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Journal articles on the topic 'NELFINAVIR RESISTANCE'

Author: Grafiati

Published: 11 September 2023

Last updated: 31 July 2025

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1

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 It has largely been replaced by next-generation HIV-PI with increased specificity and efficacy for HIV therapy, partly reflecting the significant rate of the off-target activity of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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3

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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8

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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9

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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Hammer, Scott M., Roland Bassett, Kathleen E. Squires, et al. "A Randomized Trial of Nelfinavir and Abacavir in Combination with Efavirenz and Adefovir Dipivoxil in HIV-1-Infected Persons with Virological Failure Receiving Indinavir." Antiviral Therapy 8, no. 6 (2002): 507–18. http://dx.doi.org/10.1177/135965350300800615.

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Objectives (1) To determine the efficacy and safety of nelfinavir versus placebo and abacavir versus other approved nucleoside reverse transcriptase inhibitors (NRTIs), in combination with efavirenz and adefovir dipovoxil, in subjects experiencing virological failure on an indinavir-containing regimen. (2) To determine the relationship of baseline viral drug resistance genotype and phenotype to virological outcome. Design and methods A prospective, randomized, controlled, multicentre study in non-nucleoside reverse transcriptase inhibitor (NNRTI)-naive subjects conducted by the Adult AIDS Clin

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12

Ferrarelli, Leslie K. "Repurposing an HIV drug for melanoma." Science Signaling 9, no. 423 (2016): ec85-ec85. http://dx.doi.org/10.1126/scisignal.aaf8440.

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Inhibitors of the kinases BRAF or MEK (BRAF/MEK) can reduce tumor growth in some patients with melanoma, but resistance often develops. Microphthalmia-associated transcription factor (MITF) is implicated in promoting melanoma development. Smith et al. found that long-term treatment of cell cultures and mice bearing xenografts with BRAF/MEK inhibitors increased the abundance of MITF and its transcription factor PAX3 and that silencing MITF sensitized drug-resistant melanoma cells to the inhibitors. In a screen for small molecules that could reduce the abundance of MITF or PAX3, the most effecti

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Kolli, M., A. Ozen, N. Kurt-Yilmaz, and C. A. Schiffer. "HIV-1 Protease-Substrate Coevolution in Nelfinavir Resistance." Journal of Virology 88, no. 13 (2014): 7145–54. http://dx.doi.org/10.1128/jvi.00266-14.

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Schütt, M., J. Zhou, M. Meier, and H. H. Klein. "Long-term effects of HIV-1 protease inhibitors on insulin secretion and insulin signaling in INS-1 beta cells." Journal of Endocrinology 183, no. 3 (2004): 445–54. http://dx.doi.org/10.1677/joe.1.05620.

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The mechanism by which chronic treatment with HIV (human immunodeficiency virus)-1 protease inhibitors leads to a deterioration of glucose metabolism appears to involve insulin resistance, and may also involve impaired insulin secretion. Here we investigated the long-term effects of HIV-1 protease inhibitors on glucose-stimulated insulin secretion from beta cells and explored whether altered insulin secretion might be related to altered insulin signaling. INS-1 cells were incubated for 48 h with different concentrations of amprenavir, indinavir, nelfinavir, ritonavir or saquinavir, stimulated

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15

Perrin, Virginie, and Fabrizio Mammano. "Parameters Driving the Selection of Nelfinavir-Resistant Human Immunodeficiency Virus Type 1 Variants." Journal of Virology 77, no. 18 (2003): 10172–75. http://dx.doi.org/10.1128/jvi.77.18.10172-10175.2003.

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ABSTRACT We investigated the parameters driving nelfinavir resistance, along the D30N and L90M evolutionary pathways. The advantage of the D30N mutant was mostly due to its resistance level, while the L90M mutation allowed preservation of infectivity coupled with minimal resistance. Emergence of secondary mutations further increased the selective advantage of viruses harboring D30N.

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Subeha, Mahbuba R., and Carlos M. Telleria. "The Anti-Cancer Properties of the HIV Protease Inhibitor Nelfinavir." Cancers 12, no. 11 (2020): 3437. http://dx.doi.org/10.3390/cancers12113437.

