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Artykuły w czasopismach na temat "Drug Targeting"

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Agrawal, Surendra, Vaishali Londhe i Ram Gaud. "Niosomes: Layered Delivery System For Drug Targeting". International Journal of Scientific Research 3, nr 1 (1.06.2012): 413–17. http://dx.doi.org/10.15373/22778179/jan2014/143.

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M, Vidhya. "Bioavailability – Challenges and Advances in Drug Targeting". Bioequivalence & Bioavailability International Journal 7, nr 1 (4.01.2023): 1–3. http://dx.doi.org/10.23880/beba-16000186.

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It has been a very challenging task in drug development to handle bioavailability of drug molecules during targeting. Foremost challenges include the time span involved apart from various complexities, wrong methods or failure in outcome, increasing manual and financial requirements to be managed in the drug discovery process. Among this bioavailability is one of the biggest challenges handled to successfully identify druggability in a molecule. Various methods of administration and targeting has been used including co-crystallization, micro emulsion, micellar solubilization and other traditionally which has also expanded to other methods as morphous solid dispersion, liposomes, and complexions. To enable precision in availability of drug molecule at the targeted site. There has been an increase in bioavailability of potential drugs. This review comprehensively determines challenges and methods used in drug targeting based on their bioavailability.
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Torchilin, Vladimir P. "Drug targeting". European Journal of Pharmaceutical Sciences 11 (październik 2000): S81—S91. http://dx.doi.org/10.1016/s0928-0987(00)00166-4.

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Vinson, V. K. "Drug Targeting". Science Signaling 6, nr 283 (9.07.2013): ec158-ec158. http://dx.doi.org/10.1126/scisignal.2004484.

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 . "‘Drug targeting’". Medisch-Farmaceutische Mededelingen 41, nr 9 (wrzesień 2003): 276. http://dx.doi.org/10.1007/bf03058268.

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Hampton, Tracy. "Drug Targeting". JAMA 299, nr 9 (5.03.2008): 1008. http://dx.doi.org/10.1001/jama.299.9.1008-a.

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Edman, Peter. "Drug Targeting". Journal of Pharmaceutical Sciences 75, nr 7 (lipiec 1986): 728. http://dx.doi.org/10.1002/jps.2600750733.

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Rohde, D. "„Multi-targeting drugs“ und „multi-drug targeting“ beim metastasierten Nierenzellkarzinom". Der Urologe 45, nr 3 (marzec 2006): 356–58. http://dx.doi.org/10.1007/s00120-006-1011-0.

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Salvati, Anna, i Klaas Poelstra. "Drug Targeting and Nanomedicine: Lessons Learned from Liver Targeting and Opportunities for Drug Innovation". Pharmaceutics 14, nr 1 (17.01.2022): 217. http://dx.doi.org/10.3390/pharmaceutics14010217.

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Drug targeting and nanomedicine are different strategies for improving the delivery of drugs to their target. Several antibodies, immuno-drug conjugates and nanomedicines are already approved and used in clinics, demonstrating the potential of such approaches, including the recent examples of the DNA- and RNA-based vaccines against COVID-19 infections. Nevertheless, targeting remains a major challenge in drug delivery and different aspects of how these objects are processed at organism and cell level still remain unclear, hampering the further development of efficient targeted drugs. In this review, we compare properties and advantages of smaller targeted drug constructs on the one hand, and larger nanomedicines carrying higher drug payload on the other hand. With examples from ongoing research in our Department and experiences from drug delivery to liver fibrosis, we illustrate opportunities in drug targeting and nanomedicine and current challenges that the field needs to address in order to further improve their success.
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Kinget, Renaat, Willbrord Kalala, Liesbeth Vervoort i Guy van den Mooter. "Colonic Drug Targeting". Journal of Drug Targeting 6, nr 2 (styczeń 1998): 129–49. http://dx.doi.org/10.3109/10611869808997888.

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Rozprawy doktorskie na temat "Drug Targeting"

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Abbassi, Ramzi Hussam Suleiman. "Targeting glioblastoma with microtubule-targeting agents and epigenetic modulators". Thesis, The University of Sydney, 2020. https://hdl.handle.net/2123/25072.

