Hisham A. Badreldin , Nada Alsuhebany , Mohammed Alzahrani , Abdulmajeed M. Alshehri , Maha Aldoughaim , Saleh Alqifari , Omar Yassin , Lama Alfehaid , Tariq Alqahtani
{"title":"Abelacimab: A leap forward in anticoagulation with FXI and FXIa Inhibition","authors":"Hisham A. Badreldin , Nada Alsuhebany , Mohammed Alzahrani , Abdulmajeed M. Alshehri , Maha Aldoughaim , Saleh Alqifari , Omar Yassin , Lama Alfehaid , Tariq Alqahtani","doi":"10.1016/j.crphar.2024.100179","DOIUrl":"https://doi.org/10.1016/j.crphar.2024.100179","url":null,"abstract":"<div><p>Direct Oral Anticoagulants (DOACs) have revolutionized the treatment of thromboembolic disorders, offering targeted, effective, and safer alternatives to traditional anticoagulants like heparins and vitamin K antagonists (VKAs). Despite their benefits, DOACs have drawbacks, including an increased risk of gastrointestinal bleeding and unsuitability for patients with mechanical heart valves. Recent research has highlighted Factor XI (FXI) as a promising anticoagulation target due to its significant role in pathological thrombosis and minor involvement in normal hemostasis. Abelacimab, an antibody that inhibits FXI, has shown potential in transforming anticoagulation therapy by sparing hemostasis. This review provides a comprehensive analysis of abelacimab, examining its clinical pharmacology and its pharmacokinetic and pharmacodynamic properties. It scrutinizes abelacimab's safety profile and key monitoring parameters. The current evidence supporting its use and potential future research strengthening its position in anticoagulant therapy is also discussed. The objective is to enhance understanding and contribute to discussions around developing safer anticoagulants, particularly for patients at risk for thrombosis.</p></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"6 ","pages":"Article 100179"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590257124000063/pdfft?md5=57b84c5a9c099c657260d03887e08166&pid=1-s2.0-S2590257124000063-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140163560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Molecular mechanisms and therapeutic potential of natural flavonoids in diabetic nephropathy: Modulation of intracellular developmental signaling pathways","authors":"Mahaboob Khan Sulaiman","doi":"10.1016/j.crphar.2024.100194","DOIUrl":"https://doi.org/10.1016/j.crphar.2024.100194","url":null,"abstract":"<div><p>Recognized as a common microvascular complication of diabetes mellitus (DM), diabetic nephropathy (DN) is the principal cause of chronic end-stage renal disease (ESRD). Patients with diabetes have an approximately 25% risk of developing progressive renal disease. The underlying principles of DN control targets the dual outcomes of blood glucose regulation through sodium glucose cotransporter 2 (SGLT 2) blockade and hypertension management through renin-angiotensin-aldosterone inhibition. However, these treatments are ineffective in halting disease progression to kidney failure and cardiovascular comorbidities. Recently, the dysregulation of subcellular signaling pathways has been increasingly implicated in DN pathogenesis. Natural compounds are emerging as effective and side-effect-free therapeutic agents that target intracellular pathways. This narrative review synthesizes recent insights into the dysregulation of maintenance pathways in DN, drawing from animal and human studies. To compile this review, articles reporting DN signaling pathways and their treatment with natural flavonoids were collected from PubMed, Cochrane Library Web of Science, Google Scholar and EMBASE databases since 2000. As therapeutic interventions are frequently based on the results of clinical trials, a brief analysis of data from current phase II and III clinical trials on DN is discussed.</p></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"7 ","pages":"Article 100194"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S259025712400021X/pdfft?md5=1f92eb2d0381845b0736d4728a947c8b&pid=1-s2.0-S259025712400021X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141582194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Exacerbation of atherosclerosis, hyperlipidemia and inflammation by MK886, an inhibitor of leukotriene biosynthesis, in obese and diabetic mice","authors":"Katherine Keever , Bardia Askari","doi":"10.1016/j.crphar.2024.100203","DOIUrl":"10.1016/j.crphar.2024.100203","url":null,"abstract":"<div><div>Leukotrienes are potent mediators of the inflammatory response and 5-lipoxygenase, the enzyme responsible for their synthesis, is dependent on its interaction with 5-lipoxygenase activating protein for optimum catalysis. Previous studies had demonstrated that macrophage infiltration into adipose tissue is associated with obesity and atherosclerosis in LDLR<sup>−/−</sup> mice fed a high fat-high carbohydrate. The present study was undertaken to determine whether inhibition of 5-lipoxygenase activating protein is efficacious in attenuating adipose tissue inflammation in LDLR<sup>−/−</sup> mice fed a high fat-high carbohydrate. 