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Martin J. Brodie - One of the best experts on this subject based on the ideXlab platform.
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Mutual Interaction between remacemide hydrochloride and phenytoin
Epilepsy research, 1997Co-Authors: John Paul Leach, Virginia Jamieson, Tracey Jones, Alan Richens, Jacqueline Girvan, Martin J. BrodieAbstract:Abstract A randomised, double-blind, placebo-controlled crossover study of add-on remacemide hydrochloride was carried out in epilepsy patients being treated with phenytoin (PHT) monotherapy. Eleven patients were recruited, ten of whom completed the study. Plasma concentration profiles of PHT, remacemide, and its active desglycinyl metabolite (ARL12495XX) were determined following single and multiple dosing with remacemide hydrochloride. Following 14 days' treatment with remacemide hydrochloride 300 mg twice daily, the mean AUC of PHT was increased by 11.5% ( P =0.33), C max by 13.7% ( P =0.32) and C min by 22.2% ( P =0.12) over placebo. There was an increase in trough concentrations of PHT averaging 20% during active treatment compared with placebo ( P =0.01). No symptoms of PHT toxicity were reported by any patient. There was no evidence of autoinduction of remacemide metabolism. However, average concentrations of remacemide and its active metabolite in PHT-treated patients were around 40 and 30% lower, respectively than in healthy volunteers previously receiving the same dose of remacemide hydrochloride. Thus, remacemide hydrochloride has a small inhibitory effect on PHT metabolism, which itself induces that of remacemide and its active metabolite. This Mutual Interaction is predictable and modest and should not present a barrier to their clinical use in combination.
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Mutual Interaction Between Remacemide Hydrochloride and Carbamazepine: Two Drugs with Active Metabolites
Epilepsia, 1996Co-Authors: John Paul Leach, Jackie Blacklaw, Virginia Jamieson, Tracey Jones, Alan Richens, Martin J. BrodieAbstract:Summary: Purpose: We wished to determine Mutual Interaction of two drugs with active metabolism: remacemide, hydrochloride and carbamazepine (CBZ). Methods: A randomized, double-blind, placebo-controlled cross-over study of add-on remacemide hydrochloride was performed in 10 of 14 recruited patients being treated with CBZ monotherapy. Forty-eight-hour concentration profiles of CBZ, its active epoxide metabolite (CBZ-E), remacemide, and its desglycinyl metabolite (ARL12495XX) were assayed after single and multiple dosing. Results: After patients were treated with 300 mg remacemide hydrochloride twice daily for 14 days, the mean area under the concentration-time curve (AUC) of CBZ was increased by 22% (p = 0.12), Cmax was increased by 27% (p = 0.07), and Cmin was increased by 22% (p = 0.29). Trough concentrations of CBZ were higher (p = 0.0037) during active treatment as compared with placebo treatment. CBZ-E levels were unaffected. No symptoms of CBZ toxicity were reported. There was no evidence of autoinduction of remacemide metabolism. However, in CBZ-treated patients, the AUC of remacemide and its active metabolite was 60 and 30%, respectively, of values observed in healthy volunteers treated previously with the same dose. Conclusions: Remacemide hydrochloride inhibits CBZ metabolism, which itself induces that of remacemide hydrochloride and its active metabolite. This Mutual Interaction between remacemide hydrochloride and CBZ is predictable and modest and should not present a barrier to their clinical use in combination.
John Paul Leach - One of the best experts on this subject based on the ideXlab platform.
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Mutual Interaction between remacemide hydrochloride and phenytoin
Epilepsy research, 1997Co-Authors: John Paul Leach, Virginia Jamieson, Tracey Jones, Alan Richens, Jacqueline Girvan, Martin J. BrodieAbstract:Abstract A randomised, double-blind, placebo-controlled crossover study of add-on remacemide hydrochloride was carried out in epilepsy patients being treated with phenytoin (PHT) monotherapy. Eleven patients were recruited, ten of whom completed the study. Plasma concentration profiles of PHT, remacemide, and its active desglycinyl metabolite (ARL12495XX) were determined following single and multiple dosing with remacemide hydrochloride. Following 14 days' treatment with remacemide hydrochloride 300 mg twice daily, the mean AUC of PHT was increased by 11.5% ( P =0.33), C max by 13.7% ( P =0.32) and C min by 22.2% ( P =0.12) over placebo. There was an increase in trough concentrations of PHT averaging 20% during active treatment compared with placebo ( P =0.01). No symptoms of PHT toxicity were reported by any patient. There was no evidence of autoinduction of remacemide metabolism. However, average concentrations of remacemide and its active metabolite in PHT-treated patients were around 40 and 30% lower, respectively than in healthy volunteers previously receiving the same dose of remacemide hydrochloride. Thus, remacemide hydrochloride has a small inhibitory effect on PHT metabolism, which itself induces that of remacemide and its active metabolite. This Mutual Interaction is predictable and modest and should not present a barrier to their clinical use in combination.