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Glioblastoma is one of the most lethal tumours. However, current standard of care therapy is ineffective at eradicating the entire tumour cell population. This fractional killing occurs as glioblastoma cells possess great intertumour (patient-to-patient) and intratumour (cell-to-cell) heterogeneities, leading to tumour recurrence. Microtubules are required for proliferation and other integral cell processes, thus one proposed therapeutic approach to glioblastoma is the use of microtubule-targeting agents (MTAs). It is postulated that this ‘non-targeted’ approach would kill all tumour cells. However, while classical MTAs such as taxanes and Vinca alkaloids are clinically successful anti-cancer drugs and are effective at killing glioblastoma cells in vitro, the polarity and large molecular mass of these drugs render them useless for the treatment brain tumours, as they cannot cross the blood-brain barrier. Our laboratory has been developing small-molecule MTAs, based on the lead inhibitor CMPD1, which are able to cross the blood-brain barrier and effectively kill glioblastoma cells in vivo. While the drug development of small-molecule MTAs for glioblastoma therapy is commercial-in-confidence, the overarching aim of this PhD candidature was to assess the translational potential of microtubule-targeting agents for glioblastoma therapy. We first questioned whether microtubule heterogeneity, resulting from numerous tubulin isoforms and their post-translational modifications impacts on sensitivity of glioblastoma cells to MTAs. Using a panel of 12 genetically diverse glioblastoma stem cell lines and per-division growth rate inhibition metrics we established that the total α- and β-tubulin levels impact on MTA sensitivity. The baseline levels of α- and β-tubulin were up to 40% lower in cells that were not effectively killed by MTAs. Further, low α/β-tubulin expression was associated with higher degree of stemness. Importantly, we discovered that in every glioblastoma cell line, regardless of tubulin expression levels and sensitivity to MTA, a small subpopulation of cells survived MTA treatment via reversible non-mutational dormancy. The cells that survived the treatment, known as drug-tolerant persister (DTP) cells, resumed proliferation in ‘drug holidays’ and displayed the same sensitivity to MTAs as their treatment-naïve parental population. Hence, the drug-tolerant state is a survival mechanism mediated by reversible epigenetic processes, often via changes to the histone H3 subunit of the nucleosome. We used SWATH-MS, a technique emerging as a gold-standard in large-scale proteomics, to assess changes in histone H3 post-translational modifications in DTP cells and compared these to modifications in treatment-naïve parental cells. The analysis revealed that DTP cells exhibit a global decrease in histone lysine acetylation and an increase in histone lysine methylation, which is consistent with a genetically repressive chromatin state. Assessment of transcript levels of histone lysine methyltransferases (KMTs) and demethylases (KDMs) demonstrated more increases in KMT than KDM transcripts in DTP cells relative to their treatment-naïve parental counterparts, supporting SWATH-MS findings. A screen of a library of epigenetic probes and a series of pharmacological assays using disease-relevant cell models discovered that DTP cell recovery and return to a proliferative state was hampered when treated with CMPD1 in combination with inhibitors targeting KDM4 or KDM6. Taken together, the research presented in this thesis suggests that small-molecule MTA are promising drugs to treat glioblastoma patients. However, in order to achieve complete killing of all glioblastoma cells within a tumour population, MTAs must be combined with drugs targeting DTPs. It is hypothesised that KDM inhibitors prevent the demethylation of methylated lysine residues acquired in drug-tolerant cells, and hence, prevent recovery. Further, we identified KDM4 as a potential novel target in treatment-naïve glioblastoma cells. Given the lack of orthogonal and cell-permeable KDM4 inhibitors to validate KDM4 as a target, we established a high-throughput AlphaScreen KDM4 inhibition assay to begin the drug discovery process. Using this assay, we screened a small chemical library and identified two hit molecules that offer excellent starting points for future hit-to-lead optimisation and the development of KDM4 inhibitors.
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Wright, J. J. "Targeting of colloidal drug carriers". Thesis, University of Nottingham, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381059.

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Saunders, J. E. "Drug targeting using albumin microspheres". Thesis, University of Nottingham, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381061.

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ORSATO, ALEXANDRE. "Studies on tumor drug targeting". Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/19200.