10-week old male LDLR<sup>−/−</sup> mice were fed a high fat-high carbohydrate diet for 22-weeks, with or without MK886 (40 mg/kg/day, <em>ad libitum</em>) a well-established 5-lipoxygenase activating protein inhibitor. All mice had an approximate 2-fold increase in total body weight, but a 6-week course of MK886 treatment had differential effects on adipose tissue size, without affecting macrophage accumulation. MK886 exacerbated the dyslipidemia, increased serum amyloid A content of high-density lipoproteins and caused a profound hepatomegaly. Dyslipidemia and increased serum amyloid A were concomitant with increases in atherosclerosis. In conclusion, MK886 paradoxically exacerbated hyperlipidemia and the pro-inflammatory phenotype in a mouse model of diet-induced atherosclerosis, possibly via a disruption of hepatic lipid metabolism and increased inflammation.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"7 ","pages":"Article 100203"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142527344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
George J. Dugbartey , Karl K. Alornyo , Christabel O. Dapaa-Addo , Emmanuel Botchway , Emmanuel K. Kwashie , Yvonne Harley
{"title":"Alpha-lipoic acid: A promising pharmacotherapy seen through the lens of kidney diseases","authors":"George J. Dugbartey , Karl K. Alornyo , Christabel O. Dapaa-Addo , Emmanuel Botchway , Emmanuel K. Kwashie , Yvonne Harley","doi":"10.1016/j.crphar.2024.100206","DOIUrl":"10.1016/j.crphar.2024.100206","url":null,"abstract":"<div><div>Kidney diseases have rapidly increased in prevalence over the past few decades, and have now become a major global public health concern. This has put economic burden on the public healthcare system and causing significant morbidity and mortality worldwide. Unfortunately, drugs currently in use for the management of kidney diseases have long-term major adverse effects that negatively impact the quality of life of these patients, hence making these drugs a “necessary evil”. In recent times, antioxidant therapy has been explored as a potential pharmacological avenue for treatment of kidney diseases, and could offer a better therapeutic option with less adverse effect profile. One of such antioxidants is alpha-lipoic acid (ALA), a sulphur-containing multifunctional antioxidant that is endogenously produced by lipoic acid synthase in the mitochondria of many tissues, including the kidney. Burgeoning evidence indicates that ALA is showing clinical promise in the treatment and pharmacological management of many kidney diseases through its antioxidant and other therapeutic properties by activating several protective mechanisms while inhibiting deleterious signaling pathways. In this review, we present ALA as a potent naturally occurring antioxidant, its mitochondrial biosynthesis and pharmacological properties. In addition, we also discuss within the limit of present literature, ALA and its underlying molecular mechanisms implicated in experimental and clinical treatment of various kidney conditions, and thus, may offer nephrologists an additional and/or alternative avenue in the pharmacological management and treatment of kidney diseases while giving hope to these patients.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"7 ","pages":"Article 100206"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142537363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
John Oludele Olanlokun , Oshireku Wisdom Abiodun , Adekunle Theophilus Adegbuyi , Neil Anthony Koorbanally , Olufunso Olabode Olorunsogo
