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Mansoor Ahmad - One of the best experts on this subject based on the ideXlab platform.
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Lipids bearing extruded-spheronized pellets for extended release of poorly soluble antiemetic agent—Meclizine HCl
Lipids in Health and Disease, 2017Co-Authors: Faaiza Qazi, Muhammad Harris Shoaib, Rabia Ismail Yousuf, Muhammad Iqbal Nasiri, Kamran Ahmed, Mansoor AhmadAbstract:Background Antiemetic agent Meclizine HCl, widely prescribed in vertigo, is available only in immediate release dosage forms. The approved therapeutic dose and shorter elimination half-life make Meclizine HCl a potential candidate to be formulated in extended release dosage form. This study was aimed to develop extended release Meclizine HCl pellets by extrusion spheronization using natural and synthetic lipids. Influence of lipid type, drug/lipid ratio and combinations of different lipids on drug release and sphericity of pellets were evaluated. Methods Thirty two formulations were prepared with four different lipids, Glyceryl monostearate (Geleol^®), Glyceryl palmitostearate (Precirol^®), Glyceryl behenate (Compritol^®) and Carnauba wax, utilized either alone or in combinations of drug/lipid ratio of 1:0.5–1:3. Dissolution studies were performed at variable pH and release kinetics were analyzed. Fourier transform infrared spectroscopy was conducted and no drug lipid interaction was found. Results Sphericity indicated by shape factor (e_R) varied with type and concentration of lipids: Geleol^® (e_R = 0.891–0.997), Precirol^® (e_R = 0.611–0.743), Compritol^® (e_R = 0.665–0.729) and Carnauba wax (e_R = 0.499-0.551). Highly spherical pellets were obtained with Geleol^® (Aspect ratio = 1.005–1.052) whereas irregularly shaped pellets were formed using Carnauba wax (Aspect ratio = 1.153–1.309). Drug release was effectively controlled by three different combinations of lipids: (i) Geleol^® and Compritol^®, (ii) Geleol^® and Carnauba wax and (iii) Geleol^®, Compritol^® and Carnauba wax. Scanning electron microscopy of Compritol^® pellets showed smooth surface with pores, whereas, irregular rough surface with hollow depressions was observed in Carnauba wax pellets. Energy dispersive spectroscopy indicated elemental composition of lipid matrix pellets. Kinetics of (i) Geleol^® and Compritol^® pellets, explained by Korsmeyer-Peppas (R^2 = 0.978–0.993) indicated non-Fickian diffusion ( n = 0.519-0.597). Combinations of (ii) Geleol^® and Carnauba wax and (iii) Geleol^®, Compritol^® and Carnauba wax pellets followed Zero-order (R^2 = 0.991–0.995). Similarity test was performed using combination of Geleol^® and Compritol^® (i) as a reference. Conclusions Matrices for the extended release of Meclizine HCl from extruded-spheronized pellets were successfully formed by using three lipids (Geleol^®, Compritol^® and Carnauba wax) in different combinations. The encapsulated pellets of Meclizine HCl can be effectively used for treatment of motion sickness, nausea and vertigo for extended period of time.
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Lipids bearing extruded-spheronized pellets for extended release of poorly soluble antiemetic agent-Meclizine HCl.