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Tumor drug targeting is one of the most promising therapeutic strategies in oncology. The aim of this PhD work was the study of the essential features required for the assembly of tumor targeting conjugates.This work was focused on the deveploment of ligands for the GRP receptor that should function as carrier molecules for the targeting of tumor cells overexpressing this receptor. For this purpose, non-peptide GRP mimetics were designed, using a computer-based drug design technique, synthesized and tested. Two analogue compounds based on a bicyclic scaffold exerted an antagonist behaviour on the GRP receptor. Synthetic studies have been performed to optimize their production as well as biological tests to determine their potential as carrier molecules. Apart from the targeting moiety, we also studied the antineoplastic part of tumor targeting conjugates. Akt is a proto-oncogenic kinase that has been associated to cancer development. Therefore, the Akt inhibitory activity of phosphatidylinositol phosphate analogues was exploited. A small library of iminosugar-based phosphatidylinositol phosphate analogues was designed and synthesized. During the biological evaluation, target compounds displayed low to moderate inhibitory activity for Akt, which suggests their feasibility for the development of new and more potent Akt inhibitors.
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Nacev, Aleksandar Nelson. "Magnetic drug targeting| Developing the basics". Thesis, University of Maryland, College Park, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=3587279.

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Focusing medicine to disease locations is a needed ability to treat a variety of pathologies. During chemotherapy, for example, typically less than 0.1% of the drugs are taken up by tumor cells, with the remaining 99.9% going into healthy tissue. Physicians often select the dosage by how much a patient can physically withstand rather than by how much is needed to kill all the tumor cells. The ability to actively position medicine, to physically direct and focus it to specific locations in the body, would allow better treatment of not only cancer but many other diseases.

Magnetic drug targeting (MDT) harnesses therapeutics attached to magnetizable particles, directing them to disease locations using magnetic fields. Particles injected into the vasculature will circulate throughout the body as the applied magnetic field is used to attempt confinement at target locations. The goal is to use the reservoir of particles in the general circulation and target a specific location by pulling the nanoparticles using magnetic forces.

This dissertation adds three main advancements to development of magnetic drug targeting. Chapter 2 develops a comprehensive ferrofluid transport model within any blood vessel and surrounding tissue under an applied magnetic field. Chapter 3 creates a ferrofluid mobility model to predict ferrofluid and drug concentrations within physiologically relevant tissue architectures established from human autopsy samples. Chapter 4 optimizes the applied magnetic fields within the particle mobility models to predict the best treatment scenarios for two classes of chemotherapies for treating future patients with hepatic metastatic breast cancer microtumors.

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Macadam, Anglea Brenda. "Drug targeting in the gastrointestinal tract". Thesis, University of Brighton, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306400.

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Hyde, Robert. "Drug targeting with phagocytic polymorphonuclear leucocytes". Thesis, Aston University, 1989. http://publications.aston.ac.uk/12577/.

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1. Phagocytic polymorphonuclear leucocytes (PMNLs) or neutrophils have a marked avidity for the uptake of particulate material and are the first cell type to respond to inflammatory stimuli in vivo. 2. By harnessing these pathophysiological characteristics the inherent targeting capacity of the PMNL could be exploited to carry drug loaded particles to these sites. 3. In vitro chemotaxis of PMNLs was studied in response to N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) in the Blindwell chamber assay. 4. After phagocytosis of 1.1m polystyrene latex (PSL) beads at a range of incubation concentrations (5,10,20, and 30 beads/cell) the migration of the PMNL population was not significantly different from control, without beads. 5. The distribution of the beads within the filter showed that a disproportionately large number of PSL (50%) were associated with the cells on the surface of the filter that had not penetrated the filter. Eighty per cent of the PMNL population migrated and despite containing less PSL beads/cell, 50% of the dose was carried into the filter. Between 5 and 10% of these PSL were carried beyond 60m in the assay. 6. These results suggested heterogeneity of the PMNL population and to achieve efficient targeting with these cells preferential selection of the migratory sub-population would be needed. 7. The air-pouch model was then developed to study the focal accumulation of PMNLs in vivo. The PMNL isolated did not survive long enough in the circulation due to the trauma of the isolation procedure used; an alternative method will have to be employed.
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Zhang, Qian. "Natural Product Drug Discovery Targeting Cancer". Thesis, Griffith University, 2017. http://hdl.handle.net/10072/370435.