{"title":"Mefloquine-curcumin combinations improve host mitochondrial respiration and decrease mitotoxic effects of mefloquine in Plasmodium berghei-infected mice","authors":"John Oludele Olanlokun , Oshireku Wisdom Abiodun , Adekunle Theophilus Adegbuyi , Neil Anthony Koorbanally , Olufunso Olabode Olorunsogo","doi":"10.1016/j.crphar.2024.100180","DOIUrl":"10.1016/j.crphar.2024.100180","url":null,"abstract":"<div><p><em>Plasmodium</em> infection is a health challenge. Although, antiplasmodial drugs kill the parasites, information on the effects of infection and drugs on the expression of some genes is limited.</p><p>Malaria was induced in two different studies using NK65 (chloroquine-susceptible, study 1), and ANKA (chloroquine-resistant, study 2) strains of <em>Plasmodium berghei</em> in 30 male Swiss mice (n = 5) in each study. Mice orally received 10 mL/kg distilled water, (infected control), Mefloquine (MF) (10 mg/kg), MF and Curcumin (CM) (25 mg/kg), MF and CM (50 mg/kg), CM (25 mg/kg) and CM (50 mg/kg). Five mice (un-infected) were used as the control. After treatment, total Ribonucleic acid (RNA) was isolated from liver and erythrocytes while Deoxyribonucleic acid (DNA)-free RNA were converted to cDNA. Polymerase Chain Reaction (PCR) amplification was performed and relative expressions of <em>FIKK12, AQP3, P38 MAPK, NADH</em> oxidoreductase, and cytochrome oxidase expressions were determined. Markers of glycolysis, toxicity and antioxidants were determined using ELISA assays. While the expression of <em>FIKK12</em> was blunted by MF in the susceptible study, co-treatment with curcumin (25 mg/kg) yielded the same results in the chloroquine-resistant study. Similar results were obtained on <em>AQP3</em> in both studies. Curcumin decreased <em>P38 MAPK</em> in both studies. <em>Plasmodium</em> infection decreased <em>NADH</em> oxidoreductase and cytochrome oxidase but mefloquine-curcumin restored the expression of these genes. While glycolysis and toxicity were inhibited, antioxidant systems improved in the treated groups. Curcumin is needed for effective therapeutic efficacy and prevention of toxicity. <em>Plasmodium</em> infection and treatment modulate the expressions of some genes in the host. Curcumin combination with mefloquine modulates the expression of some genes in the host.</p></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"6 ","pages":"Article 100180"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590257124000075/pdfft?md5=5c540566dbefe3538d1df92bdff79031&pid=1-s2.0-S2590257124000075-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140760778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Andrey Y. Vinokurov , Marina Y. Pogonyalova , Larisa Andreeva , Andrey Y. Abramov , Plamena R. Angelova
{"title":"Energy substrate supplementation increases ATP levels and is protective to PD neurons","authors":"Andrey Y. Vinokurov , Marina Y. Pogonyalova , Larisa Andreeva , Andrey Y. Abramov , Plamena R. Angelova","doi":"10.1016/j.crphar.2024.100187","DOIUrl":"10.1016/j.crphar.2024.100187","url":null,"abstract":"<div><p>Alteration of mitochondrial metabolism by various mutations or toxins leads to various neurological conditions. Age-related changes in energy metabolism could also play the role of a trigger for neurodegenerative disorders. Nonetheless, it is not clear if restoration of ATP production or supplementation of brain cells with substrates for energy production could be neuroprotective. Using primary neurons and astrocytes, and neurons with familial forms of neurodegenerative disorders we studied whether various substrates of energy metabolism could improve mitochondrial metabolism and stimulate ATP production, and whether increased ATP levels could protect cells against glutamate excitotoxicity and neurodegeneration. We found that supplementation of neurons with several substrates, or combination thereof, for the TCA cycle and cellular respiration, and oxidative phosphorylation resulted in an increase in mitochondrial NADH level and in mitochondrial membrane potential and led to an increased level of ATP in neurons and astrocytes. Subsequently, these cells were protected against energy deprivation during ischemia or glutamate excitotoxicity. Provision of substrates for energy metabolism to cells with familial forms of Parkinson's disease also prevented triggering of cell death. Thus, restoration of energy metabolism and increase of ATP production can play neuroprotective role in neurodegeneration. A combination of a succinate salt of choline and nicotinamide provided the best results.