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JournalISSN: 2198-641X

Current Pharmacology Reports 

Springer Science+Business Media
About: Current Pharmacology Reports is an academic journal published by Springer Science+Business Media. The journal publishes majorly in the area(s): Medicine & Cancer. It has an ISSN identifier of 2198-641X. Over the lifetime, 322 publications have been published receiving 5162 citations.

Papers published on a yearly basis

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Journal ArticleDOI
TL;DR: It is hoped that this review will provide useful and most updated therapeutic drugs to prevent, control, and treat COVID-19 patients until the approval of vaccines and specific drugs targeting SARS-CoV-2.
Abstract: The current pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has presented unprecedented challenges to the healthcare systems in almost every country around the world. Currently, there are no proven effective vaccines or therapeutic agents against the virus. Current clinical management includes infection prevention and control measures and supportive care including supplemental oxygen and mechanical ventilatory support. Evolving research and clinical data regarding the virologic SARS-CoV-2 suggest a potential list of repurposed drugs with appropriate pharmacological effects and therapeutic efficacies in treating COVID-19 patients. In this review, we will update and summarize the most common and plausible drugs for the treatment of COVID-19 patients. These drugs and therapeutic agents include antiviral agents (remdesivir, hydroxychloroquine, chloroquine, lopinavir, umifenovir, favipiravir, and oseltamivir), and supporting agents (Ascorbic acid, Azithromycin, Corticosteroids, Nitric oxide, IL-6 antagonists), among others. We hope that this review will provide useful and most updated therapeutic drugs to prevent, control, and treat COVID-19 patients until the approval of vaccines and specific drugs targeting SARS-CoV-2.

446 citations

Journal ArticleDOI
Masoud Jamei1
TL;DR: A number of drug labels are informed by simulation results generated using PBPK models, showing that either the simulations are used in lieu of conducting clinical studies or have informed the drug label that otherwise would have been silent in some specific situations.
Abstract: There is a renewed surge of interest in applications of physiologically-based pharmacokinetic (PBPK) models by the pharmaceutical industry and regulatory agencies. Developing PBPK models within a systems pharmacology context allows separation of the parameters pertaining to the animal or human body (the system) from that of the drug and the study design which is essential to develop generic drug-independent models used to extrapolate PK/PD properties in various healthy and patient populations. This has expanded the classical paradigm to a ‘predict-learn-confirm-apply’ concept. Recently, a number of drug labels are informed by simulation results generated using PBPK models. These cases show that either the simulations are used in lieu of conducting clinical studies or have informed the drug label that otherwise would have been silent in some specific situations. It will not be surprising to see applications of these models in implementing precision dosing at the point of care in the near future.

174 citations

Journal ArticleDOI
TL;DR: The current knowledge on the effect of curcumin in the treatment and/or prevention of inflammation, neurodegenerative diseases, and cancers by regulating histone deacetylases, histone acetyltransferases, and DNA methyltransferases is summarized.
Abstract: Curcumin (diferuloylmethane), a polyphenolic compound, is a component of Curcuma longa, commonly known as turmeric. It is a well-known anti-inflammatory, anti-oxidative, and anti-lipidemic agent and has recently been shown to modulate several diseases via epigenetic regulation. Many recent studies have demonstrated the role of epigenetic inactivation of pivotal genes that regulate human pathologies, such as neurocognitive disorders, inflammation, obesity, and cancers. Epigenetic changes involve changes in DNA methylation, histone modifications, or altered microRNA expression patterns which are known to be interconnected and play a key role in tumor progression and failure of conventional chemotherapy. The majority of epigenetic changes are influenced by lifestyle and diets. In this regard, dietary phytochemicals as dietary supplements have emerged as a promising source that are able to reverse these epigenetic alterations, to actively regulate gene expression and molecular targets that are known to promote tumorigenesis, and also to prevent age-related diseases through epigenetic modifications. There have been several studies which reported the role of curcumin as an epigenetic regulator in neurological disorders, inflammation, and in diabetes apart from cancers. The epigenetic regulatory roles of curcumin include (1) inhibition of DNA methyltransferases (DNMTs), which has been well defined from the recent studies on its function as a DNA hypomethylating agent; (2) regulation of histone modifications via regulation of histone acetyltransferases (HATs) and histone deacetylases (HDACs); and (3) regulation of micro RNAs (miRNA). This review summarizes the current knowledge on the effect of curcumin in the treatment and/or prevention of inflammation, neurodegenerative diseases, and cancers by regulating histone deacetylases, histone acetyltransferases, and DNA methyltransferases.

141 citations

Journal ArticleDOI
TL;DR: The cancer chemopreventive role of naturally occurring glucosinolate derivatives as inhibitors of carcinogenesis is summarized, with particular emphasis on specific molecular targets and epigenetic alterations in in vitro and in vivo human cancer animal models.
Abstract: Glucosinolates are a group of sulfur-containing glycosides found in many plant species, including cruciferous vegetables such as broccoli, cabbage, brussels sprouts, and cauliflower. Accumulating evidence increasingly supports the beneficial effects of dietary glucosinolates on overall health, including as potential anti-cancer agents, because of their role in the prevention of the initiation of carcinogenesis via the induction of cellular defense detoxifying/antioxidant enzymes and their epigenetic mechanisms, including modification of the CpG methylation of cancer-related genes, histone modification regulation and changes in the expression of miRNAs. In this context, the defense mechanism mediated by Nrf2-antioxidative stress and anti-inflammatory signaling pathways can contribute to cellular protection against oxidative stress and reactive metabolites of carcinogens. In this review, we summarize the cancer chemopreventive role of naturally occurring glucosinolate derivatives as inhibitors of carcinogenesis, with particular emphasis on specific molecular targets and epigenetic alterations in in vitro and in vivo human cancer animal models.

139 citations

Journal ArticleDOI
TL;DR: The discovery of ROS-responsive microRNAs provides a potential new strategy to specifically overcome ROS-mediated tumor progression or benefit from ROS-induced apoptosis.
Abstract: As both reactive oxygen species (ROS) production and microRNA expression signature have been associated with tumor development, progression, metastasis, and therapeutic response, it is important to understand the crosstalk between ROS and microRNAs. Indeed, growing evidence suggests a reciprocal connection between ROS signaling and microRNA pathway, resulting in diverse biological effects in cancer cells. In this mini review, we discussed the ROS-responsive microRNAs that have implications in cancer and the possible mechanisms in which ROS regulate microRNAs. We also highlighted the microRNAs which are able to modify cellular ROS homeostasis during tumorigenesis, their biological targets and subsequent functions. As the use of antioxidants is limited due to the diverse or even opposing roles of ROS signaling in cancer, the discovery of ROS-responsive microRNAs provides a potential new strategy to specifically overcome ROS-mediated tumor progression or benefit from ROS-induced apoptosis.

100 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
202319
202245
202119
202040
201942
201843