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Chemotherapy is one of the most effective approaches for cancer treatment. However, to improve efficacy, the therapeutic targets should be identified and characterised. Moreover, new drugs need to be discovered and developed to target different cancer pathways. Current therapeutics can eliminate most of the cancer cells. However, recurrence and metastasis still remain a major failure of cancer therapy. Emerging evidence demonstrates that multidrug resistance (MDR) and the existence of cancer stem cells (CSCs) are two major contributors for the failure of chemotherapy. MDR is a phenomenon in which cancer cells become resistant to structurally and functionally unrelated anticancer agents. CSCs are a small population of cells within cancer cells with capacity for self-renewal, tumor metastasis and differentiation. CSCs are also believed to be associated with chemoresistance. Thus, MDR and CSCs are the greatest challenges for cancer chemotherapy. Significant effort has been made to search for agents that specifically target MDR cells and CSCs. Consequently, some agents derived from nature have been developed to overcome MDR and CSCs. However, the developed chemotherapeutics cannot be used for all the cancers and some of them display severe cytotoxicity. Hence, there is an urgency to investigate the mechanism of drug resistance and to characterise cancer stem cells to identify potential new therapeutic targets. Natural products lie in the heart of the drug discovery. The developed chemotherapeutic compounds mainly originates from the secondary metabolites of microbes, terrestrial plants and marine organisms. In this study, MDR cancer cells were derived from tissue cultured cancer cells by the treatment the cells with fluorouracil (5-FU) and cisplatin (CDDP). CSCs were developed by treatment in serum-free medium with different factors. Fractions and compounds from Nature Bank (Griffith Institute for Drug Discovery, Griffith University), Compounds Australia (Griffith Institute for Drug Discovery, Griffith University) and Traditional Chinese Medicine (TCM) were screening by high through-put screening (HTS). As a result, one potential anticancer flavonoid was isolated from the Australian plant Cryptocarya (QID025519) which was identified by NMR spectroscopic data, in combination with LC-MS. Extracts, fractions and isolated pure compounds from Bruguiera gymnorrhiza andSchisandraviridis were identified as potential agents for the treatment of tongue cancer and breast cancer. The DCM and MeOH extracts and HPLC fractions of B. gymnorrhiza showed antiproliferation activity against cancer cells in a concentration-dependent manner. Further purification of the active fractions led to the isolation of five flavonoids namely rutin, myricetin 3-rutinoside, methoxyflavone, 5-Methoxyluteolin, and 7,3',4',5'-tetrahydroxy-5- gramrione. All five compounds showed antiproliferation activity against CAL27 and MCF7 and MDR cells in a concentration-dependent manner. Methoxyflavone demonstrated the strongest anticancer potential against CAL27 cells, MCF7 cells, CAL27 MDR cells while 7,3',4',5'-tetrahydroxy-5- gramrione illustrated the highest inhibitory effect on MCF7 MDR cells. Both aqueous and ethanol extracts showed activities against MCF7 and CAL27 cancer cells. Bioassay-guided fractionation and purification of the extracts from S.viridis resulted in six active principles, including five dibenzocyclooctene lignans namely gomisin H (1), schisandrin (2), angeloylgomisin H (3), (+)-gomisin M2 (4) and rubschisandrin (5), and one terpenoid, schisanol (6). Compounds 1-3 showed moderate anticancer activities with an IC50 value ranging from 100-200 μg/mL against MCF7 and CAL27 cell lines. Dioxane containing lignans 4-5 and triterpenoid 6 were 10 times more active with IC50 values of14.5, 13.4, 10.6 μg/mL against MCF7, and 21.2, 17.9, 11.7 μg/mL against CAL27, respectively. In addition, two compounds from Compounds Australia exhibited a potential application prospects for tongue cancer and breast cancer therapy. One compound SN00802961 exhibited significant inhibition on MCF7 cells, but low inhibitory effects on fibroblast cells. Meanwhile, it exhibited moderate inhibition on CAL27 MDR cells, CAL27 cells and CSCs. Compound SN00802961 has potently targeted the MAPK/ERK1/2 signaling pathway to induce cytotoxicity in MCF7 cells. Another agent SN00771077 for breast cancer cells in vitro was investigated. The effects of compound SN00771077 on cell viability in vitro were evaluated by treatment of MCF-7 and T47D cells. An in vitro viability assay demonstrated that compound SN00771077 inhibited the cell growth in a dose-dependent manner. The antiproliferative activity of compound SN00771077 is related to its activity on monomeric actin and the subsequent inhibition of polymerization of G-actin monomers. Exposure to compound SN00771077 induced the inhibition of Raf/MEK/ERK pathway in T47D cells. All the results indicated that compound SN00771077 had a strong cytotoxic effects on cancer cells, and shows potential in the treatment of breast cancer by causing the depolymerizing actin cytoskeleton.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Natural Sciences
Science, Environment, Engineering and Technology
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Govender, Thirumala. "Enhancing drug incorporation into nanoparticulate systems". Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299551.