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Traditional cancer treatments may lose efficacy following the emergence of novel mutations or the development of chemoradiotherapy resistance. Late diagnosis, high-cost of treatment, and the requirement of highly efficient infrastructure to dispense cancer therapies hinder the availability of adequate treatment in low-income and resource-limited settings. Repositioning approved drugs as cancer therapeutics may reduce the cost and timeline for novel drug development and expedite the availability of newer, efficacious options for patients in need. Nelfinavir is a human immunodeficiency virus (HI

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17

Mo, Hongmei, Neil Parkin, Kent D. Stewart, et al. "Identification and Structural Characterization of I84C and I84A Mutations That Are Associated with High-Level Resistance to Human Immunodeficiency Virus Protease Inhibitors and Impair Viral Replication." Antimicrobial Agents and Chemotherapy 51, no. 2 (2006): 732–35. http://dx.doi.org/10.1128/aac.00690-06.

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ABSTRACT Two novel human immunodeficiency virus protease mutations, I84C and I84A, were identified in patient isolates. The mutants with I84C displayed high-level resistance (median, at least 56-fold) to nelfinavir and saquinavir, but the majority remained susceptible to lopinavir. In contrast, isolates with the I84A mutation exhibited ≥33-fold median increased levels of resistance to nelfinavir, indinavir, amprenavir, ritonavir, lopinavir, saquinavir, and atazanavir. Isolates with the I84A or I84C mutation tended to be more resistant than the isolates with the I84V mutation. Modeling of the s

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Solas, Caroline, Alain Lafeuillade, Philippe Halfon, Stéphane Chadapaud, Gilles Hittinger, and Bruno Lacarelle. "Discrepancies between Protease Inhibitor Concentrations and Viral Load in Reservoirs and Sanctuary Sites in Human Immunodeficiency Virus-Infected Patients." Antimicrobial Agents and Chemotherapy 47, no. 1 (2003): 238–43. http://dx.doi.org/10.1128/aac.47.1.238-243.2003.

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ABSTRACT The variable penetration of antiretroviral drugs into sanctuary sites may contribute to the differential evolution of human immunodeficiency virus (HIV) and the emergence of drug resistance. We evaluated the penetration of indinavir, nelfinavir, and lopinavir-ritonavir (lopinavir/r) in the central nervous system, genital tract, and lymphoid tissue and assessed the correlation with residual viral replication. Plasma, cerebrospinal fluid (CSF), semen, and lymph node biopsy samples were collected from 41 HIV-infected patients on stable highly active antiretroviral therapy regimens to det

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Gonzalez, Luis M. F., Renato S. Aguiar, Adriana Afonso, et al. "Biological characterization of human immunodeficiency virus type 1 subtype C protease carrying indinavir drug-resistance mutations." Journal of General Virology 87, no. 5 (2006): 1303–9. http://dx.doi.org/10.1099/vir.0.81517-0.

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Human immunodeficiency virus type 1 subtype C isolates belong to one of the most prevalent strains circulating worldwide and are responsible for the majority of new infections in the sub-Saharan region and other highly populated areas of the globe. In this work, the impact of drug-resistance mutations in the protease gene of subtype C viruses was analysed and compared with that of subtype B counterparts. A series of recombinant subtype C and B viruses was constructed carrying indinavir (IDV)-resistance mutations (M46V, I54V, V82A and L90M) and their susceptibility to six FDA-approved protease

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Johnston, Elizabeth, Mark A. Winters, Soo-Yon Rhee, Thomas C. Merigan, Celia A. Schiffer, and Robert W. Shafer. "Association of a Novel Human Immunodeficiency Virus Type 1 Protease Substrate Cleft Mutation, L23I, with Protease Inhibitor Therapy and In Vitro Drug Resistance." Antimicrobial Agents and Chemotherapy 48, no. 12 (2004): 4864–68. http://dx.doi.org/10.1128/aac.48.12.4864-4868.2004.

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ABSTRACT We observed a previously uncharacterized mutation in the protease substrate cleft, L23I, in 31 of 4,303 persons undergoing human immunodeficiency virus type 1 genotypic resistance testing. In combination with V82I, L23I was associated with a sevenfold reduction in nelfinavir susceptibility and a decrease in replication capacity. In combination with other drug resistance mutations, L23I was associated with multidrug resistance and a compensatory increase in replication capacity.

