Relevant bibliographies by topics / Drug development

Academic literature on the topic 'Drug development'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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Journal articles on the topic "Drug development"

Mishra, Hara Prasad, Ayush Goel, Sahil Kumar, Mihir Chauhan, Mrinal Patnaik, and Imaad Rehman. "Drug development hit by war." Journal of Pharmacovigilance and Drug Research 3, no. 2 (June 1, 2022): 11–15. http://dx.doi.org/10.53411/jpadr.2022.3.2.3.

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Jadhav, Mr Gahininath Thansing, and Mr Rahul Bhavlal Jadhav. "Drug Discovery and Development Process." International Journal of Research Publication and Reviews 5, no. 1 (January 8, 2024): 1891–95. http://dx.doi.org/10.55248/gengpi.5.0124.0225.

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Adukondalu, D., Rajesh Rajesh, Shaik Thaslim, E. Soumya, and M. Chandana. "Regulatory Guidelines for New Drug Development." Pharmaceutics and Pharmacology Research 4, no. 3 (September 25, 2021): 01–11. http://dx.doi.org/10.31579/2693-7247/046.

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Aim: The aim of present project work is to understand the guidelines and regulatory requirements for investigational new drug and development of new drug Objectives: The objective of current project include Need of a new drug to investigate New drug development targets Understanding the properties of new dug Required protocols for submission of new drug to regulatory authority Regulatory requirements to get approval of new drug.

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Sharma, Bhavik. "DRUG DISCOVERY AND DEVELOPMENT: AN OVERVIEW." INDIAN RESEARCH JOURNAL OF PHARMACY AND SCIENCE 7, no. 2 (June 2020): 2215–26. http://dx.doi.org/10.21276/irjps.2020.7.2.14.

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Agrawal, Shrutidevi, Narisetty Sunil Thomas, Anand Babu Dhanikula, Chaman Lal Kaul, and Ramesh Panchagnula. "Antituberculosis drugs and new drug development." Current Opinion in Pulmonary Medicine 7, no. 3 (May 2001): 142–47. http://dx.doi.org/10.1097/00063198-200105000-00005.

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GRABOWSKI, H. G. "Issues of Drug Development: Orphan Drugs." Science 228, no. 4702 (May 24, 1985): 981. http://dx.doi.org/10.1126/science.228.4702.981.

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Vaalburg, Willem, N. Harry Hendrikse, and Erik F. J. de Vries. "Drug development, radiolabeled drugs and PET." Annals of Medicine 31, no. 6 (January 1999): 432–37. http://dx.doi.org/10.3109/07853899908998801.

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Flaherty, Keith T., Dung T. Le, and Steven Lemery. "Tissue-Agnostic Drug Development." American Society of Clinical Oncology Educational Book, no. 37 (May 2017): 222–30. http://dx.doi.org/10.1200/edbk_173855.

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The U.S. Food and Drug Administration (FDA) has approved drugs to treat patients with tumor types based on a single anatomic site, such as renal cell carcinoma or melanoma, rather than on a biomarker alone. This standard approach is based on a number of factors, including heterogeneity of drug effects in different biomarker-positive tumor types. Additionally, drug development for some drugs was primarily directed toward a specific genomic abnormality in a specific tumor type (e.g., drugs for anaplastic lymphoma kinase [ALK] fusion-positive non–small cell lung cancer). In such cases, differences in biology, differences in natural histories of different cancers, differences in mutation frequencies among cancers, or differences in concomitant therapies may have necessitated diverse development considerations. As described in U.S. regulations [21 CFR 201, CFR 201.57(c)(2)], the indications and usage section of drug labeling “must state that a drug is indicated for the treatment, prevention, mitigation, cure, or diagnosis of a recognized disease or condition or of a manifestation of a recognized disease or condition, or for the relief of symptoms associated with a recognized disease or condition.” Such regulations, however, do not require that disease be defined solely as a specific tumor type. This manuscript will highlight scientific/biologic issues, clinical trial designs, and regulatory issues pertaining to the development of drugs agnostic of tumor type. Although the manuscript will discuss regulatory considerations as understood by the authors regarding tissue-agnostic drug development, it should not be considered formal or binding FDA guidance or policy.

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Yamashiro, Yuichiro, Jennifer Martin, Madlen Gazarian, Sharon Kling, Hidefumi Nakamura, Akira Matsui, Salvatore Cucchiara, Marina Aloi, Erica L. Wynn, and Andrew E. Mulberg. "Drug Development." Journal of Pediatric Gastroenterology and Nutrition 55, no. 5 (November 2012): 506–10. http://dx.doi.org/10.1097/mpg.0b013e318272af1f.