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Vance, Nicholas Robert. "Targeting dynamic enzymes for drug discovery efforts". Diss., University of Iowa, 2018. https://ir.uiowa.edu/etd/6517.

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Proteins are dynamic molecules capable of performing complex biological functions necessary for life. The impact of protein dynamics in the development of medicines is often understated. Science is only now beginning to unravel the numerous consequences of protein flexibility on structure and function. This thesis will encompass two case studies in developing small molecule inhibitors targeting flexible enzymes, and provide a thorough evaluation of their inhibitory mechanisms of action. The first case study focuses on caspases, a family of cysteine proteases responsible for executing the final steps of apoptosis. Consequently, they have been the subject of intense research due to the critical role they play in the pathogenesis of various cardiovascular and neurodegenerative diseases. A fragment-based screening campaign against human caspase-7 resulted in the identification of a novel series of allosteric inhibitors, which were characterized by numerous biophysical methods, including an X-ray co-crystal structure of an inhibitory fragment with caspase-7. The fragments described herein appear to have a significant impact on the substrate binding loop dynamics and the orientation of the catalytic Cys-His dyad, which appears to be the origin of their inhibition. This screening effort serves the dual purpose of laying the foundation for future medicinal chemistry efforts targeting caspase proteins, and for probing the allosteric regulation of this interesting class of hydrolases. The second case study focuses on glutamate racemase, another dynamic enzyme responsible for the stereoinversion of glutamate, providing the essential function of D-glutamate production for the crosslinking of peptidoglycan in all bacteria. Herein, I present a series of covalent inhibitors of an antimicrobial drug target, glutamate racemase. The application of covalent inhibitors has experienced a renaissance within drug discovery programs in the last decade. To leverage the superior potency and drug target residence time of covalent inhibitors, there have been extensive efforts to develop highly specific covalent modifications to reduce off-target liabilities. A combination of enzyme kinetics, mass spectrometry, and surface-plasmon resonance experiments details a highly specific 1,4-conjugate addition of a small molecule inhibitor with the catalytic Cys74 of glutamate racemase. Molecular dynamics simulations and quantum mechanics-molecular mechanics geometry optimizations reveal, with unprecedented detail, the chemistry of the conjugate addition. Two compounds from this series of inhibitors display antimicrobial potency comparable to β-lactam antibiotics, with significant activity against methicillin-resistant S. aureus strains. This study elucidates a detailed chemical rationale for covalent inhibition and provides a platform for the development of antimicrobials with a novel mechanism of action.
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Książki na temat "Drug Targeting"

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Francis, G. E., i Cristina Delgado. Drug Targeting. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592590756.

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Ralph, Green, i Widder Kenneth J, red. Drug and enzyme targeting. Orlando: Academic Press, 1987.

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Schäfer-Korting, Monika, i Ulrich S. Schubert, red. Drug Delivery and Targeting. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-52864-4.

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J, Widder Kenneth, i Green Ralph 1940-, red. Drug and enzyme targeting. Orlando, Fla: Academic Press, 1985.