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Mutual Interaction Between Remacemide Hydrochloride and Carbamazepine: Two Drugs with Active Metabolites
Epilepsia, 1996Co-Authors: John Paul Leach, Jackie Blacklaw, Virginia Jamieson, Tracey Jones, Alan Richens, Martin J. BrodieAbstract:Summary: Purpose: We wished to determine Mutual Interaction of two drugs with active metabolism: remacemide, hydrochloride and carbamazepine (CBZ). Methods: A randomized, double-blind, placebo-controlled cross-over study of add-on remacemide hydrochloride was performed in 10 of 14 recruited patients being treated with CBZ monotherapy. Forty-eight-hour concentration profiles of CBZ, its active epoxide metabolite (CBZ-E), remacemide, and its desglycinyl metabolite (ARL12495XX) were assayed after single and multiple dosing. Results: After patients were treated with 300 mg remacemide hydrochloride twice daily for 14 days, the mean area under the concentration-time curve (AUC) of CBZ was increased by 22% (p = 0.12), Cmax was increased by 27% (p = 0.07), and Cmin was increased by 22% (p = 0.29). Trough concentrations of CBZ were higher (p = 0.0037) during active treatment as compared with placebo treatment. CBZ-E levels were unaffected. No symptoms of CBZ toxicity were reported. There was no evidence of autoinduction of remacemide metabolism. However, in CBZ-treated patients, the AUC of remacemide and its active metabolite was 60 and 30%, respectively, of values observed in healthy volunteers treated previously with the same dose. Conclusions: Remacemide hydrochloride inhibits CBZ metabolism, which itself induces that of remacemide hydrochloride and its active metabolite. This Mutual Interaction between remacemide hydrochloride and CBZ is predictable and modest and should not present a barrier to their clinical use in combination.
Alan Richens - One of the best experts on this subject based on the ideXlab platform.
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Mutual Interaction between remacemide hydrochloride and phenytoin
Epilepsy research, 1997Co-Authors: John Paul Leach, Virginia Jamieson, Tracey Jones, Alan Richens, Jacqueline Girvan, Martin J. BrodieAbstract:Abstract A randomised, double-blind, placebo-controlled crossover study of add-on remacemide hydrochloride was carried out in epilepsy patients being treated with phenytoin (PHT) monotherapy. Eleven patients were recruited, ten of whom completed the study. Plasma concentration profiles of PHT, remacemide, and its active desglycinyl metabolite (ARL12495XX) were determined following single and multiple dosing with remacemide hydrochloride. Following 14 days' treatment with remacemide hydrochloride 300 mg twice daily, the mean AUC of PHT was increased by 11.5% ( P =0.33), C max by 13.7% ( P =0.32) and C min by 22.2% ( P =0.12) over placebo. There was an increase in trough concentrations of PHT averaging 20% during active treatment compared with placebo ( P =0.01). No symptoms of PHT toxicity were reported by any patient. There was no evidence of autoinduction of remacemide metabolism. However, average concentrations of remacemide and its active metabolite in PHT-treated patients were around 40 and 30% lower, respectively than in healthy volunteers previously receiving the same dose of remacemide hydrochloride. Thus, remacemide hydrochloride has a small inhibitory effect on PHT metabolism, which itself induces that of remacemide and its active metabolite. This Mutual Interaction is predictable and modest and should not present a barrier to their clinical use in combination.
