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Role Of Drug Intake In Disease Caused In Central Nervous System
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| Author:
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MR.SANDEEP KUMAR KURMI, DIPANSHU GARG, MS.AVISHIKTA RAY DAS, MS.SAMBRITA BOSE
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| Abstract:
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Single doses of GPI 5693 were provided to healthy volunteers in a double-blind placebo-controlled, exploratory experiment in the range of 100 mg to 1125 mg. 750, 1125, and 1500 mg doses were tested in an open-label and parallel extension study. For pharmacokinetic and biochemical/hematological safety studies, vital signs, ECG, and adverse event checks were done every 48 hours. Following the drug's ingestion into rats' bodies, the effects on the central nervous system were evaluated using eye movements, adaptive tracking, EEG, body sway, and Visual Analogue Scales (VAS) (VAS). There were significant reductions in adaptive tracking, VAS alertness, and VAS mood, as well as an increase in EEG occipital alpha and theta power consistent with CNS effects following the 1125 mg dosage. Gastrointestinal (GI) side effects were more prevalent in those taking higher dosages. There was no change in the ECG or vital signs throughout any of the treatments. The therapeutically relevant concentration range (950–11100 ng ml1) was already attained after a single dosage of 300 mg. T1/2 was 2.54 h for 300 mg and 4.78 h for 750 mg, with a Cmax of 2868 ng ml1 in both cases.3.4 The Cmax and AUC were reduced by about 66% and 40%, respectively, when the 750 mg and 1125 mg doses were taken with meals. Also, the dose-normalized Cmax reduced by 5.6 (CI: 2.26 to 8.7) ng ml1 mg1 following meal intake, which was a significant reduction. In the 300 and 750 mg dosages, the pharmacokinetic variability was the largest, resulting in a pharmacokinetic variability of about half the Cmax.
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| Keyword:
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Pharmacokinetics, Central Nervous System, NAALAD-As-Inhibitor.
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| EOI:
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| DOI:
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https://doi.org/10.31838/ijpr/2020.12.02.437
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| Download:
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