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Peter, Buchwald, red. Retrometabolic drug design and targeting. Hoboken, N.J: John Wiley & Sons, 2013.

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1955-, Andreev Boris, i Egorov Vasily, red. Handbook of drug targeting and monitoring. Hauppauge, N.Y: Nova Science Publishers, 2009.

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Perrie, Yvonne. Pharmaceutics: Drug delivery and targeting. London [u.a.]: Pharmaceutical Press, 2010.

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Bodor, Nicholas, i Peter Buchwald. Retrometabolic Drug Design and Targeting. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118407738.

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Muzykantov, Vladimir, i Vladimir Torchilin, red. Biomedical Aspects of Drug Targeting. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-4627-3.

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Ulloa-Aguirre, Alfredo, i Ya-Xiong Tao, red. Targeting Trafficking in Drug Development. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-74164-2.

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Części książek na temat "Drug Targeting"

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Weissig, Volkmar, Gerard D’ Souza i Vladimir P. Torchilin. "Targeting Mitochondria". W Biomedical Aspects of Drug Targeting, 473–95. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-4627-3_25.

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Lindner, Jonathan R., Alexander L. Klibanov i Klaus Ley. "Targeting Inflammation". W Biomedical Aspects of Drug Targeting, 149–72. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-4627-3_8.

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Palma Abriata, Juliana, Marcela Tavares Luiz, Giovanni Loureiro Raspantini, Patrícia Mazureki Campos i Juliana Maldonado Marchetti. "Liposomal Drug Carriers". W Nanocarriers for Brain Targeting, 349–76. Includes bibliographical references and index.: Apple Academic Press, 2019. http://dx.doi.org/10.1201/9780429465079-12.

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Han, Jingyan, Jena B. Goodman i Mo Zhang. "Cardiovascular Drug Delivery". W Organelle and Molecular Targeting, 279–306. New York: CRC Press, 2021. http://dx.doi.org/10.1201/9781003092773-9.

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Eedara, Basanth Babu, Wafaa Alabsi, David Encinas-Basurto, Robin Polt, Don Hayes, Stephen M. Black i Heidi M. Mansour. "Pulmonary Drug Delivery". W Organelle and Molecular Targeting, 227–78. New York: CRC Press, 2021. http://dx.doi.org/10.1201/9781003092773-8.

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Hochdörffer, Katrin, Giuseppina Di Stefano, Hiroshi Maeda i Felix Kratz. "Liver Tumor Targeting". W Drug Delivery in Oncology, 1519–68. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527634057.ch47.

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Guan, Xiangming. "Metabolic Activation and Drug Targeting". W Drug Delivery, 383–434. Hoboken, NJ: John Wiley & Sons, Inc, 2016. http://dx.doi.org/10.1002/9781118833322.ch17.

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Leontien van der Bent, M., Remco T. P. van Cruchten i Derick G. Wansink. "CHAPTER 7. Targeting Toxic Repeats". W Drug Discovery, 126–50. Cambridge: Royal Society of Chemistry, 2019. http://dx.doi.org/10.1039/9781788015714-00126.

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Guan, Xiangming. "Metabolic Activation and Drug Targeting". W Drug Delivery, 201–44. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2005. http://dx.doi.org/10.1002/0471475734.ch11.

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Stella, V. J., i A. S. Kearney. "Pharmacokinetics of Drug Targeting: Specific Implications for Targeting via Prodrugs". W Targeted Drug Delivery, 71–103. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75862-1_4.

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Streszczenia konferencji na temat "Drug Targeting"

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Kamali, Reza, i Gholamreza Keshavarzi. "Computational Simulation of Magnetic Drug Targeting in Human Body". W ASME 2011 9th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2011. http://dx.doi.org/10.1115/icnmm2011-58115.

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Development of novel particle carrier methods has led to enhanced advances in targeted drug delivery. This paper has aimed the investigation of targeting drugs via attached magnetic particles into human body. This goal was approached by inducing a magnetic field near a specific part of the human body to target the drug or as it is called magnetic drug targeting (MDT). Blood flow and magnetic particles are simulated under the presence of the specified properties of a magnetic field. In order to demonstrate a more realistic simulation, the flow was considered pulsatile. Finally, the results provided show valuable information on magnetic drug targeting in human body.
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Schmieg, Jaime, Alicia Williams i Pavlos Vlachos. "Magnetic Drug Targeting: Drug Delivery in Large Vasculature". W ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193157.