</p></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"6 ","pages":"Article 100187"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590257124000142/pdfft?md5=fa4f852b11d98e050ced37db3c1bf9e8&pid=1-s2.0-S2590257124000142-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141139119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Targeting c-Met in breast cancer: From mechanisms of chemoresistance to novel therapeutic strategies","authors":"Emeka Eze Joshua Iweala , Doris Nnenna Amuji , Abimbola Mary Oluwajembola , Eziuche Amadike Ugbogu","doi":"10.1016/j.crphar.2024.100204","DOIUrl":"10.1016/j.crphar.2024.100204","url":null,"abstract":"<div><div>Breast cancer presents a significant challenge due to its heterogeneity and propensity for developing chemoresistance, particularly in the triple-negative subtype. c-Mesenchymal epithelial transition factor (c-Met), a receptor tyrosine kinase, presents a promising target for breast cancer therapy due to its involvement in disease progression and poor prognosis. However, the heterogeneous expression of c-Met within breast cancer subtypes and individual tumors complicates targeted therapy. Also, cancer cells can develop resistance to c-Met inhibitors through various mechanisms, including bypass signaling pathways and genetic mutations. The off-target effects of c-Met inhibitors further limit their clinical utility, necessitating the development of more selective agents. To overcome these challenges, personalized treatment approaches and combination therapies are being explored to improve treatment efficacy while minimizing adverse effects. Novel c-Met inhibitors with improved selectivity and reduced off-target toxicity show promise in preclinical studies. Additionally, targeted delivery systems aim to enhance drug localization and reduce systemic toxicity. Future directions involve refining inhibitor design and integrating c-Met inhibition into personalized treatment regimens guided by molecular profiling. This review explores the mechanisms by which c-Met contributes to chemoresistance in breast cancer and current challenges in targeting c-Met for breast cancer therapy. It discusses strategies to optimize treatment outcomes, ultimately improving patient prognosis and reducing mortality rates associated with this devastating disease.</div></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"7 ","pages":"Article 100204"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142527348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Liraglutide improves adipose tissue remodeling and mitochondrial dynamics in a visceral obesity model induced by a high-fat diet","authors":"Vanessa Touceda , Florencia Fontana Estevez , Leonardo Cacciagiú , Paola Finocchietto , Romina Bustos , Agustina Vidal , Gabriela Berg , Celina Morales , Germán González , Veronica Miksztowicz","doi":"10.1016/j.crphar.2024.100185","DOIUrl":"10.1016/j.crphar.2024.100185","url":null,"abstract":"<div><p>Central obesity is characterized by visceral adipose tissue (VAT) expansion, considered one of the main risk factors for metabolic complications. In recent years, new drugs have been studied for obesity treatment. Liraglutide (LGT), a GLP-1 agonist, decreases body weight, however, several mechanisms of action on VAT are still unknown.</p></div><div><h3>Aim</h3><p>to study the effect of LGT on factors associated with VAT remodeling and mitochondrial dynamics in mice fed a high-fat diet (HFD).</p></div><div><h3>Methods</h3><p>C57BL/6 mice were divided into Control (C) and HFD. After 15 weeks of feeding, each group was subdivided according to LGT administration for 5 weeks: C, C + LGT, HFD, and HFD + LGT. In epididymal AT (EAT) we evaluated histological and mitochondrial characteristics, vascularity, gelatinase activity (MMPs), and galectin-3 expression.</p></div><div><h3>Results</h3><p>HFD presented larger adipocytes (p < 0.05), and lower vascular density and MMP-9 activity (p < 0.01) than C, while a major number of smaller adipocytes (p < 0.05) and an increase in vascularity (p < 0.001) and MMP-9 activity (p < 0.01) was observed in HFD + LGT. Collagen content was higher (p < 0.05) in EAT from HFD and decreased in HFD + LGT. In C, C + LGT, and HFD + LGT, mitochondria were predominantly tubular-shaped while in HFD mitochondria were mostly spherical (p < 0.001).</p></div><div><h3>Conclusion</h3><p>LGT positively influences VAT behavior by modulating gelatinase activity, enhancing vascularization, and improving adipocyte histological characteristics. Additionally, LGT improves mitochondrial dynamics, a process that would favor VAT functionality.</p></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"6 ","pages":"Article 100185"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590257124000129/pdfft?md5=2d5a86602bcffd980508a12e69fbcb26&pid=1-s2.0-S2590257124000129-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141130313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Edgar G. Ordóñez-Rubiano MD, PhD (c) , Nicolás Rincón-Arias MD , Sebastian Espinosa MD , William J. Shelton MD , Andres F. Salazar , Alba Cómbita MSc, PhD , Matías Baldoncini MD , Sabino Luzzi MD, PhD , César Payán-Gómez MD, PhD , Diego F. Gómez- Amarillo MD, MSc , Fernando Hakim MD , Javier G. Patiño-Gómez MD , Rafael Parra- Medina MD, PhD
