Relevant bibliographies by topics / NELFINAVIR RESISTANCE

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'NELFINAVIR RESISTANCE'

Author: Grafiati
Published: 11 September 2023
Last updated: 31 July 2025

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Journal articles on the topic "NELFINAVIR RESISTANCE"

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Besse, Andrej, Lenka Besse, Sara C. Stolze, et al. "Nelfinavir Overcomes Proteasome Inhibitor Resistance in Multiple Myeloma By Modulating Membrane Lipid Bilayer Composition and Fluidity." Blood 136, Supplement 1 (2020): 11. http://dx.doi.org/10.1182/blood-2020-136253.

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INTRODUCTION Nelfinavir is a highly lipophilic, first generation HIV-protease inhibitor (HIV-PI) approved for HIV treatment. It has largely been replaced by next-generation HIV-PI with increased specificity and efficacy for HIV therapy, partly reflecting the significant rate of the off-target activity of nelfinavir. Increasing preclinical and clinical evidence shows that nelfinavir has broad anti-cancer activity as a single agent and in combination, potentially related to its off-target activity in mammalian cells. Nelfinavir is particularly effective in the treatment of proteasome inhibitor-r
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Fassmannová, Dominika, František Sedlák, Jindřich Sedláček, Ivan Špička, and Klára Grantz Šašková. "Nelfinavir Inhibits the TCF11/Nrf1-Mediated Proteasome Recovery Pathway in Multiple Myeloma." Cancers 12, no. 5 (2020): 1065. http://dx.doi.org/10.3390/cancers12051065.

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Proteasome inhibitors are the backbone of multiple myeloma therapy. However, disease progression or early relapse occur due to development of resistance to the therapy. One important cause of resistance to proteasome inhibition is the so-called bounce-back response, a recovery pathway driven by the TCF11/Nrf1 transcription factor, which activates proteasome gene re-synthesis upon impairment of the proteasome function. Thus, inhibiting this recovery pathway potentiates the cytotoxic effect of proteasome inhibitors and could benefit treatment outcomes. DDI2 protease, the 3D structure of which re
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Patick, A. K., M. Duran, Y. Cao, et al. "Genotypic and Phenotypic Characterization of Human Immunodeficiency Virus Type 1 Variants Isolated from Patients Treated with the Protease Inhibitor Nelfinavir." Antimicrobial Agents and Chemotherapy 42, no. 10 (1998): 2637–44. http://dx.doi.org/10.1128/aac.42.10.2637.

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ABSTRACT Nelfinavir mesylate (formerly AG1343) is a potent and selective inhibitor of human immunodeficiency virus (HIV) protease approved for the treatment of individuals infected with HIV. Nucleotide sequence analysis of protease genes from plasma HIV type 1 (HIV-1) RNA revealed a unique aspartic acid (D)-to-asparagine (N) substitution at residue 30 (D30N) in 25 of 55 patients treated with nelfinavir for a median of 13 weeks. Although the appearance of D30N was occasionally associated with concurrent or sequential emergence of other changes (e.g., at residues 35, 36, 46, 71, 77, and 88), gen
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Yerly, Sabine, Martin Rickenbach, Matei Popescu, et al. "Drug Resistance Mutations in HIV-1-Infected Subjects during Protease Inhibitor-Containing Highly Active Antiretroviral Therapy with Nelfinavir or Indinavir." Antiviral Therapy 6, no. 3 (2000): 185–89. http://dx.doi.org/10.1177/135965350100600304.

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Objectives The aim of this retrospective study was to evaluate treatment outcome and characterize the pattern of genotype mutations in subjects with treatment failure on highly active antiretroviral therapy (HAART) containing nelfinavir or indinavir. Study design and methods The database of the Swiss HIV Cohort Study was screened for all subjects naive to protease inhibitor (PI) treatment who started HAART with nelfinavir or indinavir, responded initially (HIV-RNA <400 copies/ml) and received >24 weeks of treatment. Responders with subsequent treatment failure (HIV-RNA >1000 copies/ml
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Kachko, Ilana, Adva Maissel, Livnat Mazor, et al. "Postreceptoral Adipocyte Insulin Resistance Induced by Nelfinavir Is Caused by Insensitivity of PKB/Akt to Phosphatidylinositol-3,4,5-Trisphosphate." Endocrinology 150, no. 6 (2009): 2618–26. http://dx.doi.org/10.1210/en.2008-1205.