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Magnetic drug targeting (MDT) is a novel drug delivery method with potential to dramatically revolutionize clinical approaches of the treatment of many diseases. In fact, MDT has been proposed for ailments ranging from vascular disease to cancer [1, 2]. Conventional drug delivery methods utilize large doses of medication to account for the dispersion of the drug throughout the body in the hope that a sufficient concentration of medicine arrives at the diseased site. Unfortunately, many medications can have caustic effects on healthy systems leaving patients with discomfort, weakened immunity or lowered quality of life. Alternatively, MDT aims to reduce potentially harmful global dosage levels by localizing medication at the diseased site. Additionally, magnetic drug targeting not only reduces chemicals seen by healthy areas of the body, it may provide a higher concentration of drug capable of remaining at the damaged location for a longer duration than typically seen for current treatment practices. Possibly the most important advantage of MDT is the method’s ability to enhance delivery while providing no additional invasive procedures.
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"Targeting peroxisomal transport in trypanosoma". W 4th International Conference on Biological & Health Sciences (CIC-BIOHS’2022). Cihan University, 2022. http://dx.doi.org/10.24086/biohs2022/paper.566.

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Human infection with Trypanosoma parasites (Chagas disease and Human African Trypanosomiasis) affects around 10 million people worldwide resulting in life-threatening disease. Treatment options are limited to historic drugs characterized by significant side effects and decreasing efficacy while new drug development efforts are largely neglected. Here, we review drug discovery effort in human trypanosomiasis undertaken in academia. Peroxisomal (Pex) transport system was validated as a target in Chagas disease and a number of compounds were delivered which have shown promising results in animal experiments. Future perspectives of exploring the Pex system in anti-trypanosoma drug development are discussed.
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Ayati, Marzieh, Golnaz Taheri, Shahriar Arab, Limsoon Wong i Changiz Eslahchi. "Overcoming drug resistance by co-targeting". W 2010 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2010. http://dx.doi.org/10.1109/bibm.2010.5706562.

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VOLTAIRAS, P. A., D. I. FOTIADIS, L. K. MICHALIS i C. V. MASSALAS. "SOME ANALYTICAL ESTIMATES FOR MAGNETIC DRUG TARGETING". W Proceedings of the Sixth International Workshop. WORLD SCIENTIFIC, 2004. http://dx.doi.org/10.1142/9789812702593_0066.

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Lueshen, Eric, Indu Venugopal i Andreas Linninger. "Intrathecal Magnetic Drug Targeting: A New Approach to Treating Diseases of the Central Nervous System". W ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93117.

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Intrathecal (IT) drug delivery is a standard technique which involves direct injection of drugs into the cerebrospinal fluid (CSF)-filled space within the spinal canal to treat many diseases of the central nervous system. Currently, in order to reach the therapeutic drug concentration at certain locations within the spinal canal, high drug doses are used. With no method to deliver the large drug doses locally, current IT drug delivery treatments are hindered with wide drug distributions throughout the central nervous system (CNS) which cause harmful side effects. In order to overcome the current limitations of IT drug delivery, we have developed the novel method of intrathecal magnetic drug targeting (IT-MDT). Gold-coated magnetite nanoparticles are infused into a physiologically and anatomically relevant in vitro human spine model and then targeted to a specific site using external magnetic fields, resulting in a substantial increase in therapeutic nanoparticle localization at the site of interest. Experiments aiming to determine the effect of key parameters such as magnet strength, duration of magnetic field exposure, location of magnetic field, and ferrous implants on the collection efficiency of our superparamagnetic nanoparticles in the targeting region were performed. Our experiments indicate that intrathecal magnetic drug targeting and implant-assisted IT-MDT are promising techniques for concentrating and localizing drug-functionalized nanoparticles at required target sites within the spinal canal for potential treatment of diseases affecting the central nervous system.
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Dereli-Korkut, Zeynep, i Sihong Wang. "Microfluidic Cell Arrays to Mimic 3D Tissue Microenvironment". W ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80411.