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Williams, Ian. "Drug Development." Science 277, no. 5322 (July 4, 1997): 17.6–21. http://dx.doi.org/10.1126/science.277.5322.17-f.

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Dissertations / Theses on the topic "Drug development"

Zhang, Huarui. "Design, synthesis and activity evaluation of novel exosome inhibitors." HKBU Institutional Repository, 2020. https://repository.hkbu.edu.hk/etd_oa/849.

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Background: Exosomes are extracellular vesicles (EVs) that produced in the endosomal compartment of most eukaryotic cells, and have observed increasing attentions over the past decades. They play important roles in cell- to-cell communications, they can carry varieties of substances, like proteins, nucleic acids and lipids, to the target cells they encounter. These cargos could influence the function of recipient cells. This novel mode of intercellular communication is found to be of critical importance to many cellular activities. However, exosomes are involved in various diseases processes. Tumor- derived exosomes could promote cancer progression, and our preliminary study indicated that exosome released from osteoclasts could inhibit bone formation. We also found that osteoarthritis (OA) progression in OA mice could be attenuated by inhibiting exosomes released by osteoclasts. Therefore, inhibition of exosome release has potential value in the treatment of diseases. The exosome release is under control by RAB27A, which is a protein involved in protein transport and signal transduction. It is reported that a compound named Nexinhib20 could selectively inhibit RAB27A, but this compound is highly toxic to RAW264.7 cells, which IC 50 is 1.5 µM. Therefore, for safety concerns, it has to be chemically modified to reduce toxicity. Aim: (1) To design and synthesize a series compounds based on the structure of Nexinhib20. (2) To evaluate the toxicity and exosome inhibiting activity of the synthesized compounds and discuss the structure-activity relationships (SAR) of them. Materials and Methods: Nexinhib20 derivatives were synthesized by aldol reaction. The cytotoxicity of these compounds was evaluated by MTT assay. The exosome inhibiting activity of these compounds was evaluated through exosome isolation and quantitation. Result: A series of compounds were synthesized and their structures were confirmed by LC-MS and NMR. The structure-activity relationships of these compounds were discussed, and the results showed that compounds A3, A23 and B2 exhibited lower toxicity compared to Nexinhib20 and strong exosome inhibiting ability. Conclusion: The results of this project indicate that A3, A23 and B2 exhibited low toxicity and good exosome inhibiting activity. Based on this, further chemical modification could be applied to develop new exosome inhibitors with better efficacy

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Larson, Joeanna Lee. "Perinatal Drug Abuse Intervention: Policy Development for Drug Screening." ScholarWorks, 2016. https://scholarworks.waldenu.edu/dissertations/2555.

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Perinatal drug abuse is becoming a profound issue facing the health and wellbeing of neonates. The community serviced by the project site, which lies within the boundaries of an Indian Reservation, suffers from perinatal drug abuse at a higher rate than state and federal averages. The purpose of this project was to provide the project site with a policy to consistently screen for perinatal drug abuse. Lave's theory of situational learning and the Sanford Way model for quality improvement framed this project. To guide policy development, data were compiled through a systematic review of current literature, national and state guidelines, state law, local tribal government, and community stakeholders. Data included: (a) studies completed in the past 10 years specifically targeting drug abuse in child-bearing aged women, with intentional exclusion of tobacco and alcohol studies; (b) prevalence of illicit drug abuse in child bearing aged women at a local, state, and national levels; and (c) local, state, and national guidelines, as well as state law, for perinatal drug abuse intervention and screening. In addition, interviews and meetings with local stakeholders were completed and their feedback was incorporated into the development of the perinatal drug abuse screening and intervention policy. To evaluate policy effectiveness, it is proposed that perinatal drug screens ordered at the project site be monitored for six months prior to and after implementation of the new policy. The desired outcome will be that providers consistently intervene with perinatal drug abuse in a non-biased fashion. This quality improvement project will create a positive social change by allowing non-biased intervention with perinatal drug abuse using evidence-based practice and by promoting nursing-driven policy development.

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Hartmann, Neil Godfried. "Intercalative drugs in cancer chemotherapy : two approaches towards drug development." Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292983.

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Mawad, Damia Graduate School of Biomedical Engineering Faculty of Engineering UNSW. "Development of Novel hydrogels for protein drug delivery." Awarded by:University of New South Wales. Graduate School of Biomedical Engineering, 2005. http://handle.unsw.edu.au/1959.4/25221.