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Gong, Yi-Fei, Brett S. Robinson, Ronald E. Rose, et al. "In Vitro Resistance Profile of the Human Immunodeficiency Virus Type 1 Protease Inhibitor BMS-232632." Antimicrobial Agents and Chemotherapy 44, no. 9 (2000): 2319–26. http://dx.doi.org/10.1128/aac.44.9.2319-2326.2000.

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ABSTRACT BMS-232632 is an azapeptide human immunodeficiency virus (HIV) type 1 (HIV-1) protease inhibitor that displays potent anti-HIV-1 activity (50% effective concentration [EC50], 2.6 to 5.3 nM; EC90, 9 to 15 nM). In vitro passage of HIV-1 RF in the presence of inhibitors showed that BMS-232632 selected for resistant variants more slowly than nelfinavir or ritonavir did. Genotypic and phenotypic analysis of three different HIV strains resistant to BMS-232632 indicated that an N88S substitution in the viral protease appeared first during the selection process in two of the three strains. An

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Grossman, Zehava, Ellen E. Paxinos, Diana Averbuch, et al. "Mutation D30N Is Not Preferentially Selected by Human Immunodeficiency Virus Type 1 Subtype C in the Development of Resistance to Nelfinavir." Antimicrobial Agents and Chemotherapy 48, no. 6 (2004): 2159–65. http://dx.doi.org/10.1128/aac.48.6.2159-2165.2004.

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ABSTRACT Differences in baseline polymorphisms between subtypes may result in development of diverse mutational pathways during antiretroviral treatment. We compared drug resistance in patients with human immunodeficiency virus subtype C (referred to herein as “subtype-C-infected patients”) versus subtype-B-infected patients following protease inhibitor (PI) therapy. Genotype, phenotype, and replication capacity (Phenosense; Virologic) were determined. We evaluated 159 subtype-C- and 65 subtype-B-infected patients failing first PI treatment. Following nelfinavir treatment, the unique nelfinavi

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Sugiura, Wataru, Zene Matsuda, Yoshiyuki Yokomaku, et al. "Interference between D30N and L90M in Selection and Development of Protease Inhibitor-Resistant Human Immunodeficiency Virus Type 1." Antimicrobial Agents and Chemotherapy 46, no. 3 (2002): 708–15. http://dx.doi.org/10.1128/aac.46.3.708-715.2002.

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ABSTRACT We studied the evolutionary relationships between the two protease inhibitor (PI) resistance mutations, D30N and L90M, of human immunodeficiency virus type 1 (HIV-1). The former is highly specific for nelfinavir resistance, while the latter is associated with resistance to several PIs, including nelfinavir. Among patients with nelfinavir treatment failure, we found that D30N acquisition was strongly suppressed when L90M preexisted. Thus, D30N/L90M double mutations not only were detected in a very limited number of patients but also accounted for a minor fraction within each patient. I

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Gupta, Vinay, Christian G. Samuleson, Susan Su, and Thomas C. Chen. "Nelfinavir potentiation of imatinib cytotoxicity in meningioma cells via survivin inhibition." Neurosurgical Focus 23, no. 4 (2007): E9. http://dx.doi.org/10.3171/foc-07/10/e9.

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✓ Although most meningiomas are treated surgically, it may not be possible to completely remove atypical, malignant, and surgically inaccessible meningiomas; in the majority of these cases there is tumor recurrence. The authors have already reported initial preclinical results on the efficacy of imatinib in the treatment of meningiomas; however, a recent Phase II trial of imatinib in patients with recurrent meningiomas did not demonstrate significant antitumor activity. To enhance the activity of imatinib, the authors investigated the use of a combination therapy with nelfinavir on primary men

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Winters, Mark A., Jonathan M. Schapiro, Jody Lawrence, and Thomas C. Merigan. "Human Immunodeficiency Virus Type 1 Protease Genotypes and In Vitro Protease Inhibitor Susceptibilities of Isolates from Individuals Who Were Switched to Other Protease Inhibitors after Long-Term Saquinavir Treatment." Journal of Virology 72, no. 6 (1998): 5303–6. http://dx.doi.org/10.1128/jvi.72.6.5303-5306.1998.