{"title":"The potential of miRNA-based approaches in glioblastoma: An update in current advances and future perspectives","authors":"Edgar G. Ordóñez-Rubiano MD, PhD (c) , Nicolás Rincón-Arias MD , Sebastian Espinosa MD , William J. Shelton MD , Andres F. Salazar , Alba Cómbita MSc, PhD , Matías Baldoncini MD , Sabino Luzzi MD, PhD , César Payán-Gómez MD, PhD , Diego F. Gómez- Amarillo MD, MSc , Fernando Hakim MD , Javier G. Patiño-Gómez MD , Rafael Parra- Medina MD, PhD","doi":"10.1016/j.crphar.2024.100193","DOIUrl":"https://doi.org/10.1016/j.crphar.2024.100193","url":null,"abstract":"<div><p>Glioblastoma (GBM) is the most common malignant central nervous system tumor. The emerging field of epigenetics stands out as particularly promising. Notably, the discovery of micro RNAs (miRNAs) has paved the way for advancements in diagnosing, treating, and prognosticating patients with brain tumors. We aim to provide an overview of the emergence of miRNAs in GBM and their potential role in the multifaceted management of this disease. We discuss the current state of the art regarding miRNAs and GBM. We performed a narrative review using the MEDLINE/PUBMED database to retrieve peer-reviewed articles related to the use of miRNA approaches for the treatment of GBMs. MiRNAs are intrinsic non-coding RNA molecules that regulate gene expression mainly through post-transcriptional mechanisms. The deregulation of some of these molecules is related to the pathogenesis of GBM. The inclusion of molecular characterization for the diagnosis of brain tumors and the advent of less-invasive diagnostic methods such as liquid biopsies, highlights the potential of these molecules as biomarkers for guiding the management of brain tumors such as GBM. Importantly, there is a need for more studies to better examine the application of these novel molecules. The constantly changing characterization and approach to the diagnosis and management of brain tumors broaden the possibilities for the molecular inclusion of novel epigenetic molecules, such as miRNAs, for a better understanding of this disease.</p></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"7 ","pages":"Article 100193"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590257124000208/pdfft?md5=e3fb5cee84b6f649ec2a936785e8f6e2&pid=1-s2.0-S2590257124000208-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141540070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mujahed I. Mustafa , Awad A. Alzebair , Ahmed Mohammed
{"title":"Development of Recombinant Antibody by Yeast Surface Display Technology","authors":"Mujahed I. Mustafa , Awad A. Alzebair , Ahmed Mohammed","doi":"10.1016/j.crphar.2024.100174","DOIUrl":"10.1016/j.crphar.2024.100174","url":null,"abstract":"<div><p>Recombinant antibodies have emerged as powerful tools in various fields, including therapeutics, diagnostics, and research applications. The selection of high-affinity antibodies with desired specificity is a crucial step in the development of recombinant antibody-based products. In recent years, yeast surface display technology has gained significant attention as a robust and versatile platform for antibody selection. This graphical review provides an overview of the yeast surface display technology and its applications in recombinant antibody selection. We discuss the key components involved in the construction of yeast surface display libraries, including the antibody gene libraries, yeast host strains, and display vectors. Furthermore, we highlight the strategies employed for affinity maturation and optimization of recombinant antibodies using yeast surface display. Finally, we discuss the advantages and limitations of this technology compared to other antibody selection methods. Overall, yeast surface display technology offers a powerful and efficient approach for the selection of recombinant antibodies, enabling the rapid generation of high-affinity antibodies for various applications.</p></div>","PeriodicalId":10877,"journal":{"name":"Current Research in Pharmacology and Drug Discovery","volume":"6 ","pages":"Article 100174"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590257124000014/pdfft?md5=6b65539c630be8a3142504caae389fe9&pid=1-s2.0-S2590257124000014-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139632723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}