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Introduction: Embolic agents are used to block blood flow of hypervascular tumours, ultimately resulting in target tissue necrosis. However, this therapy is limited by the formation of new blood vessels within the tumour, a process known as angiogenesis. Targeting angiogenesis led to the discovery of anti-angiogenic factors, large molecular weight proteins that can block the angiogenic process. The aim of this research is development of poly (vinyl alcohol) (PVA) aqueous solutions that cross-link in situ to form a hydrogel that functions as an embolic agent for delivery of macromolecular drugs. Methods: PVA (14 kDa, 83% hydrolysed), functionalised by 7 acrylamide groups per chain, was used to prepare 10, 15, and 20wt% non-degradable hydrogels, cured by UV or redox initiation. Structural properties were characterised and the release of FITCDextran (20kDa) was quantified. Degradable networks were then prepared by attaching to PVA (83% and 98 % hydrolysed) ester linkages with an acrylate end group. The effect on degradation profiles was assessed by varying parameters such as macromer concentration, cross-linking density, polymer backbone and curing method. To further enhance the technology, radiopaque degradable PVA was synthesised, and degradation profiles were determined. Cell growth inhibition of modified PVA and degradable products were also investigated. Results: Redox initiation resulted in non-degradable PVA networks of well-controlled structural properties. Increasing the solid content from 10 to 20wt% prolonged the release time from few hours to ~ 2 days but had no effect on the percent release, with only a maximum release of 65% achieved. Ester attachment to the PVA allowed flexibility in designing networks of variable swelling behaviors and degradation times allowing ease of tailoring for specific clinical requirements. Synthesis of radiopaque degradable PVA hydrogels was successful without affecting the polymer solubility in water or its ability to polymerize by redox. This suggested that this novel hydrogel is a potential liquid embolic with enhanced X-ray visibility. Degradable products had negligible cytotoxicity. Conclusion: Novel non-degradable and radiopaque degradable PVA hydrogels cured by redox initiation were developed in this research. The developed PVA hydrogels showed characteristics in vitro that are desirable for the in vivo application as release systems for anti-angiogenic factors.

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Fagnan, David Erik. "Analytics for financing drug development." Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/98572.

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Thesis: Ph. D., Massachusetts Institute of Technology, Sloan School of Management, Operations Research Center, 2015.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references (pages 133-139).
Financing drug development has a particular set of challenges including long development times, high chance of failure, significant market valuation uncertainty, and high costs of development. The earliest stages of translational research pose the greatest risks, which have been termed the "valley of death" as a result of a lack of funding. This thesis focuses on an exploration of financial engineering techniques aimed at addressing these concerns. Despite the recent financial crisis, many suggest that securitization is an appropriate tool for financing such large social challenges. Although securitization has been demonstrated effectively at later stages of drug development for drug royalties of approved drugs, it has yet to be utilized at earlier stages. This thesis starts by extending the model of drug development proposed by Fernandez et al. (2012). These extensions significantly influence the resulting performance and optimal securitization structures. Budget-constrained venture firms targeting high financial returns are incentivized to fund only the best projects, thereby potentially stranding less-attractive projects. Instead, such projects have the potential to be combined in larger portfolios through techniques such as securitization which reduce the cost of capital. In addition to modeling extensions, we provide examples of a model calibrated to orphan drugs, which we argue are particularly suited to financial engineering techniques. Using this model, we highlight the impact of our extensions on financial performance and compare with previously published results. We then illustrate the impact of incorporating a credit enhancement or guarantee, which allows for added flexibility of the capital structure and therefore greater access to lower costing capital. As an alternative to securitization, we provide some examples of a structured equity approach, which may allow for increased access to or efficiency of capital by matching investor objectives. Finally, we provide examples of optimizing the Sortino ratio through constrained Bayesian optimization.
by David Erik Fagnan.
Ph. D.

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Voyi, Kuku Vinolia Vuyelwa. "Development of an antirheumatic drug." Doctoral thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/17187.

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Includes bibliographical references.
The diamino-diamide ligands have been investigated in an attempt to develop an antirheumatic drug. The ligands N,N'-di-(2-dimethylamino)ethyloxamide and N,N'di-(2-diethylamino)ethyloxamide, were synthesised and characterised using the physical techniques, NMR, mass- and infrared spectrometry. The stability constants of the complexes of Mg, Ca, Zn and several first transition metal-ions with the ligands were determined potentiometrically. The solution conformation of the CuII complexes were determined using visible spectrophotometry. Finally the physico-chemical studies were carried out. Firstly by studying the interaction of the copper complex with albumin at the physiological pH 7.4 using visible spectrophotometry. Secondly by determining the superoxide dismutase activity of the ligand by reduction of nitrobluetetrazolium using visible spectrophotometry. Lastly the ligands and the carr, CuII, MgII and ZnII metalions were monitored in vitro using the computer blood plasma model.

