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Please use this identifier to cite or link to this item: http://repository.iitr.ac.in/handle/123456789/20153
Title: Ibuprofen-based advanced therapeutics: breaking the inflammatory link in cancer, neurodegeneration, and diseases
Authors: Upadhyay A.
Amanullah A.
Joshi V.
Dhiman R.
Prajapati V.K.
Poluri, Krishna Mohan
Mishra A.
Published in: Drug Metabolism Reviews
Abstract: Ibuprofen is a classical nonsteroidal anti-inflammatory drug (NSAID) highly prescribed to reduce acute pain and inflammation under an array of conditions, including rheumatoid arthritis, osteoarthritis, dysmenorrhea, and gout. Ibuprofen acts as a potential inhibitor for cyclooxygenase enzymes (COX-1 and COX-2). In the past few decades, research on this small molecule has led to identifying other possible therapeutic benefits. Anti-tumorigenic and neuroprotective functions of Ibuprofen are majorly recognized in recent literature and need further consideration. Additionally, several other roles of this anti-inflammatory molecule have been discovered and subjected to experimental assessment in various diseases. However, the major challenge faced by Ibuprofen and other drugs of similar classes is their side effects, and tendency to cause gastrointestinal injury, generate cardiovascular risks, modulate hepatic and acute kidney diseases. Future research should also be conducted to deduce new methods and approaches of suppressing the unwanted toxic changes mediated by these drugs and develop new therapeutic avenues so that these small molecules continue to serve the purposes. This article primarily aims to develop a comprehensive and better understanding of Ibuprofen, its pharmacological features, therapeutic benefits, and possible but less understood medicinal properties apart from major challenges in its future application.KEY POINTS Ibuprofen, an NSAID, is a classical anti-inflammatory therapeutic agent. Pro-apoptotic roles of NSAIDs have been explored in detail in the past, holding the key in anti-cancer therapies. Excessive and continuous use of NSAIDs may have several side effects and multiple organ damage. Hyperactivated Inflammation initiates multifold detrimental changes in multiple pathological conditions. Targeting inflammatory pathways hold the key to several therapeutic strategies against many diseases, including cancer, microbial infections, multiple sclerosis, and many other brain diseases. © 2021 Informa UK Limited, trading as Taylor & Francis Group.
Citation: Drug Metabolism Reviews, 53(1): 100-121
URI: https://doi.org/10.1080/03602532.2021.1903488
http://repository.iitr.ac.in/handle/123456789/20153
Issue Date: 2021
Publisher: Taylor and Francis Ltd.
Keywords: COX
ibuprofen
neurodegeneration
neuroprotection
NSAIDs
ISSN: 3602532
Author Scopus IDs: 57189335137
56188291700
56189143600
30467506200
24468880500
55842079400
57214220793
Author Affiliations: Upadhyay, A., Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Jodhpur, Rajasthan, India
Amanullah, A., Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Jodhpur, Rajasthan, India
Joshi, V., Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Jodhpur, Rajasthan, India
Dhiman, R., Laboratory of Mycobacterial Immunology, Department of Life Science, National Institute of Technology, Rourkela, Odisha, India
Prajapati, V.K., Department of Biochemistry, School of Life Sciences, Central University of Rajasthan, Ajmer, Rajasthan, India
Poluri, K.M., Department of Biotechnology, Indian Institute of Technology Roorkee, Roorkee, Uttarakhand, India
Mishra, A., Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Jodhpur, Rajasthan, India
Funding Details: The work was supported by the Science & Engineering Research Board (SERB), Department of Science & Technology, Government of India grant to AM [EMR/2016/000716]. EMR/2016/000716; Science and Engineering Research Board, SERB
Corresponding Author: Mishra, A.; Cellular and Molecular Neurobiology Unit, India
Appears in Collections:Journal Publications [BT]

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