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Adipocyte insulin resistance can be caused by proximal insulin signaling defects but also from postreceptor mechanisms, which in large are poorly characterized. Adipocytes exposed for 18 h to the HIV protease inhibitor nelfinavir manifest insulin resistance characterized by normal insulin-stimulated tyrosine phosphorylation of the insulin receptor and insulin receptor substrate proteins, preserved in vitro phosphatidylinositol 3-kinase (PI 3-kinase) assay activity but impaired activation of PKB/Akt and stimulation of glucose uptake. Here we aimed to assess whether impaired PKB/Akt activation i
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&NA;. "Nelfinavir + saquinavir resistance testing in HIV management." Inpharma Weekly &NA;, no. 1325 (2002): 20. http://dx.doi.org/10.2165/00128413-200213250-00052.

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Petrich, Adam M., Violetta V. Leshchenko, Pei-Yu Kuo, B. Hilda Ye, Joseph A. Sparano, and Samir Parekh. "Genomic and Pathway Connectivity Analyses Identify Novel Strategies to Overcome mTOR Inhibitor Resistance In DLBCL." Blood 116, no. 21 (2010): 436. http://dx.doi.org/10.1182/blood.v116.21.436.436.

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Abstract Abstract 436 mTOR inhibitors have been used with clinical success in solid tumors and non-Hodgkin lymphoma (NHL), and are attractive therapeutic options for DLBCL (diffuse large B-cell lymphoma, which has been shown to have constitutively active mTOR signaling). However, resistance to this class of agents remains problematic, and mechanisms of resistance are poorly understood. We performed candidate drug discovery using connectivity mapping and global gene expression profiling (GEP) to understand the pathways and genes responsible for resistance to the mTOR inhibitor Rapamycin (Siroli
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Chow, W. A., S. Guo, and F. Valdes-Albini. "HIV protease inhibitor (PI) therapy for liposarcoma." Journal of Clinical Oncology 24, no. 18_suppl (2006): 9564. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.9564.

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9564 Background: Liposarcomas are the second most common soft-tissue sarcoma. Highly-active anti-retroviral therapy (HAART) with HIV PIs results in “HIV-1 protease inhibitor associated lipodystrophy syndrome,” characterized by peripheral fat wasting, central fat accumulation, insulin resistance, and hyperlipidemia. Based upon this syndrome, we hypothesized that HIV PIs might represent a novel liposarcoma therapy. Methods: SW872, LiSa-2, and FU-DDLS-1 liposarcoma, and control 293 embryonic kidney and HT1080 fibrosarcoma cell lines were treated with HIV PIs and subjected to cellular and molecula
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Schmidt, Barbara, Klaus Korn, Brigitte Moschik, Christiane Paatz, Klaus Überla, and Hauke Walter. "Low Level of Cross-Resistance to Amprenavir (141W94) in Samples from Patients Pretreated with Other Protease Inhibitors." Antimicrobial Agents and Chemotherapy 44, no. 11 (2000): 3213–16. http://dx.doi.org/10.1128/aac.44.11.3213-3216.2000.

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ABSTRACT The therapeutic success of an antiretroviral salvage regimen containing protease inhibitors (PI) is limited by PI-resistant viral strains exhibiting various degrees of resistance and cross-resistance. To evaluate the extent of cross-resistance to the new PI amprenavir, 155 samples from 132 human immunodeficiency virus type 1-infected patients were analyzed for viral genotype by direct sequencing of the protease gene. Concomitantly, drug sensitivity to indinavir, saquinavir, ritonavir, nelfinavir, and amprenavir was analyzed by a recombinant virus assay. A total of 111 patients had bee
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Ford, Jennifer, David Cornforth, Patrick G. Hoggard, et al. "Intracellular and Plasma Pharmacokinetics of Nelfinavir and M8 in HIV-Infected Patients: Relationship with P-Glycoprotein Expression." Antiviral Therapy 9, no. 1 (2004): 77–84. http://dx.doi.org/10.1177/135965350400900101.