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ABSTRACT An understanding of the mechanisms of virologic cross-resistance between human immunodeficiency virus type 1 protease inhibitors is important for the establishment of effective treatment strategies for patients who no longer respond to their initial protease inhibitor. Protease gene sequencing results from patients treated with saquinavir showed significant increases in the frequency of the G48V protease mutation in patients receiving higher doses of the drug. In addition, all six patients who developed the G48V mutation during saquinavir therapy developed the V82A mutation either on

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Kirk, Ole, Jens D. Lundgren, Court Pedersen, et al. "A Randomized Trial Comparing Initial Haart Regimens of Nelfinavir/Nevirapine and Ritonavir/Saquinavir in Combination with Two Nucleoside Reverse Transcriptase Inhibitors." Antiviral Therapy 8, no. 6 (2002): 595–602. http://dx.doi.org/10.1177/135965350300800611.

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Background A triple-class HAART regimen may be associated with a better virological effect than conventional regimens, but may also lead to toxicity and more profound resistance. Methods Randomized, controlled, open-label trial of 233 protease inhibitor- and non-nucleoside reverse transcriptase inhibitor-naive HIV-infected patients allocated to a regimen of nelfinavir and nevirapine (1250/200 mg twice daily; n=118) or ritonavir and saquinavir (400/400 mg twice daily; n=115), both in combination with two nucleoside reverse transcriptase inhibitors. The primary end-point was HIV RNA ≤20 copies/m

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Doualla-Bell, Florence, Ava Avalos, Tendani Gaolathe, et al. "Impact of Human Immunodeficiency Virus Type 1 Subtype C on Drug Resistance Mutations in Patients from Botswana Failing a Nelfinavir-Containing Regimen." Antimicrobial Agents and Chemotherapy 50, no. 6 (2006): 2210–13. http://dx.doi.org/10.1128/aac.01447-05.

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ABSTRACT Among 16 human immunodeficiency virus-infected (subtype C) Batswana patients who failed nelfinavir (NFV)-containing regimens, the most prevalent mutation observed was D30N (54%), followed by L90M (31%). L89I, K20T/I, and E35D polymorphic changes were also identified. These findings suggest that subtype C viruses in Botswana may develop resistance to NFV via subtype-specific pathways.

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Ziermann, Rainer, Kay Limoli, Kalyan Das, Edward Arnold, Christos J. Petropoulos, and Neil T. Parkin. "A Mutation in Human Immunodeficiency Virus Type 1 Protease, N88S, That Causes In Vitro Hypersensitivity to Amprenavir." Journal of Virology 74, no. 9 (2000): 4414–19. http://dx.doi.org/10.1128/jvi.74.9.4414-4419.2000.

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ABSTRACT Amprenavir (Agenerase, 141-W94, VX-478) is a human immunodeficiency virus type 1 (HIV-1) protease inhibitor (PRI) recently approved for the treatment of HIV-1 infection in the United States. A major cause of treatment failure is the development of resistance to PRIs. One potential use for amprenavir is as salvage therapy for patients for whom treatment that includes one (or more) of the other four currently approved PRIs—saquinavir, indinavir, ritonavir, and nelfinavir—has failed. We evaluated the cross-resistance to amprenavir of viruses that evolved during treatment with the two mos

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Sugiura, Wataru, Tsuyoshi Oishi, Aiko Okano, et al. "Two Possible Pathways for Acquisition of Mutations Related to Nelfinavir Resistance." Japanese Journal of Infectious Diseases 52, no. 4 (1999): 175–76. http://dx.doi.org/10.7883/yoken.52.175.

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Liu, Wei, Qiang Meng, Yaoting Sun, et al. "Targeting P-Glycoprotein: Nelfinavir Reverses Adriamycin Resistance in K562/ADR Cells." Cellular Physiology and Biochemistry 51, no. 4 (2018): 1616–31. http://dx.doi.org/10.1159/000495650.

