BIJO MATHEW

Dr. BIJO MATHEW

Amrita School of Pharmacy

Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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28 December 2019 in Environmental Science and Pollution Research
Verified
Journal Article
Closed access
PDF file
JJJobin Jose
Jobin Jose
RKRajesh Kumar
Rajesh Kumar
SHSeetha Harilal
Seetha Harilal
GMGitha Elizabeth Mathew
Githa Elizabeth Mathew
DPDella Grace Thomas Parambi
Della Grace Thomas Parambi
BIJO MATHEWBIJO MATHEW
BIJO MATHEW

11 October 2022 in Processes
Verified
Journal Article
Open access
PDF file
ANAathira Sujathan Nair
Aathira Sujathan Nair
ASAshutosh Kumar Singh
Ashutosh Kumar Singh
AKAstik Kumar
Astik Kumar
SKSUNIL KUMAR
SUNIL KUMAR
SSSunitha Sukumaran
Sunitha Sukumaran
BIJO MATHEWBIJO MATHEW
BIJO MATHEW
As people around the world regard 2020 as the year of COVID-19, the medical community considers this year to be the second-best year, shared with the year 1996, with respect to the number of drug molecules approved by the US Food and Drug Administration (FDA). Both years, 2020 and 1996, had a record of 53 new drug molecules approved by the FDA. In the year 2020, 53 new chemical entities and 13 biological medicines were approved, including 10 monoclonal antibodies, 2 antibody-drug conjugates, 3 peptides, and 2 oligonucleotides. Among them, most of the compounds were found to have fluorine or fluorine-containing functional groups exhibiting numerous pharmacological activities. Herein, we summarized the trifluoromethyl (TFM, -CF3)-group-containing FDA-approved drugs for the last 20 years. This article specially features and details the previous 20-year literature data, covering CF3-incorporated potential drug molecules, including their syntheses and uses for various diseases and disorders. The review covers the detailed chemistry of 19 FDA-approved drugs in the past 20 years, which contains the TFM group as one of the pharmacophores.

Verified
Journal Article
Open access
PDF file
TKTanvir Kabir
Tanvir Kabir
SUSahab Uddin
Sahab Uddin
AMAbdullah Al Mamun
Abdullah Al Mamun
Philippe JeandetPhilippe Jeandet
Philippe Jeandet
Lotfi AleyaLotfi Aleya
Lotfi Aleya
Mohamed Abdel-DaimMohamed Abdel-Daim
Mohamed Abdel-Daim
Alzheimer’s disease (AD) is the leading cause of dementia worldwide. Even though the number of AD patients is rapidly growing, there is no effective treatment for this neurodegenerative disorder. At present, implementation of effective treatment approaches for AD is vital to meet clinical needs. In AD research, priorities concern the development of disease-modifying therapeutic agents to be used in the early phases of AD and the optimization of the symptomatic treatments predominantly dedicated to the more advanced AD stages. Until now, available therapeutic agents for AD treatment only provide symptomatic treatment. Since AD pathogenesis is multifactorial, use of a multimodal therapeutic intervention addressing several molecular targets of AD-related pathological processes seems to be the most practical approach to modify the course of AD progression. It has been demonstrated through numerous studies, that the clinical efficacy of combination therapy (CT) is higher than that of monotherapy. In case of AD, CT is more effective, mostly when started early, at slowing the rate of cognitive impairment. In this review, we have covered the major studies regarding CT to combat AD pathogenesis. Moreover, we have also highlighted the safety, tolerability, and efficacy of CT in the treatment of AD.

3 September 2019 in Archiv der Pharmazie
Verified
Journal Article
Closed access
PDF file
BIJO MATHEWBIJO MATHEW
BIJO MATHEW
DPDella G. T. Parambi
Della G. T. Parambi
GMGitha E. Mathew
Githa E. Mathew
SUSahab Uddin
Sahab Uddin
SISini T. Inasu
Sini T. Inasu
Simone CarradoriSimone Carradori
Simone Carradori

1 September 2019 in Journal of Pharmacy and Pharmacology
Verified
Journal Article
Closed access
SHSeetha Harilal
Seetha Harilal
JJJobin Jose
Jobin Jose
DPDella Grace Thomas Parambi
Della Grace Thomas Parambi
RKRajesh Kumar
Rajesh Kumar
GMGitha Elizabeth Mathew
Githa Elizabeth Mathew
BIJO MATHEWBIJO MATHEW
BIJO MATHEW

11 March 2020 in Molecules
Verified
Journal Article
Open access
PDF file
SUSahab Uddin
Sahab Uddin
TKTanvir Kabir
Tanvir Kabir
KNKamal Niaz
Kamal Niaz
Philippe JeandetPhilippe Jeandet
Philippe Jeandet
Christophe ClémentChristophe Clément
Christophe Clément
Lotfi AleyaLotfi Aleya
Lotfi Aleya
Alzheimer’s disease (AD) is one of the utmost chronic neurodegenerative disorders, which is characterized from a neuropathological point of view by the aggregates of amyloid beta (Aβ) peptides that are deposited as senile plaques and tau proteins which form neurofibrillary tangles (NFTs). Even though advancement has been observed in order to understand AD pathogenesis, currently available therapeutic methods can only deliver modest symptomatic relief. Interestingly, naturally occurring dietary flavonoids have gained substantial attention due to their antioxidative, anti-inflammatory, and anti-amyloidogenic properties as alternative candidates for AD therapy. Experimental proof provides support to the idea that some flavonoids might protect AD by interfering with the production and aggregation of Aβ peptides and/or decreasing the aggregation of tau. Flavonoids have the ability to promote clearance of Aβ peptides and inhibit tau phosphorylation by the mTOR/autophagy signaling pathway. Moreover, due to their cholinesterase inhibitory potential, flavonoids can represent promising symptomatic anti-Alzheimer agents. Several processes have been suggested for the aptitude of flavonoids to slow down the advancement or to avert the onset of Alzheimer’s pathogenesis. To enhance cognitive performance and to prevent the onset and progress of AD, the interaction of flavonoids with various signaling pathways is proposed to exert their therapeutic potential. Therefore, this review elaborates on the probable therapeutic approaches of flavonoids aimed at averting or slowing the progression of the AD pathogenesis.