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We developed a functional high throughput 3D microfluidic living cell array (MLC) for anti-cancer drug screening and mechanism discovery. Contemporary drug screening methods suffer from low sample throughput and lack of abilities of mimicking the 3D microenvironment of mammalian tissues. The poor performance of anti-cancer drugs limits the efficacy at controlling the complex disease system like cancer. Systematic studies of apoptotic signaling pathways can be prominent approaches for searching active and effective treatments with less drug resistance. Hence, innovative bio-devices are needed to represent tumor microenvironment to understand the molecular signatures of apoptosis for testing new anticancer therapies targeting apoptosis. Our novel 3D MLC design is the prototype of a high-throughput drug screening platform targeting apoptotic signaling pathways.
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"Lymphatic targeting drug delivery system and tumor treatment". W 2018 International Conference on Medicine, Biology, Materials and Manufacturing. Francis Academic Press, 2018. http://dx.doi.org/10.25236/icmbmm.2018.73.

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Yu Jin Kim, Il-Kyu Park, Jin Soo Kim, Joon Hwang, Eui-Sik Chung, Kang Moo Huh i Yong-kyu Lee. "Anticancer drug delivery for tumor targeting and therapy". W 2009 4th IEEE International Conference on Nano/Micro Engineered and Molecular Systems. IEEE, 2009. http://dx.doi.org/10.1109/nems.2009.5068724.

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Ernsting, Mark J., Arthur Worthington, Jonathan P. May, Tatsuaki Tagami, Michael C. Kolios i Shyh-Dar Li. "Ultrasound drug targeting to tumors with thermosensitive liposomes". W 2011 IEEE International Ultrasonics Symposium (IUS). IEEE, 2011. http://dx.doi.org/10.1109/ultsym.2011.0001.

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Raporty organizacyjne na temat "Drug Targeting"

1

Hiscott, John. Oncolytic Virotherapy Targeting Lung Cancer Drug Resistance. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2013. http://dx.doi.org/10.21236/ada589848.

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Nolan, Linda L. Chemotherapy and Drug Targeting in the Treatment of Leishmaniasis. Fort Belvoir, VA: Defense Technical Information Center, styczeń 1993. http://dx.doi.org/10.21236/ada283541.

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Nolan, Linda L. Chemotherapy and Drug Targeting in the Treatment of Leishmaniasis. Fort Belvoir, VA: Defense Technical Information Center, maj 1989. http://dx.doi.org/10.21236/ada237253.

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Nolan, Linda L. Chemotherapy and Drug Targeting in the Treatment of Leishmaniasis. Fort Belvoir, VA: Defense Technical Information Center, maj 1991. http://dx.doi.org/10.21236/ada238236.

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Nolan, Linda L. Chemotherapy and Drug Targeting in the Treatment of Leishmaniasis. Fort Belvoir, VA: Defense Technical Information Center, maj 1990. http://dx.doi.org/10.21236/ada238768.

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Nolan, Linda L. Chemotherapy and Drug Targeting in the Treatment of Leishmaniasis. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 1988. http://dx.doi.org/10.21236/ada242584.

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Watkins, Linda R., Steven Maier, Ryan Bachtell, Jonathan Katz i Betty Diamond. Combating Drug Abuse by Targeting Toll-Like Receptor 4 (TLR4). Fort Belvoir, VA: Defense Technical Information Center, październik 2013. http://dx.doi.org/10.21236/ada593126.

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Pasinelli, Piera, i Dena Jacob. Rethinking Drug Treatment Approaches in ALS by Targeting ABC Efflux Transporters. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2014. http://dx.doi.org/10.21236/ada615391.

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Yang, Dajun. Strategies of Discovering Small Molecule Drugs Targeting Growth Factor Heregulin. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2002. http://dx.doi.org/10.21236/ada435287.

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Collins, Tammy R., i Tao-shih Hsieh. Mechanistic Basis of Sensitivity/Resistance Towards Anti-Cancer Drugs Targeting Topoisomerase II. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2005. http://dx.doi.org/10.21236/ada437191.

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