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Background/Aims: The emergence of multidrug resistance (MDR) caused by P-glycoprotein (P-gp) overexpression is a serious obstacle to the treatment of chronic myelocytic leukemia. In recent years, some clinical trials have shown that nelfinavir (NFV), a traditional anti-HIV drug, has anti-cancer effects. Some researchers have also shown NFV might be a potential P-gp inhibitor. This study is aimed at investigating whether nelfinavir can act as an MDR-reversal drug and to clarify its molecular mechanism as well. Methods: K562 and K562/ADR cell lines were applied in the study. Cytotoxicity was det

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Atkinson, B., J. Isaacson, M. Knowles, E. Mazabel, and A. K. Patick. "Correlation between Human Immunodeficiency Virus Genotypic Resistance and Virologic Response in Patients Receiving Nelfinavir Monotherapy or Nelfinavir with Lamivudine and Zidovudine." Journal of Infectious Diseases 182, no. 2 (2000): 420–27. http://dx.doi.org/10.1086/315726.

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Rufo, Paul A., Patricia W. Lin, Adriana Andrade, et al. "Diarrhea-associated HIV-1 APIs potentiate muscarinic activation of Cl- secretion by T84 cells via prolongation of cytosolic Ca2+ signaling." American Journal of Physiology-Cell Physiology 286, no. 5 (2004): C998—C1008. http://dx.doi.org/10.1152/ajpcell.00357.2003.

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Aspartyl protease inhibitors (APIs) effectively extend the length and quality of life in human immunodeficiency virus (HIV)-infected patients, but dose-limiting side effects such as lipodystrophy, insulin resistance, and diarrhea have limited their clinical utility. Here, we show that the API nelfinavir induces a secretory form of diarrhea in HIV-infected patients. In vitro studies demonstrate that nelfinavir potentiates muscarinic stimulation of Cl- secretion by T84 human intestinal cell monolayers through amplification and prolongation of an apical membrane Ca2+-dependent Cl- conductance. Th

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Walter, Hauke, Barbara Schmidt, Astrid Rascu, et al. "Phenotypic HIV-1 Resistance Correlates with Treatment Outcome of Nelfinavir Salvage Therapy." Antiviral Therapy 5, no. 4 (1999): 249–56. http://dx.doi.org/10.1177/135965350000500403.

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In order to analyse whether drug sensitivity testing would be beneficial for clinical decision-making in heavily pretreated patients, we retrospectively studied viral genotype and phenotypic drug resistance in 12 HIV-1-infected patients, each of them with a history of failing at least one therapeutic regimen including one or two protease inhibitors (PIs). The salvage therapy included nelfinavir as new PI in all cases. Four patients showed a sustained and five patients a transient viral load decrease. Three patients failed to show a significant decline of plasma HIV-1 RNA. In the baseline sampl

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Bakker, Andreas. "Predictive Value of Genotypic and Phenotypic Resistance in 2 Nelfinavir‐Experienced Patients." Journal of Infectious Diseases 181, no. 5 (2000): 1862–63. http://dx.doi.org/10.1086/315480.

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Gonzalez, Luis M. F., Rodrigo M. Brindeiro, Renato S. Aguiar, et al. "Impact of Nelfinavir Resistance Mutations on In Vitro Phenotype, Fitness, and Replication Capacity of Human Immunodeficiency Virus Type 1 with Subtype B and C Proteases." Antimicrobial Agents and Chemotherapy 48, no. 9 (2004): 3552–55. http://dx.doi.org/10.1128/aac.48.9.3552-3555.2004.

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ABSTRACT Human immunodeficiency virus type 1 subtype B and C proteases were manipulated to contain 90M, 88D, or 89L, and their in vitro biological properties were studied. We showed that D30N has significantly more impact in subtype C than in subtype B counterparts, accounting for the reported low prevalence of this mutation in patients failing nelfinavir-based regimens.

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Gonsalves, Wilson I., Shaji Kumar, Gabriela Perez, et al. "Trial in Progress: Phase I Open-Label Study of Metformin and Nelfinavir in Combination with Bortezomib in Patients with Relapsed and/or Refractory Multiple Myeloma." Blood 138, Supplement 1 (2021): 2735. http://dx.doi.org/10.1182/blood-2021-149437.