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Alkhaldi, Abdulsalam Abdulhadi. "Drug development against kinetoplastid parasites." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3637/.

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Human African trypanosomiasis and leishmaniasis are caused by parasites belonging to the genera Trypanosoma and Leishmania, respectively. Significant numbers of people are affected by these diseases worldwide, which are fatal if untreated. Animals can also be infected, posing agricultural and economic hindrances, especially in poor countries. Although chemotherapy can be used for treatment, many problems are associated with it, including drug toxicity, resistance, lack of guaranteed supply, and high treatment cost. Therefore, there is an urgent need for new treatment approaches. Here, we aim to examine the in vitro efficacy of curcumin and phosphonium compounds against these parasites, assay their toxicity to human kidney cells in vitro, and investigate the mechanism of antiparasite activity of curcumin. The Alamar blue assay was used to test 158 curcumin analogues against Leishmania major promastigotes and Leishmania mexicana promastigotes and axenic amastigotes to obtain in vitro EC50 values. Many curcumin compounds such as AS-HK122 and AS-HK126 exhibited anti-leishmanial activities similar to or better than the current clinical drug pentamidine. Similarly, EC50 values of 83 phosphonium compounds against Trypanosoma brucei brucei bloodstream forms were determined. More than 20% of the tested compounds were found to be more active than the standard veterinary drug diminazene aceturate. Multi-drug resistant strains were used to determine that there is no cross-resistance between the tested compounds and the diamidine or melaminophenyl arsenical classes of trypanocides. Structure activity relationship (SAR) analysis revealed that mono-O-demethylated curcumin compounds showed 10-fold higher activity against the parasites than curcumin. The addition of one or two pentyl pyridinium (C10H15N) groups on specific positions of the aromatic ring also increased the activity of these compounds. Furthermore, curcumin compounds with an isoxazole ring instead of the diketo motif showed higher activity and the lowest EC50 values. Similarly, pentyl bromide (OC5H10Br) substitutions on the phenyl rings improved the antiparasitic activity. Curcuminoids with trienone linkers showed increased antiparasitic activity against all parasites tested. Eighty-three phosphonium analogues were tested against T. brucei brucei. SAR analysis indicated that the bulky substituents surrounding the bisphosphonium cations led to strong antiparasitic activity while the nature of the linker had less effect on the activity. Some monophosphonium analogues registered the lowest EC50 values of all the phosphonium compounds. The toxicity of the curcumin and phosphonium analogues to HEK cells was analysed in vitro. All curcumin and phosphonium compounds demonstrated lower toxicity to HEK cells than to the parasites. Of the 83 phosphonium compounds, 60 displayed >200-fold in vitro selectivity index (SI). We also investigated the mode of antiparasitic activity of curcumin compounds. Preliminary toxicity tests had revealed that AS-HK014 caused rapid depletion of glutathione content in rat hepatocytes. Therefore, we tested AS-HK014 activity in the presence of different concentrations of L-glutathione, and AS-HK014 activity was found to decrease with increased L-glutathione concentrations, strongly suggesting that glutathione reacted with the active compound. Indeed, a chemical adduct was observed between the two compounds and identified through mass spectrometry. A trypanosome cell line (TA014) adapted to AS-HK014 was produced. TA014 and wild-type T. brucei brucei were treated with AS-HK014 and compared with each other and with untreated controls. The glutathione and trypanothione levels were lower in the treated WT cells than in the untreated cells. However, there was no change in the glutamate, ornithine, or spermidine levels, providing no evidence for the inhibition of trypanothione synthesis, suggesting that the effect is probably not metabolic but chemical. AS-HK014 did not significantly affect thiol levels in TA014; this might reflect a higher level of trypanothione synthesis through increased glutathione synthetase (GS) and/or γ-glutamylcysteine synthetase (γ-GCS) expression. Therefore, we analysed the protein levels using western blotting, and sequenced the encoding genes in both WT and TA014 to identify any mutations in the open reading frames (ORFs). However, we found no changes in the GS and γ-GCS protein levels in resistant trypanosomes and no mutations were found in the GS and γ-GCS ORFs. It is clear that the resistance is to the reactive enone motif of AS-HK014 rather than to curcumin and curcuminoids in general, since TA014 only displayed resistance to AS-HK014 analogues bearing the enone motif while sensitivity to curcumin remained unchanged, confirming that this motif is responsible for the higher activity of AS-HK014 compared to curcumin. The effects of bisphosphonium analogues on T. brucei brucei bloodstream forms were investigated to identify the target. All tested analogues rapidly reduced the T. brucei brucei mitochondrial membrane potential Ψm and decreased the intracellular ATP level after one hour of incubation, suggesting that the compounds may be targeting the mitochondria. The intracellular Ca2+ levels increased gradually after eight hours, suggesting that the damaged mitochondria are unable to retain the stored Ca2+ as their membrane potential dissipates. We also studied the trypanosome cell cycle after incubating the parasites with bisphosphonium compounds. The cell cycle defects became apparent after eight hours of incubation: DNA synthesis could not be initiated, leading to a dramatic reduction of cells in the S phase. This result was also confirmed by fluorescence microscopic assessment of DNA configuration. After eight hours of incubation with the bisphosphonium compound CD38, the number of 2K1N cells significantly decreased as compared with the control. There may be a causal relationship between mitochondrial damage and cell cycle defects. Transmission electron microscopy images of the cells obtained after 12 h of exposure to CD38 also revealed the presence of mitochondrial damage. We tested whether bisphosphonium compounds can induce programmed cell death in trypanosomes. A TUNEL assay was used to detecting DNA fragmentation; the results showed increased DNA fragmentation after 24-h treatment with two different bisphosphonium compounds, CD38 and EFpI7. This result indicates is consistent with apoptosis occurring in treated cells but there was no evidence suggesting that bisphosophonium-induced cell death in trypanosomes is dependent on new protein synthesis. In conclusion, curcumin and phosphonium analogues exhibit promising antiparasitic activity, and some analogues could be optimised for in vivo evaluation. Further investigations on the site of action of phosphonium compounds in the mitochondrion are in progress.