Lipids in Health and Disease, 2017Co-Authors: Faaiza Qazi, Muhammad Harris Shoaib, Rabia Ismail Yousuf, Muhammad Iqbal Nasiri, Kamran Ahmed, Mansoor AhmadAbstract:Antiemetic agent Meclizine HCl, widely prescribed in vertigo, is available only in immediate release dosage forms. The approved therapeutic dose and shorter elimination half-life make Meclizine HCl a potential candidate to be formulated in extended release dosage form. This study was aimed to develop extended release Meclizine HCl pellets by extrusion spheronization using natural and synthetic lipids. Influence of lipid type, drug/lipid ratio and combinations of different lipids on drug release and sphericity of pellets were evaluated. Thirty two formulations were prepared with four different lipids, Glyceryl monostearate (Geleol®), Glyceryl palmitostearate (Precirol®), Glyceryl behenate (Compritol®) and Carnauba wax, utilized either alone or in combinations of drug/lipid ratio of 1:0.5–1:3. Dissolution studies were performed at variable pH and release kinetics were analyzed. Fourier transform infrared spectroscopy was conducted and no drug lipid interaction was found. Sphericity indicated by shape factor (eR) varied with type and concentration of lipids: Geleol® (eR = 0.891–0.997), Precirol® (eR = 0.611–0.743), Compritol® (eR = 0.665–0.729) and Carnauba wax (eR = 0.499-0.551). Highly spherical pellets were obtained with Geleol® (Aspect ratio = 1.005–1.052) whereas irregularly shaped pellets were formed using Carnauba wax (Aspect ratio = 1.153–1.309). Drug release was effectively controlled by three different combinations of lipids: (i) Geleol® and Compritol®, (ii) Geleol® and Carnauba wax and (iii) Geleol®, Compritol® and Carnauba wax. Scanning electron microscopy of Compritol® pellets showed smooth surface with pores, whereas, irregular rough surface with hollow depressions was observed in Carnauba wax pellets. Energy dispersive spectroscopy indicated elemental composition of lipid matrix pellets. Kinetics of (i) Geleol® and Compritol® pellets, explained by Korsmeyer-Peppas (R2 = 0.978–0.993) indicated non-Fickian diffusion (n = 0.519-0.597). Combinations of (ii) Geleol® and Carnauba wax and (iii) Geleol®, Compritol® and Carnauba wax pellets followed Zero-order (R2 = 0.991–0.995). Similarity test was performed using combination of Geleol® and Compritol® (i) as a reference. Matrices for the extended release of Meclizine HCl from extruded-spheronized pellets were successfully formed by using three lipids (Geleol®, Compritol® and Carnauba wax) in different combinations. The encapsulated pellets of Meclizine HCl can be effectively used for treatment of motion sickness, nausea and vertigo for extended period of time.
Ella W. Englander - One of the best experts on this subject based on the ideXlab platform.
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Cisplatin Toxicity in Dorsal Root Ganglion Neurons Is Relieved by Meclizine via Diminution of Mitochondrial Compromise and Improved Clearance of DNA Damage.
Molecular neurobiology, 2016Co-Authors: Murat F. Gorgun, Ming Zhuo, Ella W. EnglanderAbstract:Chemotherapy-induced neurotoxicity of peripheral nervous system (PNS) hinders efficacy of cancer treatments. Mechanisms initiating PNS injury by anticancer drugs are incompletely understood delaying development of effective management strategies. To understand events triggered in PNS by cancer drugs, we exposed dorsal root ganglion (DRG) neurons to cisplatin, a drug from platinum-based class of chemotherapeutics frequently implicated in peripheral neuropathies. While cisplatin enters cancer cells and forms cisplatin/DNA crosslinks that block cell proliferation, circulating cisplatin can also reach the PNS and produce crosslinks that impede critical DNA transactions in postmitotic neurons. Cisplatin forms crosslinks with both, nuclear and mitochondrial DNA (mtDNA). Crosslinks are repairable primarily via the nucleotide excision repair (NER) pathway, which is present in nuclei but absent from mitochondrial compartment. Hence, high mitochondrial content and limited shielding by blood nerve barrier make DRG neurons particularly vulnerable to mitochondrial injury by cisplatin. We report that in DRG neurons, cisplatin elevates reactive oxygen species, depletes mtDNA, and impairs mitochondrial respiration, whereas concomitant Meclizine supplementation preserves redox balance, attenuates mitochondrial compromise, and augments DNA repair. Meclizine is an antihistamine drug recently implicated in neuroprotection via modulation of energy metabolism. Our data demonstrate that in the mitochondria-rich DRG neurons, Meclizine mitigates cisplatin-induced mitochondrial compromise via enhancement of pentose phosphate pathway and repletion of nicotinamide adenine dinucleotide phosphate (NADPH) and glutathione stores. The findings suggest that Meclizine-mediated preservation of redox balance sustains mitochondrial respiration and supports execution of cellular processes, including timely removal of cisplatin crosslinks from nuclear DNA, thereby attenuating cisplatin toxicity in DRG neurons. Collectively, the findings reveal potential for pharmacologic modulation of dorsal root ganglion neurons metabolism for protection against toxicity of chemotherapeutic drugs.
