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In Silico Approach to Cancer Therapy
Published in Anjana Pandey, Saumya Srivastava, Recent Advances in Cancer Diagnostics and Therapy, 2022
Anjana Pandey, Saumya Srivastava
In anticancer pharmaceutics, repurposing the obsolete FDA-approved drugs for novel therapeutic use became a fascinating approach (Hsieh et al., 2019; Lo and Torres, 2019; Melge et al., 2019; Costa et al., 2020; Dinić et al., 2020; GNS et al., 2020; Irham et al., 2020; De et al., 2021; Mahdian et al., 2021). This process is also called drug repurposing. The primary benefit of this process is associated with the cost of drug and time issues. Drug repurposing significantly reduces drug development’s associated risk and expense and curtails the time gap from drug finding to its availability for patients because of having suitable and appropriate pharmacokinetics and clinical data (Shaughnessy, 2011; Papapetropoulos and Szabo, 2018; Fayed et al., 2021; Issa et al., 2021; Karaman Mayack and Sippl, 2021; Li et al., 2021; Mottini et al., 2021; Sankhe et al., 2021; Sohraby and Aryapour, 2021; Zhang et al., 2021). Generally, experimental-driven drug repurposing is just a matter of uncertainty; it can’t be driven hypothetically. Instead, it can be obtained from screening drug experiments or by the target similarities identification in different diseases (Wilkinson and Pritchard, 2015). In the case of cancer, examples of current drug repurposing include (i) Disulfiram, which was initially used for the treatment of alcoholism and discovered as therapeutics for cancer treatment (Iljin et al., 2009; Huang et al., 2016; Skrott et al., 2017); (ii) Valproic Acid, an antiepileptic repurposed to the anticancer drug in many clinical trials (Chateauvieux et al., 2010); (iii) Nelfinavir, originally used to treat HIV infection and now it is under clinical trials for the treatment of breast, lung, and melanoma cancers (Shim and Liu, 2014).
Pleural disease induced by drugs
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Valproic acid, a carboxylic acid derivative, is used for the treatment of specific seizure disorders and acute manic episodes in patients with bipolar disorder. It has also been used for migraine headache prophylaxis and other psychiatric conditions. Common adverse effects include somnolence, tremor, nausea and vomiting; hepatic failure has also been reported.
Metabolomics profiling of valproic acid-induced symptoms resembling autism spectrum disorders using 1H NMR spectral analysis in rat model
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Hyang Yeon Kim, Yong-Jae Lee, Sun Jae Kim, Jung Dae Lee, Suhkmann Kim, Mee Jung Ko, Ji-Woon Kim, Chan Young Shin, Kyu-Bong Kim
There have been many studies on neurotoxicity and its causal factors (Li and Li 2021; Tsai et al. 2021; Wilson et al. 2021). Although many etiologies for ASD have been proposed, the precise causal mechanism for this disorder remains unknown. In addition, single-gene disorders, inborn errors in metabolism, heavy metals, and maternal drug exposure are known to increase the risk of ASD development (Ghaziuddin and Al-Owain 2013; Hill et al. 2015; Rossignol and Frye 2014; Shin et al. 2021). Exposure to drugs, such as valproic acid (VPA), may also be associated with ASD development (Williams et al. 2001). Clinical investigators reported that administration of VPA during pregnancy increased the risk of incidence of neural tube defects, including ASD (Christensen et al. 2013; Williams et al. 2001). Valproic acid is used to treat epilepsy and bipolar disorder, as well as modulating gamma-aminobutyric acid (GABA) neurotransmission and preventing migraine headaches. In a follow-up study of children exposed to VPA during pregnancy, the rate of ASD was elevated approximately 8-fold concomitant with reduction in number of eye motor neurons, shortened tail regions in the facial nucleus, and decreased number of Purkinje cells (Baker et al. 2015). It is of interest that several investigators noted treatment with VPA during pregnancy led to fetal valproate syndrome (FVS), which results in abnormal and delayed development, organ malformations, and deficits in social function or communication ASD (Christensen et al. 2013; Williams et al. 2001).
Anticlastogenic and hepatoprotective effects of Kolaviron on sodium valproate-induced oxidative toxicity in Wistar rats
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Olaniyi Solomon Ola, Kayode Ezekiel Adewole
Off-target toxicity of many effective modern day drugs against neurological diseases is a major concern to some patients undergoing treatments, as some drugs have adverse effects on major organs that expressed their metabolizing enzymes in addition to their purported pharmacological activities. Valproic acid (VPA) also known as 2-propylpentanoic acid is a front-line synthetic drug used for treatment of some types of epilepsy and myriads of neurological conditions, such as bipolar disorder, neuropathic pain and migraine [1,2]. It is a choice drug for the treatment of epilepsy and neurodegenerative diseases that affect more than 70 million people worldwide [3,4]. However, administration of VPA could elevate hepatic damage markers in patients as well as in experimental rat models [5,6] and cause definite liver damage that may lead to resultant fatal liver failure [7,8]. VPA was linked with rare fatal hepatotoxicity [9] due to oxidative stress resulting from overproduction of reactive species, and its reactive metabolites were suggested to play a key role in the etiology of its toxicity [10]. Cytochrome P450 metabolize VPA to electrophilic metabolite (E) 2, 4-diene-VPA which was a suggested marker for assessing oxidative stress in liver cells and a major cause of necrotic cell death and hepatotoxicity in human [10]. Since treatment with VPA was associated with oxidative stress through dose-dependent increase in plasma and hepatic level of endogenous lipid peroxidation (LPO) markers [11], it is very important to search for new therapeutic agent that can counteract its undesirable hepatotoxic effects and therefore preserve its desirable therapeutic outcomes.