Abstract
Objectives: This study aimed to develop simple UV spectrophotometric methods for simultaneous determination of pravastatin sodium and pioglitazone hydrochloride without previous separation. Methods. The first method is the first derivative, where the peak amplitudes of first derivative of absorption spectra were measured at 249.7 and 277 nm for pravastatin sodium and pioglitazone hydrochloride respectively. The second method is the first derivative of the ratio spectra, where the peak amplitudes were measured at 249.6 and 276.6 nm for pravastatin sodium and pioglitazone hydrochloride respectively. Results. The proposed methods were validated according to International Conference on Harmonization (ICH) guidelines and successfully applied for simultaneous determination of both drugs in their combined dosage form. Conclusion. The proposed methods are simple, rapid, economic, accurate and precise to simultaneously determine pravastatin and pioglitazone in pure form and in pharmaceutical dosage form without previous separation steps.
Highlights
Pravastatin sodium (PRV), (Figure 1a), is sodium (3R,5R)-7-{(1S,2S,6S,8S,8aR)-1,2,6,7,8,8ahexahydro-6-hydroxy-2-methyl-8-[(S)-2-methylbutyryloxy]-1-naphthyl}-3,5 dihydroxyheptan-oate.[1,2] It is a selective and competitive inhibitor of 3-hydroxy-3methylglutaryl -coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme that converts HMG-CoA to mevalonate, a precursor of cholesterol.[3]
It increases the number of hepatic low density lipoprotein (LDL) receptors on the cell surface to enhance uptake and catabolism of LDL
PRV inhibits hepatic synthesis of very low density lipoprotein (VLDL), which reduces the total number of VLDL and LDL particles.[4]
Summary
Pravastatin sodium (PRV), (Figure 1a), is sodium (3R,5R)-7-{(1S,2S,6S,8S,8aR)-1,2,6,7,8,8ahexahydro-6-hydroxy-2-methyl-8-[(S)-2-methylbutyryloxy]-1-naphthyl}-3,5 dihydroxyheptan-oate.[1,2] It is a selective and competitive inhibitor of 3-hydroxy-3methylglutaryl -coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme that converts HMG-CoA to mevalonate, a precursor of cholesterol.[3] PRV is a member of the class of statins, used to treat hypercholesterolemia and related conditions and to prevent cardiovascular disease. It increases the number of hepatic low density lipoprotein (LDL) receptors on the cell surface to enhance uptake and catabolism of LDL. PRV inhibits hepatic synthesis of very low density lipoprotein (VLDL), which reduces the total number of VLDL and LDL particles.[4]
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