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Augmentation of glycolytic metabolism by Meclizine is indispensable for protection of dorsal root ganglion neurons from hypoxia-induced mitochondrial compromise
Free radical biology & medicine, 2016Co-Authors: Ming Zhuo, Murat F. Gorgun, Ella W. EnglanderAbstract:Abstract To meet energy demands, dorsal root ganglion (DRG) neurons harbor high mitochondrial content, which renders them acutely vulnerable to disruptions of energy homeostasis. While neurons typically rely on mitochondrial energy production and have not been associated with metabolic plasticity, new studies reveal that Meclizine, a drug, recently linked to modulations of energy metabolism, protects neurons from insults that disrupt energy homeostasis. We show that Meclizine rapidly enhances glycolysis in DRG neurons and that glycolytic metabolism is indispensable for Meclizine-exerted protection of DRG neurons from hypoxic stress. We report that supplementation of Meclizine during hypoxic exposure prevents ATP depletion, preserves NADPH and glutathione stores, curbs reactive oxygen species (ROS) and attenuates mitochondrial clustering in DRG neurites. Using extracellular flux analyzer, we show that in cultured DRG neurons Meclizine mitigates hypoxia-induced loss of mitochondrial respiratory capacity. Respiratory capacity is a measure of mitochondrial fitness and cell ability to meet fluctuating energy demands and therefore, a key determinant of cellular fate. While Meclizine is an ‘old’ drug with long record of clinical use, its ability to modulate energy metabolism has been uncovered only recently. Our findings documenting neuroprotection by Meclizine in a setting of hypoxic stress reveal previously unappreciated metabolic plasticity of DRG neurons as well as potential for pharmacological harnessing of the newly discovered metabolic plasticity for protection of peripheral nervous system under mitochondria compromising conditions.
Vishal M Gohil - One of the best experts on this subject based on the ideXlab platform.
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Meclizine preconditioning protects the kidney against ischemia reperfusion injury
EBioMedicine, 2015Co-Authors: Seiji Kishi, Vishal M Gohil, Fabiana Perocchi, Gabriela Campanholle, Craig R. Brooks, Ryuji Morizane, Venkata Sabbisetti, Takaharu Ichimura, Vamsi K. Mootha, Joseph V. BonventreAbstract:Abstract Global or local ischemia contributes to the pathogenesis of acute kidney injury (AKI). Currently there are no specific therapies to prevent AKI. Potentiation of glycolytic metabolism and attenuation of mitochondrial respiration may decrease cell injury and reduce reactive oxygen species generation from the mitochondria. Meclizine, an over-the-counter anti-nausea and -dizziness drug, was identified in a ‘nutrient-sensitized' chemical screen. Pretreatment with 100mg/kg of Meclizine, 17h prior to ischemia protected mice from IRI. Serum creatinine levels at 24h after IRI were 0.13±0.06mg/dl (sham, n=3), 1.59±0.10mg/dl (vehicle, n=8) and 0.89±0.11mg/dl (Meclizine, n=8). Kidney injury was significantly decreased in Meclizine treated mice compared with vehicle group (p
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Meclizine Preconditioning Protects the Kidney Against Ischemia–Reperfusion Injury
EBioMedicine, 2015Co-Authors: Seiji Kishi, Vishal M Gohil, Fabiana Perocchi, Gabriela Campanholle, Craig R. Brooks, Ryuji Morizane, Venkata Sabbisetti, Takaharu Ichimura, Vamsi K. Mootha, Joseph V. BonventreAbstract:Abstract Global or local ischemia contributes to the pathogenesis of acute kidney injury (AKI). Currently there are no specific therapies to prevent AKI. Potentiation of glycolytic metabolism and attenuation of mitochondrial respiration may decrease cell injury and reduce reactive oxygen species generation from the mitochondria. Meclizine, an over-the-counter anti-nausea and -dizziness drug, was identified in a ‘nutrient-sensitized' chemical screen. Pretreatment with 100mg/kg of Meclizine, 17h prior to ischemia protected mice from IRI. Serum creatinine levels at 24h after IRI were 0.13±0.06mg/dl (sham, n=3), 1.59±0.10mg/dl (vehicle, n=8) and 0.89±0.11mg/dl (Meclizine, n=8). Kidney injury was significantly decreased in Meclizine treated mice compared with vehicle group (p
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Meclizine inhibits mitochondrial respiration through direct targeting of cytosolic phosphoethanolamine metabolism
Journal of Biological Chemistry, 2013Co-Authors: Vishal M Gohil, Lin Zhu, Charli D Baker, Valentin Cracan, Abbas Yaseen, Mohit Jain, Clary B Clish, Paul S. BrookesAbstract:Abstract We recently identified Meclizine, an over-the-counter drug, as an inhibitor of mitochondrial respiration. Curiously, Meclizine blunted respiration in intact cells but not in isolated mitochondria, suggesting an unorthodox mechanism. Using a metabolic profiling approach, we now show that treatment with Meclizine leads to a sharp elevation of cellular phosphoethanolamine, an intermediate in the ethanolamine branch of the Kennedy pathway of phosphatidylethanolamine biosynthesis. Metabolic labeling and in vitro enzyme assays confirmed direct inhibition of the cytosolic enzyme CTP:phosphoethanolamine cytidylyltransferase (PCYT2). Inhibition of PCYT2 by Meclizine led to rapid accumulation of its substrate, phosphoethanolamine, which is itself an inhibitor of mitochondrial respiration. Our work identifies the first pharmacologic inhibitor of the Kennedy pathway, demonstrates that its biosynthetic intermediate is an endogenous inhibitor of respiration, and provides key mechanistic insights that may facilitate repurposing Meclizine for disorders of energy metabolism.