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Abstract Background: GLUT4 inhibition is an attractive therapeutic option in multiple myeloma (MM) given the dependence of MM cells on glucose transport. Furthermore, combining a GLUT4 inhibitor with an oxidative phosphorylation inhibitor in MM cells to counter the possibility of therapeutic resistance to GLUT4 inhibition has demonstrated synergistic promise (Dalva-Aydemir et al, Clin Can Res 2015). Using a GLUT4 inhibitor such as the HIV protease inhibitor nelfinavir is an attractive choice since it not only inhibits the transport function of GLUT4, but it also lowers the cytotoxicity resista

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Pellegrin, Isabelle, Dominique Breilh, François Montestruc, et al. "Virologic response to nelfinavir-based regimens: pharmacokinetics and drug resistance mutations (VIRAPHAR study)." AIDS 16, no. 10 (2002): 1331–40. http://dx.doi.org/10.1097/00002030-200207050-00004.

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Antunes, Dinler A., Maurício M. Rigo, Marialva Sinigaglia, et al. "New Insights into the In Silico Prediction of HIV Protease Resistance to Nelfinavir." PLoS ONE 9, no. 1 (2014): e87520. http://dx.doi.org/10.1371/journal.pone.0087520.

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Quiros-Roldan, E., F. Moretti, C. Torti, V. Tirelli, S. Casari, and G. Carosi. "HIV-1 genotype resistance pattern and evolution in patients failing nelfinavir-containing regimens." Journal of Clinical Laboratory Analysis 19, no. 1 (2005): 26–29. http://dx.doi.org/10.1002/jcla.20051.

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Chandra, Surabhi, Subramanyam N. Murthy, Debasis Mondal, and Krishna C. Agrawal. "Therapeutic effects of Nigella sativa on chronic HAART-induced hyperinsulinemia in ratsThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 2 of a 2-part Special Issue)." Canadian Journal of Physiology and Pharmacology 87, no. 4 (2009): 300–309. http://dx.doi.org/10.1139/y09-014.

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Prolonged use of highly active antiretroviral therapy (HAART) is associated with insulin resistance in HIV-1-positive patients. Small animal models that recapitulate the long-term effects of HAART may facilitate the identification of therapeutic agents to suppress these side effects. We investigated the protective effects of black seed oil (BSO) from Nigella sativa in Sprague–Dawley rats treated with a daily HAART regimen for 7 months. The antiretroviral drugs, consisting of nelfinavir (200 mg/kg), zidovudine (50 mg/kg), and efavirenz (20 mg/kg), were mixed with diet with or without BSO (400 µ

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Driessen, Christoph, Jürgen Bader, Marianne Kraus, et al. "SAKK 65/08: A Phase I Dose Escalation Study of Bortezomib in Combination with Nelfinavir in Patients with Advanced Hematologic Malignancies." Blood 124, no. 21 (2014): 4747. http://dx.doi.org/10.1182/blood.v124.21.4747.4747.

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Abstract Rationale: Overcoming proteasome inhibitor (PI) resistance is a challenge in multiple myeloma (MM) therapy since most MM patients ultimately develop PI resistance. Induction of excessive activation of the unfolded protein response (UPR) is the major mechanism of PI-induced cytotoxicity in MM. The UPR is a complex transcriptional response that balances biosynthesis, folding and proteasomal destruction of cellular protein. UPR inactivation results in PI resistance in vitro, and MM cells with low UPR activation accumulate and drive the relapse in PI-resistant MM patients. Pharmacologic a

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Chandler, Becky, Maria Detsika, Andrew Owen, et al. "Effect of Transporter Modulation on the Emergence of Nelfinavir Resistance In Vitro." Antiviral Therapy 12, no. 5 (2007): 831–34. http://dx.doi.org/10.1177/135965350701200515.

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Background HIV drug resistance is of increasing concern and could result from inadequate drug potency, poor therapy adherence and the existence of pharmacological sanctuary sites for viral replication. One contributing factor to the generation of such sites could be drug efflux transporters, which have been shown capable of effluxing HIV protease inhibitors from cells. Methods In this ‘proof-of-concept’ study, the ability of the efflux transport inhibitor verapamil to modulate the intracellular accumulation of radiolabeled nelfinavir (NFV) and the antiviral effect of NFV was assessed in MT4 ce

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Kumar, Pranav, Robert Lodge, Frédéric Raymond, et al. "Gene expression modulation and the molecular mechanisms involved in Nelfinavir resistance inLeishmania donovaniaxenic amastigotes." Molecular Microbiology 89, no. 3 (2013): 565–82. http://dx.doi.org/10.1111/mmi.12298.