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Mutual Interaction Between Remacemide Hydrochloride and Carbamazepine: Two Drugs with Active Metabolites
Epilepsia, 1996Co-Authors: John Paul Leach, Jackie Blacklaw, Virginia Jamieson, Tracey Jones, Alan Richens, Martin J. BrodieAbstract:Summary: Purpose: We wished to determine Mutual Interaction of two drugs with active metabolism: remacemide, hydrochloride and carbamazepine (CBZ). Methods: A randomized, double-blind, placebo-controlled cross-over study of add-on remacemide hydrochloride was performed in 10 of 14 recruited patients being treated with CBZ monotherapy. Forty-eight-hour concentration profiles of CBZ, its active epoxide metabolite (CBZ-E), remacemide, and its desglycinyl metabolite (ARL12495XX) were assayed after single and multiple dosing. Results: After patients were treated with 300 mg remacemide hydrochloride twice daily for 14 days, the mean area under the concentration-time curve (AUC) of CBZ was increased by 22% (p = 0.12), Cmax was increased by 27% (p = 0.07), and Cmin was increased by 22% (p = 0.29). Trough concentrations of CBZ were higher (p = 0.0037) during active treatment as compared with placebo treatment. CBZ-E levels were unaffected. No symptoms of CBZ toxicity were reported. There was no evidence of autoinduction of remacemide metabolism. However, in CBZ-treated patients, the AUC of remacemide and its active metabolite was 60 and 30%, respectively, of values observed in healthy volunteers treated previously with the same dose. Conclusions: Remacemide hydrochloride inhibits CBZ metabolism, which itself induces that of remacemide hydrochloride and its active metabolite. This Mutual Interaction between remacemide hydrochloride and CBZ is predictable and modest and should not present a barrier to their clinical use in combination.
Virginia Jamieson - One of the best experts on this subject based on the ideXlab platform.
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Mutual Interaction between remacemide hydrochloride and phenytoin
Epilepsy research, 1997Co-Authors: John Paul Leach, Virginia Jamieson, Tracey Jones, Alan Richens, Jacqueline Girvan, Martin J. BrodieAbstract:Abstract A randomised, double-blind, placebo-controlled crossover study of add-on remacemide hydrochloride was carried out in epilepsy patients being treated with phenytoin (PHT) monotherapy. Eleven patients were recruited, ten of whom completed the study. Plasma concentration profiles of PHT, remacemide, and its active desglycinyl metabolite (ARL12495XX) were determined following single and multiple dosing with remacemide hydrochloride. Following 14 days' treatment with remacemide hydrochloride 300 mg twice daily, the mean AUC of PHT was increased by 11.5% ( P =0.33), C max by 13.7% ( P =0.32) and C min by 22.2% ( P =0.12) over placebo. There was an increase in trough concentrations of PHT averaging 20% during active treatment compared with placebo ( P =0.01). No symptoms of PHT toxicity were reported by any patient. There was no evidence of autoinduction of remacemide metabolism. However, average concentrations of remacemide and its active metabolite in PHT-treated patients were around 40 and 30% lower, respectively than in healthy volunteers previously receiving the same dose of remacemide hydrochloride. Thus, remacemide hydrochloride has a small inhibitory effect on PHT metabolism, which itself induces that of remacemide and its active metabolite. This Mutual Interaction is predictable and modest and should not present a barrier to their clinical use in combination.
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Mutual Interaction Between Remacemide Hydrochloride and Carbamazepine: Two Drugs with Active Metabolites
Epilepsia, 1996Co-Authors: John Paul Leach, Jackie Blacklaw, Virginia Jamieson, Tracey Jones, Alan Richens, Martin J. BrodieAbstract:Summary: Purpose: We wished to determine Mutual Interaction of two drugs with active metabolism: remacemide, hydrochloride and carbamazepine (CBZ). Methods: A randomized, double-blind, placebo-controlled cross-over study of add-on remacemide hydrochloride was performed in 10 of 14 recruited patients being treated with CBZ monotherapy. Forty-eight-hour concentration profiles of CBZ, its active epoxide metabolite (CBZ-E), remacemide, and its desglycinyl metabolite (ARL12495XX) were assayed after single and multiple dosing. Results: After patients were treated with 300 mg remacemide hydrochloride twice daily for 14 days, the mean area under the concentration-time curve (AUC) of CBZ was increased by 22% (p = 0.12), Cmax was increased by 27% (p = 0.07), and Cmin was increased by 22% (p = 0.29). Trough concentrations of CBZ were higher (p = 0.0037) during active treatment as compared with placebo treatment. CBZ-E levels were unaffected. No symptoms of CBZ toxicity were reported. There was no evidence of autoinduction of remacemide metabolism. However, in CBZ-treated patients, the AUC of remacemide and its active metabolite was 60 and 30%, respectively, of values observed in healthy volunteers treated previously with the same dose. Conclusions: Remacemide hydrochloride inhibits CBZ metabolism, which itself induces that of remacemide hydrochloride and its active metabolite. This Mutual Interaction between remacemide hydrochloride and CBZ is predictable and modest and should not present a barrier to their clinical use in combination.