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Meclizine is neuroprotective in models of Huntington's disease
Human molecular genetics, 2010Co-Authors: Vishal M Gohil, Sunil A Sheth, Nicolas Offner, James A. Walker, Elisa Fossale, James F. Gusella, Marcy E. Macdonald, Christian Neri, Vamsi K. MoothaAbstract:Defects in cellular energy metabolism represent an early feature in a variety of human neurodegenerative diseases. Recent studies have shown that targeting energy metabolism can protect against neuronal cell death in such diseases. Here, we show that Meclizine, a clinically used drug that we have recently shown to silence oxidative metabolism, suppresses apoptotic cell death in a murine cellular model of polyglutamine (polyQ) toxicity. We further show that this protective effect extends to neuronal dystrophy and cell death in Caenorhabditis elegans and Drosophila melanogaster models of polyQ toxicity. Meclizine’s mechanism of action is not attributable to its anti-histaminergic or anti-muscarinic activity, but rather, strongly correlates with its ability to suppress mitochondrial respiration. Since Meclizine is an approved drug that crosses the blood–brain barrier, it may hold therapeutic potential in the treatment of polyQ toxicity disorders, such as Huntington’s disease.
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nutrient sensitized screening for drugs that shift energy metabolism from mitochondrial respiration to glycolysis
Nature Biotechnology, 2010Co-Authors: Vishal M Gohil, Sunil A Sheth, Roland Nilsso, Andrew P Wojtovich, Jeong Hyu Lee, Fabiana PerocchiAbstract:Most cells have the inherent capacity to shift their reliance on glycolysis relative to oxidative metabolism, and studies in model systems have shown that targeting such shifts may be useful in treating or preventing a variety of diseases ranging from cancer to ischemic injury. However, we currently have a limited number of mechanistically distinct classes of drugs that alter the relative activities of these two pathways. We screen for such compounds by scoring the ability of >3,500 small molecules to selectively impair growth and viability of human fibroblasts in media containing either galactose or glucose as the sole sugar source. We identify several clinically used drugs never linked to energy metabolism, including the antiemetic Meclizine, which attenuates mitochondrial respiration through a mechanism distinct from that of canonical inhibitors. We further show that Meclizine pretreatment confers cardioprotection and neuroprotection against ischemia-reperfusion injury in murine models. Nutrient-sensitized screening may provide a useful framework for understanding gene function and drug action within the context of energy metabolism.
Fabiana Perocchi - One of the best experts on this subject based on the ideXlab platform.
