Abstract
A simple, sensitive, and accurate HPLC-DAD method has been developed and validated for the simultaneous determination of pantoprazole and etodolac in rat plasma as a tool for therapeutic drug monitoring. Optimal chromatographic separation of the analytes was achieved on a Waters Symmetry C18 column using a mobile phase that consisted of phosphate buffer pH~4.0 as eluent A and acetonitrile as eluent B in a ratio of A : B, 55 : 45 v/v for 6 min, pumped isocratically at a flow rate of 0.8 mL min−1. The eluted analytes were monitored using photodiode array detector set to quantify samples at 254 nm. The method was linear withr2=0.9999for PTZ andr2=0.9995for ETD at a concentration range of 0.1–15 and 5–50 μgmL−1for PTZ and ETD, respectively. The limits of detection were found to be 0.033 and 0.918 μgmL−1for PTZ and ETD, respectively. The method was statistically validated for linearity, accuracy, precision, and selectivity following the International Conference for Harmonization (ICH) guidelines. The reproducibility of the method was reliable with the intra- and interday precision (% RSD) <7.76% for PTZ and <7.58 % for ETD.
Highlights
Pantoprazole (5-(difluoromethoxy)-2-[(3,4-dimethoxy-2-pyridyl)methylsulfinyl]1H-benzimidazole, PTZ, Figure 1(a)) is a selective long-acting proton pump inhibitor [1]
Concurrent administration of proton pump inhibitors and nonsteroidal anti-inflammatory drugs (NSAIDs) has been previously reported due to the gastrointestinal problems arising from the chronic administration of NSAIDs alone
The method was extensively validated for the assay of PTZ and ETD in rat plasma which allows the quantification of PTZ and ETD in biological plasma samples for the purpose of bioequivalence study in the range of 0.1–15 μgmL−1 and 5– 50 μgmL−1 for PTZ and ETD, respectively
Summary
Pantoprazole (5-(difluoromethoxy)-2-[(3,4-dimethoxy-2-pyridyl)methylsulfinyl]1H-benzimidazole, PTZ, Figure 1(a)) is a selective long-acting proton pump inhibitor [1]. It is used for peptic ulcers, gastroesophageal reflux disease (GERD), Barrett’s esophagus, and Zollinger-Ellison syndrome, as well as the eradication of Helicobacter pylori as part of combination regimens [2]. NSAIDs have been reported to cause gastrointestinal (GI) lesions and result in dyspeptic symptoms and ulcerations and lead to increased risk of serious GI complications [4, 5]. 20 million patients in the US consume NSAIDs on a regular basis; the risk for hospitalization for serious GI adverse effects is 1-2%, resulting in approximately 200,000 to 400,000 hospitalizations per year [6]. Many patients are likely to receive both NSAIDs (either nonselective [7, 8] or selective COX-2 inhibitors [9]) and proton pump inhibitors
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