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Svedhem, Veronica, A. Lindkvist, T. Bergroth, Lidman Knut, and A. Sönnerborg. "Diverse pattern of protease inhibitor resistance mutations in HIV-1 infected patients failing nelfinavir." Journal of Medical Virology 76, no. 4 (2005): 447–51. http://dx.doi.org/10.1002/jmv.20381.

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Snoeck, Joke, Rami Kantor, Robert W. Shafer, et al. "Discordances between Interpretation Algorithms for Genotypic Resistance to Protease and Reverse Transcriptase Inhibitors of Human Immunodeficiency Virus Are Subtype Dependent." Antimicrobial Agents and Chemotherapy 50, no. 2 (2006): 694–701. http://dx.doi.org/10.1128/aac.50.2.694-701.2006.

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ABSTRACT The major limitation of drug resistance genotyping for human immunodeficiency virus remains the interpretation of the results. We evaluated the concordance in predicting therapy response between four different interpretation algorithms (Rega 6.3, HIVDB-08/04, ANRS [07/04], and VGI 8.0). Sequences were gathered through a worldwide effort to establish a database of non-B subtype sequences, and demographic and clinical information about the patients was gathered. The most concordant results were found for nonnucleoside reverse transcriptase (RT) inhibitors (93%), followed by protease inh

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Casado, Jose L., Santiago Moreno, Kurt Hertogs, et al. "Plasma drug levels, genotypic resistance, and virological response to a nelfinavir plus saquinavir-containing regimen." AIDS 16, no. 1 (2002): 47–52. http://dx.doi.org/10.1097/00002030-200201040-00007.

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Kakehasi, Fabiana M., Unaí Tupinambás, Silvia Cleto, et al. "Persistence of Genotypic Resistance to Nelfinavir among Women Exposed to Prophylactic Antiretroviral Therapy during Pregnancy." AIDS Research and Human Retroviruses 23, no. 12 (2007): 1515–20. http://dx.doi.org/10.1089/aid.2007.0025.

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Kraus, M., J. Bader, H. Overkleeft, and C. Driessen. "Nelfinavir augments proteasome inhibition by bortezomib in myeloma cells and overcomes bortezomib and carfilzomib resistance." Blood Cancer Journal 3, no. 3 (2013): e103-e103. http://dx.doi.org/10.1038/bcj.2013.2.

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Lagathu, Claire, Brenda Eustace, Matthieu Prot, et al. "Some HIV Antiretrovirals Increase Oxidative Stress and Alter Chemokine, Cytokine or Adiponectin Production in Human Adipocytes and Macrophages." Antiviral Therapy 12, no. 4 (2007): 489–500. http://dx.doi.org/10.1177/135965350701200407.

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Objectives Adipose tissue from patients with HIV-related lipodystrophy presents a state of chronic inflammation. Altered expression of cytokines/adipokines and macrophage infiltration could be involved in patients’ insulin resistance and lipoatrophy. We tested whether antiretrovirals affected adipokine release by human subcutaneous adipocytes and cytokine/chemokine production by human macrophages and examined whether reactive oxygen species (ROS) hyperproduction was related to the effect of antiretrovirals. Methods Differentiated human adipocytes and PMA-THP-1 macrophages were treated with pro

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Kim, Sanggu, Yun-Cheol Kim, Hangfei Qi, Kunkai Su, Sherie L. Morrison, and Samson A. Chow. "Efficient Identification of Human Immunodeficiency Virus Type 1 Mutants Resistant to a Protease Inhibitor by Using a Random Mutant Library." Antimicrobial Agents and Chemotherapy 55, no. 11 (2011): 5090–98. http://dx.doi.org/10.1128/aac.00687-11.

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ABSTRACTEmergence of drug-resistant mutant viruses during the course of antiretroviral therapy is a major hurdle that limits the success of chemotherapeutic treatment to suppress human immunodeficiency virus type 1 (HIV-1) replication and AIDS progression. Development of new drugs and careful patient management based on resistance genotyping data are important for enhancing therapeutic efficacy. However, identifying changes leading to drug resistance can take years of clinical studies, and conventionalin vitroassays are limited in generating reliable drug resistance data. Here we present an ef

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