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Meclizine preconditioning protects the kidney against ischemia reperfusion injury
EBioMedicine, 2015Co-Authors: Seiji Kishi, Vishal M Gohil, Fabiana Perocchi, Gabriela Campanholle, Craig R. Brooks, Ryuji Morizane, Venkata Sabbisetti, Takaharu Ichimura, Vamsi K. Mootha, Joseph V. BonventreAbstract:Abstract Global or local ischemia contributes to the pathogenesis of acute kidney injury (AKI). Currently there are no specific therapies to prevent AKI. Potentiation of glycolytic metabolism and attenuation of mitochondrial respiration may decrease cell injury and reduce reactive oxygen species generation from the mitochondria. Meclizine, an over-the-counter anti-nausea and -dizziness drug, was identified in a ‘nutrient-sensitized' chemical screen. Pretreatment with 100mg/kg of Meclizine, 17h prior to ischemia protected mice from IRI. Serum creatinine levels at 24h after IRI were 0.13±0.06mg/dl (sham, n=3), 1.59±0.10mg/dl (vehicle, n=8) and 0.89±0.11mg/dl (Meclizine, n=8). Kidney injury was significantly decreased in Meclizine treated mice compared with vehicle group (p
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Meclizine Preconditioning Protects the Kidney Against Ischemia–Reperfusion Injury
EBioMedicine, 2015Co-Authors: Seiji Kishi, Vishal M Gohil, Fabiana Perocchi, Gabriela Campanholle, Craig R. Brooks, Ryuji Morizane, Venkata Sabbisetti, Takaharu Ichimura, Vamsi K. Mootha, Joseph V. BonventreAbstract:Abstract Global or local ischemia contributes to the pathogenesis of acute kidney injury (AKI). Currently there are no specific therapies to prevent AKI. Potentiation of glycolytic metabolism and attenuation of mitochondrial respiration may decrease cell injury and reduce reactive oxygen species generation from the mitochondria. Meclizine, an over-the-counter anti-nausea and -dizziness drug, was identified in a ‘nutrient-sensitized' chemical screen. Pretreatment with 100mg/kg of Meclizine, 17h prior to ischemia protected mice from IRI. Serum creatinine levels at 24h after IRI were 0.13±0.06mg/dl (sham, n=3), 1.59±0.10mg/dl (vehicle, n=8) and 0.89±0.11mg/dl (Meclizine, n=8). Kidney injury was significantly decreased in Meclizine treated mice compared with vehicle group (p
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nutrient sensitized screening for drugs that shift energy metabolism from mitochondrial respiration to glycolysis
Nature Biotechnology, 2010Co-Authors: Vishal M Gohil, Sunil A Sheth, Roland Nilsso, Andrew P Wojtovich, Jeong Hyu Lee, Fabiana PerocchiAbstract:Most cells have the inherent capacity to shift their reliance on glycolysis relative to oxidative metabolism, and studies in model systems have shown that targeting such shifts may be useful in treating or preventing a variety of diseases ranging from cancer to ischemic injury. However, we currently have a limited number of mechanistically distinct classes of drugs that alter the relative activities of these two pathways. We screen for such compounds by scoring the ability of >3,500 small molecules to selectively impair growth and viability of human fibroblasts in media containing either galactose or glucose as the sole sugar source. We identify several clinically used drugs never linked to energy metabolism, including the antiemetic Meclizine, which attenuates mitochondrial respiration through a mechanism distinct from that of canonical inhibitors. We further show that Meclizine pretreatment confers cardioprotection and neuroprotection against ischemia-reperfusion injury in murine models. Nutrient-sensitized screening may provide a useful framework for understanding gene function and drug action within the context of energy metabolism.
Faaiza Qazi - One of the best experts on this subject based on the ideXlab platform.
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Lipids bearing extruded-spheronized pellets for extended release of poorly soluble antiemetic agent—Meclizine HCl
Lipids in Health and Disease, 2017Co-Authors: Faaiza Qazi, Muhammad Harris Shoaib, Rabia Ismail Yousuf, Muhammad Iqbal Nasiri, Kamran Ahmed, Mansoor AhmadAbstract:Background Antiemetic agent Meclizine HCl, widely prescribed in vertigo, is available only in immediate release dosage forms. The approved therapeutic dose and shorter elimination half-life make Meclizine HCl a potential candidate to be formulated in extended release dosage form. This study was aimed to develop extended release Meclizine HCl pellets by extrusion spheronization using natural and synthetic lipids. Influence of lipid type, drug/lipid ratio and combinations of different lipids on drug release and sphericity of pellets were evaluated. Methods Thirty two formulations were prepared with four different lipids, Glyceryl monostearate (Geleol^®), Glyceryl palmitostearate (Precirol^®), Glyceryl behenate (Compritol^®) and Carnauba wax, utilized either alone or in combinations of drug/lipid ratio of 1:0.5–1:3. Dissolution studies were performed at variable pH and release kinetics were analyzed. Fourier transform infrared spectroscopy was conducted and no drug lipid interaction was found. Results Sphericity indicated by shape factor (e_R) varied with type and concentration of lipids: Geleol^® (e_R = 0.891–0.997), Precirol^® (e_R = 0.611–0.743), Compritol^® (e_R = 0.665–0.729) and Carnauba wax (e_R = 0.499-0.551). Highly spherical pellets were obtained with Geleol^® (Aspect ratio = 1.005–1.052) whereas irregularly shaped pellets were formed using Carnauba wax (Aspect ratio = 1.153–1.309). Drug release was effectively controlled by three different combinations of lipids: (i) Geleol^® and Compritol^®, (ii) Geleol^® and Carnauba wax and (iii) Geleol^®, Compritol^® and Carnauba wax. Scanning electron microscopy of Compritol^® pellets showed smooth surface with pores, whereas, irregular rough surface with hollow depressions was observed in Carnauba wax pellets. Energy dispersive spectroscopy indicated elemental composition of lipid matrix pellets. Kinetics of (i) Geleol^® and Compritol^® pellets, explained by Korsmeyer-Peppas (R^2 = 0.978–0.993) indicated non-Fickian diffusion ( n = 0.519-0.597). Combinations of (ii) Geleol^® and Carnauba wax and (iii) Geleol^®, Compritol^® and Carnauba wax pellets followed Zero-order (R^2 = 0.991–0.995). Similarity test was performed using combination of Geleol^® and Compritol^® (i) as a reference. Conclusions Matrices for the extended release of Meclizine HCl from extruded-spheronized pellets were successfully formed by using three lipids (Geleol^®, Compritol^® and Carnauba wax) in different combinations. The encapsulated pellets of Meclizine HCl can be effectively used for treatment of motion sickness, nausea and vertigo for extended period of time.
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Lipids bearing extruded-spheronized pellets for extended release of poorly soluble antiemetic agent-Meclizine HCl.
Lipids in Health and Disease, 2017Co-Authors: Faaiza Qazi, Muhammad Harris Shoaib, Rabia Ismail Yousuf, Muhammad Iqbal Nasiri, Kamran Ahmed, Mansoor AhmadAbstract:Antiemetic agent Meclizine HCl, widely prescribed in vertigo, is available only in immediate release dosage forms. The approved therapeutic dose and shorter elimination half-life make Meclizine HCl a potential candidate to be formulated in extended release dosage form. This study was aimed to develop extended release Meclizine HCl pellets by extrusion spheronization using natural and synthetic lipids. Influence of lipid type, drug/lipid ratio and combinations of different lipids on drug release and sphericity of pellets were evaluated. Thirty two formulations were prepared with four different lipids, Glyceryl monostearate (Geleol®), Glyceryl palmitostearate (Precirol®), Glyceryl behenate (Compritol®) and Carnauba wax, utilized either alone or in combinations of drug/lipid ratio of 1:0.5–1:3. Dissolution studies were performed at variable pH and release kinetics were analyzed. Fourier transform infrared spectroscopy was conducted and no drug lipid interaction was found. Sphericity indicated by shape factor (eR) varied with type and concentration of lipids: Geleol® (eR = 0.891–0.997), Precirol® (eR = 0.611–0.743), Compritol® (eR = 0.665–0.729) and Carnauba wax (eR = 0.499-0.551). Highly spherical pellets were obtained with Geleol® (Aspect ratio = 1.005–1.052) whereas irregularly shaped pellets were formed using Carnauba wax (Aspect ratio = 1.153–1.309). Drug release was effectively controlled by three different combinations of lipids: (i) Geleol® and Compritol®, (ii) Geleol® and Carnauba wax and (iii) Geleol®, Compritol® and Carnauba wax. Scanning electron microscopy of Compritol® pellets showed smooth surface with pores, whereas, irregular rough surface with hollow depressions was observed in Carnauba wax pellets. Energy dispersive spectroscopy indicated elemental composition of lipid matrix pellets. Kinetics of (i) Geleol® and Compritol® pellets, explained by Korsmeyer-Peppas (R2 = 0.978–0.993) indicated non-Fickian diffusion (n = 0.519-0.597). Combinations of (ii) Geleol® and Carnauba wax and (iii) Geleol®, Compritol® and Carnauba wax pellets followed Zero-order (R2 = 0.991–0.995). Similarity test was performed using combination of Geleol® and Compritol® (i) as a reference. Matrices for the extended release of Meclizine HCl from extruded-spheronized pellets were successfully formed by using three lipids (Geleol®, Compritol® and Carnauba wax) in different combinations. The encapsulated pellets of Meclizine HCl can be effectively used for treatment of motion sickness, nausea and vertigo for extended period of time.