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Mavridis, Lazaros. "High throughput virtual drug screening using spherical harmonic molecular surface representations." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25936.

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Wang, Shining. "DRUG DEVELOPMENT OF TARGETED ANTICANCER DRUGS BASED ON PK/PD INVESTIGATIONS." Diss., Temple University Libraries, 2008. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/2535.

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Pharmaceutics
Ph.D.
EGFR inhibitors, such as gefitinib, are examples of targeted anticancer drugs whose drug sensitivity is related to gene mutations that adds a pharmacogenetic [PG] dimension to any pharmacokinetic [PK] and pharmacodynamic [PD] analysis. The goal of this project was to characterize the PK/PD properties of gefitinib in tumors and then apply these results to design rational drug design regimens, and provide a foundation for future studies with EGFR inhibitors. Progressions of in vitro and in vivo studies were completed to understand the PK and PD behavior of gefitinib. In vitro cytotoxicity assays were first conducted to confirm the gefitinib sensitivity differences in a pair of human glioblastoma cell lines, LN229-wild-type EGFR and LN229-EGFRvIII mutant, an EGFR inhibitor-sensitizing mutation. Subsequent in vitro PD studies identified phosphorylated-ERK1/2 (pERK) as a common PD marker for both cell lines. To describe the most salient features of drug disposition and dynamics in the tumor, groups of mice bearing either subcutaneous LN229-wild-type EGFR or LN229-EGFRvIII mutant tumors were administered gefitinib at doses of 10 mg/kg intravenously (IV), 50 mg/kg intraarterially (IA) and 150 mg/kg orally (PO). In each group, gefitinib plasma and tumor concentrations were quantitated, as were tumoral pERK. Hybrid physiologically-based PK/PD models were developed for each tumor type, which consisted of a forcing function describing the plasma drug concentration-profile, a tumor compartment depicting drug disposition in the tumor, and a mechanistic target-response PD model characterizing pERK in the tumor. Gefitinib showed analogous PK properties in each tumor type, yet different PD characteristics consistent with the EGFR status of the tumors. Using the PK/PD model for each tumor type, simulations were done to define multiple-dose regimens for gefitinib that yielded equivalent PD profiles of pERK in each tumor type. Based on the designed PK/PD equivalent dosing regimens for each tumor type, gefitinib 150 mg/kg PO qd × 15 days and 65 mg/kg PO qd × 15 days multiple-dose studies were conducted in wild-type EGFR and EGFRvIII mutant tumor groups, respectively. In each tumor group, gefitinib plasma and tumor concentrations were measured on both day 1 and day 15, as were tumoral amounts of pERK. Different from single-dose model simulations, gefitinib showed nonlinear PK property in the wild-type tumor due to the down-regulation of membrane transporter ABCG2. Moreover, acquired resistance of tumoral pERK inhibition was observed in both tumor types. Nevertheless, gefitinib had an analogous growth suppression action in both tumor groups, supporting the equivalent PD dosing strategy. Overall, single-dose gefitinib PK/PD investigations in a pair of genetically distinct glioblastomas facilitated the development of hybrid physiologically-based PK/PD models for each tumor type, and further introduced a novel concept of PK/PD equivalent dosing regimens which could be applied in novel drug development paradigms. Preliminary multiple-dose gefitinib studies revealed more complex PK/PD characteristics that needed to be further explored.
Temple University--Theses