Tracey Jones - One of the best experts on this subject based on the ideXlab platform.
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Mutual Interaction between remacemide hydrochloride and phenytoin
Epilepsy research, 1997Co-Authors: John Paul Leach, Virginia Jamieson, Tracey Jones, Alan Richens, Jacqueline Girvan, Martin J. BrodieAbstract:Abstract A randomised, double-blind, placebo-controlled crossover study of add-on remacemide hydrochloride was carried out in epilepsy patients being treated with phenytoin (PHT) monotherapy. Eleven patients were recruited, ten of whom completed the study. Plasma concentration profiles of PHT, remacemide, and its active desglycinyl metabolite (ARL12495XX) were determined following single and multiple dosing with remacemide hydrochloride. Following 14 days' treatment with remacemide hydrochloride 300 mg twice daily, the mean AUC of PHT was increased by 11.5% ( P =0.33), C max by 13.7% ( P =0.32) and C min by 22.2% ( P =0.12) over placebo. There was an increase in trough concentrations of PHT averaging 20% during active treatment compared with placebo ( P =0.01). No symptoms of PHT toxicity were reported by any patient. There was no evidence of autoinduction of remacemide metabolism. However, average concentrations of remacemide and its active metabolite in PHT-treated patients were around 40 and 30% lower, respectively than in healthy volunteers previously receiving the same dose of remacemide hydrochloride. Thus, remacemide hydrochloride has a small inhibitory effect on PHT metabolism, which itself induces that of remacemide and its active metabolite. This Mutual Interaction is predictable and modest and should not present a barrier to their clinical use in combination.
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Mutual Interaction Between Remacemide Hydrochloride and Carbamazepine: Two Drugs with Active Metabolites
Epilepsia, 1996Co-Authors: John Paul Leach, Jackie Blacklaw, Virginia Jamieson, Tracey Jones, Alan Richens, Martin J. BrodieAbstract:Summary: Purpose: We wished to determine Mutual Interaction of two drugs with active metabolism: remacemide, hydrochloride and carbamazepine (CBZ). Methods: A randomized, double-blind, placebo-controlled cross-over study of add-on remacemide hydrochloride was performed in 10 of 14 recruited patients being treated with CBZ monotherapy. Forty-eight-hour concentration profiles of CBZ, its active epoxide metabolite (CBZ-E), remacemide, and its desglycinyl metabolite (ARL12495XX) were assayed after single and multiple dosing. Results: After patients were treated with 300 mg remacemide hydrochloride twice daily for 14 days, the mean area under the concentration-time curve (AUC) of CBZ was increased by 22% (p = 0.12), Cmax was increased by 27% (p = 0.07), and Cmin was increased by 22% (p = 0.29). Trough concentrations of CBZ were higher (p = 0.0037) during active treatment as compared with placebo treatment. CBZ-E levels were unaffected. No symptoms of CBZ toxicity were reported. There was no evidence of autoinduction of remacemide metabolism. However, in CBZ-treated patients, the AUC of remacemide and its active metabolite was 60 and 30%, respectively, of values observed in healthy volunteers treated previously with the same dose. Conclusions: Remacemide hydrochloride inhibits CBZ metabolism, which itself induces that of remacemide hydrochloride and its active metabolite. This Mutual Interaction between remacemide hydrochloride and CBZ is predictable and modest and should not present a barrier to their clinical use in combination.
