CLL patients, and the reduction of bcl-2 levels in combination with doxorubicin was greater than additive. These results may be beneficial in possible future combination therapy with AN-9 in B-CLL.
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Butyric Acid and pivaloyloxymethyl butyrate, AN-9, a novel Butyric Acid Derivative, induce apoptosis in HL-60 cells
Journal of Cancer Research and Clinical Oncology, 1997Co-Authors: Yael Zimra, Lea Maron, Abraham Nudelman, Mati Shaklai, Lina Wasserman, Ada RephaeliAbstract:A novel Butyric Acid Derivative, pivaloyloxymethyl butyrate, AN-9, was previously shown to be a potent differentiating agent. AN-9 exerts a significant anticancer activity in vitro and in vivo. In all the activities examined, AN-9 was more potent than Butyric Acid. Here we show that AN-9 and Butyric Acid induce cell death by apoptosis. Exposure of HL-60 cells to Butyric Acid and AN-9 decreased cell numbers and induced cell differentiation and the appearance of typical apoptotic features. Induction of apoptosis and/or differentiation by AN-9 and Butyric Acid was dependent on the concentration and the time of exposure to the drugs. The advantage of AN- 9 over Butyric Acid was further confirmed. Apoptosis induced by AN-9 occurred after a shorter exposure and at lower drug concentrations than that induced by Butyric Acid. Apoptosis by AN-9 was accompanied by reduction in Bcl-2 expression. Preincubation with antioxidants did not protect HL-60 cells from apoptosis induced by AN-9. HL-60 cells that were induced to differentiate by preincubation with retinoic Acid or low AN-9 concentrations were more resistant to apoptosis, induced later by high concentrations of AN-9, than were undifferentiated cells.