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Alavi, Hajar Karimi. "Development of mechanistic mathematical models for gene-mediated drug-drug interactions." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/development-of-mechanistic-mathematical-models-for-genemediated-drugdrug-interactions(b38da88a-bb2a-4667-9809-21a09c8feeeb).html.

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The glucocorticoid receptor (GR) is a member of the nuclear hormone receptors family and has been shown to exert significant effects on the induction of cytochrome P450 (CYP) enzymes responsible for the metabolism of many xenobiotics. CYP3A4/5 and CYP2C9 are important CYP enzymes which metabolise more that 60% of drugs. Induction or inhibition of the enzymatic activity and the levels of these enzymes can have significant effects on drug metabolism. Understanding the role of GR and other nuclear receptors, pregnane X receptor (PXR) and the constitutive androstane receptor (CAR), in the mechanisms effecting CYP3A4/5 and CYP2C9 levels and activity can aid in the development of in vitro and in vivo models which have become a target for scientists in the clinic and the industry. The commonly prescribed synthetic glucocorticoid (GC) drug, dexamethasone (Dex), can induce GR, PXR and CAR and was used in this study to analyse its effects on the CYP enzymes studied. The hypothesis of this project was that changes in CYP3A4/5 and CYP2C9 gene expression affect drug metabolism and changes in gene expression of these CYP enzymes was under GR, PXR and CAR control, thus affecting the concentration and therapeutic activity of drugs metabolized by these enzymes during chronic use of GCs in conditions such as rheumatoid arthritis and asthma. This study aimed to measure mRNA, protein, ROS and enzymatic activity levels in human HepG2 hepatocytes treated with Dex for 120 h and analyze the results for various time points to produce a mathematical model. Our study has shown that changes in mRNA, protein and enzymatic activity levels of CYP3A4/5 and CYP2C9 in HepG2 cells were induced by Dex at sub-micromolar (0.1 µM) and supra-micromolar (1.5 mM) concentrations. The induction of CYP3A4/5 and CYP2C9 enzymes during 120 h treatment with Dex may be affected by the NRs studied; GR, phosphorylated GR, PXR and CAR protein levels were also shown to be induced by Dex. The efflux transporter, P-gp’s protein levels were also induced by 0.1 µM Dex, highlighting the importance of considering bioavailability of other drugs co-administered with Dex. The results of some of these laboratory experiments have been used to produce mechanistic mathematical models by MATLAB software with reference to previous studies in rats concentrating on the effects of steroids on GR. The models developed were not effective at the lower Dex concentration of 0.1 µM but were better modelled at the higher Dex concentration of 1.5 mM. The basic mechanistic models developed using HepG2 cells in this study can be utilised to design and conduct drug-drug interaction (DDI) analyses of the induction of CYP3A4/5 and CYP2C9 in other human liver cells and starting pre-clinical studies in animals to aid in drug development.

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Books on the topic "Drug development"

Gaginella, Timothy S., and Antonio Guglietta, eds. Drug Development. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-202-9.

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E, Hamner Charles, ed. Drug development. 2nd ed. Boca Raton, Fla: CRC Press, 1990.

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C, Rogge Mark, and Taft David R, eds. Preclinical drug development. Boca Raton: Taylor & Francis, 2005.

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Dikshit, Madhu, ed. Drug Discovery and Drug Development. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-8002-4.

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G, Welling Peter, Lasagna Louis 1923-, and Banakar Umesh V. 1956-, eds. The drug development process. New York: M. Dekker, 1996.

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C, Rogge Mark, and Taft David R, eds. Preclinical drug development. 2nd ed. New York: Informa Healthcare, 2010.

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De Clercq, Erik, and Richard T. Walker, eds. Antiviral Drug Development. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-7275-2.

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Mulberg, Andrew E., Dianne Murphy, Julia Dunne, and Lisa L. Mathis, eds. Pediatric Drug Development. Chichester, UK: John Wiley & Sons Ltd., 2013. http://dx.doi.org/10.1002/9781118312087.

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Giordanetto, Fabrizio Giordanetto, ed. Early Drug Development. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2018. http://dx.doi.org/10.1002/9783527801756.