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One of the targets of antiretroviral therapy is within cells infected with HIV. In order to improve therapeutic efficacy, it is therefore important that the intracellular pharmacokinetics of drugs, such as nelfinavir mesylate and its active metabolite M8, are studied in addition to plasma pharmacokinetics. Previously, the intracellular accumulation of protease inhibitors has been reported in vivo, displaying the following hierarchy: nelfinavir > saquinavir > ritonavir > indinavir. Multidrug resistance transporters, such as P-glycoprotein (P-gp), may result in a lower intracellular con
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Dissertations / Theses on the topic "NELFINAVIR RESISTANCE"

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Lisovsky, Irene. "Emergence of Nelfinavir and Lopinavir resistance relative to a clinically relevant human immunodeficiency virus type-1 single nucleotide polymorphism at position 36 in protease enzyme «in vitro»." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86996.

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The genetic differences and polymorphisms between HIV-1 subtype B and non-B subtypes have been well documented. Classically, however, antiretrovirals (ARVs), including protease inhibitors (PIs), have been designed based on structural and functional information obtained utilizing subtype B HIV-1. With the advent of antiretroviral therapy (ART) in developing countries and the emergence of non-B infections in developed countries, the impact of these polymorphisms must be evaluated in terms of ART efficacy.<br>The 36th amino acid in the viral protease (PR) of B subtypes is Methionine (M), while no
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GUPTA, ANKITA. "COMPUTATIONAL CHARACTERIZATION OF NON-ACTIVE SITE MUTATION V77I IN HIV-1 PROTEASE: POSSIBLE CONTRIBUTION TO NELFINAVIR RESISTANCE AND DEVELOPMENT OF NEW DRUG LEADS TARGETING HIV-1 PROTEASE." Thesis, 2016. http://dspace.dtu.ac.in:8080/jspui/handle/repository/16058.

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BACKGROUND The Human immunodeficiency virus (HIV-1) protease is an attractive target for antiviral treatment and a number of therapeutically useful inhibitors have been designed against it. The emergence of drug resistant mutants of HIV-1 pose a serious problem for the conventional therapies been used so far. Here we have tried to study the effect of V77I mutation along with the co-occurring mutations L33F and K20T through multinanosecond molecular dynamics simulations. V77I
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Book chapters on the topic "NELFINAVIR RESISTANCE"

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Raposo, L. M., M. B. Arruda, R. M. Brindeiro, and F. F. Nobre. "Logistic Regression Models for Predicting Resistance to HIV Protease Inhibitor Nelfinavir." In IFMBE Proceedings. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-00846-2_306.

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Unissa, Ameeruddin Nusrath, and Luke Elizabeth Hanna. "Dissection of HIV-1 Protease Subtype B Inhibitors Resistance Through Molecular Modeling Approaches." In Big Data Analytics in HIV/AIDS Research. IGI Global, 2018. http://dx.doi.org/10.4018/978-1-5225-3203-3.ch007.

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Protease (PR) is an important enzyme required for the posttranslational processing of the viral gene products of type-1 human immunodeficiency virus (HIV-1). Protease inhibitors (PI) act as competitive inhibitors that bind to the active site of PR. The I84V mutation contributes resistance to multiple PIs, and structurally, this mutation affects both sides of the enzyme active site. In order to get insights about this major resistance site to PR inhibitors using in silico approaches, in this chapter, the wild-type (WT) and mutant (MT) I84V of PR were modeled and docked with all PR inhibitors: A
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Conference papers on the topic "NELFINAVIR RESISTANCE"

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"Probabilistic Neural Network for Predicting Resistance to HIV-Protease Inhibitor Nelfinavir." In International Conference on Bioinformatics Models, Methods and Algorithms. SCITEPRESS - Science and and Technology Publications, 2014. http://dx.doi.org/10.5220/0004735900170023.

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Guan, Min. "Abstract 2653: Nelfinavir induces apoptosis in hormone-resistant prostate cancer cells through inhibition of regulated intramembrane proteolysis of SREBP-1 and ATF6." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2653.

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