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Cayen, Mitchell N., ed. Early Drug Development. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470613191.

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Book chapters on the topic "Drug development"

Upchurch Sweeney, C. Renn, J. Rick Turner, J. Rick Turner, Chad Barrett, Ana Victoria Soto, William Whang, Carolyn Korbel, et al. "Drug Development." In Encyclopedia of Behavioral Medicine, 632. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_100513.

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Duda-Seiman, Corina, Daniel Duda-Seiman, and Mihai V. Putz. "Drug Development." In New Frontiers in Nanochemistry, 175–83. Includes bibliographical references and indexes. | Contents: Volume 1. Structural nanochemistry – Volume 2. Topological nanochemistry – Volume 3. Sustainable nanochemistry.: Apple Academic Press, 2020. http://dx.doi.org/10.1201/9780429022951-10.

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Guan, Zhi-Zhong, Yi Zhao, and Chang-Xue Wu. "Drug Development." In Coal-burning Type of Endemic Fluorosis, 421–39. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1498-9_25.

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Schmidt, Marco F. "Drug Development." In Chemical Biology, 11–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2022. http://dx.doi.org/10.1007/978-3-662-64412-6_3.

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Wallace, John L. "The Arachidonic Acid Pathway." In Drug Development, 1–20. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-202-9_1.

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Tepperman, B. L., and B. J. R. Whittle. "Therapeutic Implications of the Nitric Oxide Pathway in Gastrointestinal Diseases." In Drug Development, 21–60. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-202-9_2.

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Levine, Alan D., and Claudio Fiocchi. "Cytokines." In Drug Development, 61–87. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-202-9_3.

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Guglietta, Antonio, and Marija Veljača. "Peptide Growth Factors in Gastrointestinal Disorder Therapeutics." In Drug Development, 89–112. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-202-9_4.

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Holzer, Peter. "Tachykinins." In Drug Development, 113–46. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-202-9_5.

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D’Amato, Massimo, Francesco Makovec, and Lucio C. Rovati. "CCKA Receptors in Gastrointestinal Disorders." In Drug Development, 147–76. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-202-9_6.

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Conference papers on the topic "Drug development"

Posinasetty, Ms Bhargavi, G. S. Gayathri, Vivekanand Pandey, Aayushi Jain, S. B. G. Tilak Babu, and Yashpal Singh. "AI-Enhanced Drug Screening: Accelerating Drug Development." In 2024 5th International Conference on Recent Trends in Computer Science and Technology (ICRTCST). IEEE, 2024. http://dx.doi.org/10.1109/icrtcst61793.2024.10578548.

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Yi, Xiaole. "Drug development and drug design for hepatocellular carcinoma." In Third International Conference on Biological Engineering and Medical Science (ICBioMed2023), edited by Alan Wang. SPIE, 2024. http://dx.doi.org/10.1117/12.3013166.

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Lammertsma, Adriaan A. "PET in drug development." In 2012 IEEE 9th International Symposium on Biomedical Imaging (ISBI 2012). IEEE, 2012. http://dx.doi.org/10.1109/isbi.2012.6235698.

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Sathiaseelan, Allimalar, Chong Seng Shit, and Tsun-Thai Chai. "ANTI-BIOFILM ACTIVITY OF FERMENTED SOYBEAN TEMPEH EXTRACTS AND FRACTIONS AGAINST ORAL PRIMARY COLONIZER BACTERIA." In International Conference on Drug Discovery & Development. The International Institute of Knowledge Management (TIIKM), 2018. http://dx.doi.org/10.17501/icddd.2017.1101.

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Gaynor, Richard B. "Abstract PL07-02: Rational cancer drug development for targeted drugs." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-pl07-02.

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Ghosh, Priyanka, Sam G. Raney, and Markham C. Luke. "Role of visualizing and quantifying drugs in dermal drug development." In Visualizing and Quantifying Drug Distribution in Tissue VII, edited by Conor L. Evans and Kin Foong Chan. SPIE, 2023. http://dx.doi.org/10.1117/12.2648378.

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Bose, Mausumi Bose. "CROSSOVER DESIGNS FOR DRUG DEVELOPMENT." In 41st International Academic Conference, Venice. International Institute of Social and Economic Sciences, 2018. http://dx.doi.org/10.20472/iac.2018.041.009.

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van der Geest, Ronald, Diana Nijholt, and Wil den Hollander. "Clinical Development in Drug Repurposing." In RExPO22. ScienceOpen, 2022. http://dx.doi.org/10.14293/s2199-rexpo22003.v1.

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Rokyta, O. "DRUG-INDUCED MYOCARDITIS." In EDUCATION AND SCIENCE OF TODAY: INTERSECTORAL ISSUES AND DEVELOPMENT OF SCIENCES, Chair O. Nishkumay, A. Kovalenko, O. Aleksieienko, and K. Cherniaieva. European Scientific Platform, 2021. http://dx.doi.org/10.36074/logos-19.03.2021.v3.52.

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Aditi and Kushal Qanungo. "Nano particles as drug delivery agents for antitubercular drugs." In INTERNATIONAL CONFERENCE ON HUMANS AND TECHNOLOGY: A HOLISTIC AND SYMBIOTIC APPROACH TO SUSTAINABLE DEVELOPMENT: ICHT 2022. AIP Publishing, 2023. http://dx.doi.org/10.1063/5.0112810.

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Reports on the topic "Drug development"

Basu, Sayani. Pharmacognosy in Drug Development. Spring Library, April 2021. http://dx.doi.org/10.47496/nl.blog.23.

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Seol, Dai-Wu. TRAIL-Based Anticancer Drug Development. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407205.

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Tignor, Gregory H. Drug Development against Viral Diseases. Fort Belvoir, VA: Defense Technical Information Center, February 1987. http://dx.doi.org/10.21236/ada201949.

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Krieger, Joshua, Danielle Li, and Dimitris Papanikolaou. Missing Novelty in Drug Development. Cambridge, MA: National Bureau of Economic Research, May 2018. http://dx.doi.org/10.3386/w24595.

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Novotny, Jaroslav F. Preparation of Bulk Drug for the U.S. Army Drug Development Program. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada425622.

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Novotny, Jaroslav. Preparation of Bulk Drug for the U.S. Army Drug Development Program. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada392524.

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Novotny, Jaroslav. Preparation of Chemicals and Bulk Drug Substance for the U.S. Army Drug Development Program. Fort Belvoir, VA: Defense Technical Information Center, March 2000. http://dx.doi.org/10.21236/ada382468.

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Novotny, Jaroslav F. Preparation of Chemicals and Bulk Drug Substances for the U.S. Army Drug Development Program. Fort Belvoir, VA: Defense Technical Information Center, December 1997. http://dx.doi.org/10.21236/adb232976.

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Chandra, Amitabh, Craig Garthwaite, and Ariel Dora Stern. Characterizing the Drug Development Pipeline for Precision Medicines. Cambridge, MA: National Bureau of Economic Research, November 2017. http://dx.doi.org/10.3386/w24026.

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Collington, Rosie, and William Lazonick. Pricing for Medicine Innovation: A Regulatory Approach to Support Drug Development and Patient Access. Institute for New Economic Thinking Working Paper Series, January 2022. http://dx.doi.org/10.36687/inetwp176.

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Abstract:

The United States represents the world’s largest market for pharmaceutical drugs. It is also the only advanced economy in the world that does not regulate drug prices. There is no upper threshold for the prices of medicines in the United States. List prices are instead set by manufacturers in negotiation with supply-chain intermediaries, though some federal programs have degrees of discretion in price determinations. In practice, this deregulated system means that drug prices in the United States are generally far higher than in other advanced economies, adversely affecting patient accessibility and system affordability. In this paper, we draw on the “theory of innovative enterprise” to develop a framework that provides both a critique of the existing pricing system in the United States and a foundation for developing a new model of pricing regulation to support safety and effectiveness through drug development as well as accessibility and affordability in the distribution of approved medicines to patients. We introduce a regulatory approach we term “Pricing for Medicine Innovation” (PMI), which departs dramatically from the market-equilibrium assumptions of conventional (neoclassical) economics. The PMI approach recognizes the centrality of collective investments by government agencies and business firms in the productive capabilities that underpin the drug development process. PMI specifies the conditions under which, at the firm level, drug pricing can support both sustained investment in these capabilities and improved patient access. PMI can advance both of these objectives simultaneously by regulating not just the level of corporate profit but also its allocation to reinvestment in the drug development process. PMI suggests that although price caps are likely to improve drug affordability, there remain two potential issues with this pricing approach. Firstly, in an innovation system where a company’s sales revenue is the source of its finance for further drug development, price caps may deprive a firm of the means to invest in innovation. Secondly, even with adequate profits available for investment in innovation, a firm that is run to maximize shareholder value will tend to use those profits to fund distributions to shareholders rather than for investment in drug innovation. We argue that, if implemented properly, PMI could both improve the affordability of medicines and enhance the innovative performance of pharmaceutical companies.

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