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Journal articles on the topic 'Indinavir drug'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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1

D. V. R. N., Bhikshapathi, Shiva Krishna A, Ramesh M, Suresh G, and Jyothi Sri S. "Erythrocytes as Carriers of Indinavir: Preparation, Characterization, In vitro and In vivo Pharmacokinetic Evaluation in Rats." International Journal of Pharmaceutical Sciences and Nanotechnology 10, no. 1 (2017): 3573–81. http://dx.doi.org/10.37285/ijpsn.2017.10.1.2.

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Indinavir is a protease inhibitor of the human immuno-deficiency virus. Indinavir is commercially available as capsule of 200 mg and 400 mg. Adult dose is 800 mg every 8 h. i.e., 2400 mg per day is equivalent to 6 capsules per day. No other dosage form is available in the market. Sustained release dosage form of indinavir can produce maximum therapeutic effect with minimum side effects and achieve better patient compliance. Various carriers have been used for the drug targeting among which cellular carriers such as erythrocytes offer greater potential advantages than other system. The drug is

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2

Hugen, Patricia WH, David M. Burger, Kees Brinkman, et al. "Carbamazepine–Indinavir Interaction Causes Antiretroviral Therapy Failure." Annals of Pharmacotherapy 34, no. 4 (2000): 465–70. http://dx.doi.org/10.1345/aph.19211.

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OBJECTIVE: To report a case of antiretroviral therapy failure caused by an interaction between carbamazepine and indinavir. CASE SUMMARY: A 48-year-old HIV-positive white man was treated with antiretroviral triple therapy, consisting of indinavir, zidovudine, and lamivudine. His HIV-RNA (viral load) became undetectable (<400 copies/mL) less than two months after this therapy was started; this was confirmed one month later. Shortly after the start of antiretroviral therapy, the patient developed herpes zoster, which was treated with famciclovir. Tramadol was initially prescribed for postherp

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3

Haas, David W., Benjamin Johnson, Janet Nicotera, et al. "Effects of Ritonavir on Indinavir Pharmacokinetics in Cerebrospinal Fluid and Plasma." Antimicrobial Agents and Chemotherapy 47, no. 7 (2003): 2131–37. http://dx.doi.org/10.1128/aac.47.7.2131-2137.2003.

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ABSTRACT Therapeutic control of human immunodeficiency virus type 1 (HIV-1) in peripheral compartments does not assure control in the central nervous system. Inadequate drug penetration may provide a sanctuary from which resistant virus can emerge or allow development of psychomotor abnormalities. To characterize the effect of ritonavir on indinavir disposition into cerebrospinal fluid, seven HIV-infected adults underwent intensive sampling at steady-state while receiving twice-daily indinavir (800 mg) and ritonavir (100 mg). Serial cerebrospinal fluid and plasma samples were obtained at 10 ti

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4

Kharasch, Evan D., Christine Hoffer, Dale Whittington, Alysa Walker, and Pamela Sheffels Bedynek. "Methadone Pharmacokinetics Are Independent of Cytochrome P4503A (CYP3A) Activity and Gastrointestinal Drug Transport." Anesthesiology 110, no. 3 (2009): 660–72. http://dx.doi.org/10.1097/aln.0b013e3181986a9a.

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Background Methadone clearance is highly variable, and drug interactions are problematic. Both have been attributed to CYP3A, but actual mechanisms are unknown. Drug interactions can provide such mechanistic information. Ritonavir/indinavir, one of the earliest protease inhibitor combinations, may inhibit CYP3A. We assessed ritonavir/indinavir effects on methadone pharmacokinetics and pharmacodynamics, intestinal and hepatic CYP3A activity, and intestinal transporters (P-glycoprotein) activity. CYP3A and transporters were assessed with alfentanil and fexofenadine, respectively. Methods Twelve

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5

T, Rajkumar, Sivasanker Reddy L, Sivasanker Reddy L, Rajeswari V, and Rajeswari V. "SYNTHESIS AND CHARACTERIZATION OF INDINAVIR-Cu COMPLEX." Asian Journal of Pharmaceutical and Clinical Research 10, no. 7 (2017): 289. http://dx.doi.org/10.22159/ajpcr.2017.v10i7.15359.

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Objective: The main objective of the present work is to synthesize Cu (II) indinavir, complex.Methods: The indinavir complexes were discussed with the help of spectroscopic instrumental methods such as infrared, ultraviolet, nuclear magnetic resonance, and mass and titrimetry methods (iodometry and potentiometry). Drug and drug metal complex are screened against antimicrobial activity.Results: The spectral studies show that the metal is coordinated to the drug in a bidentate manner. The titrimetry method, i.e., iodometric titration shows that metal bind to the drug in proportion of 1:1. The po

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Kharasch, Evan D., Pamela Sheffels Bedynek, Christine Hoffer, Alysa Walker, and Dale Whittington. "Lack of Indinavir Effects on Methadone Disposition Despite Inhibition of Hepatic and Intestinal Cytochrome P4503A (CYP3A)." Anesthesiology 116, no. 2 (2012): 432–47. http://dx.doi.org/10.1097/aln.0b013e3182423478.

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Background Methadone disposition and pharmacodynamics are highly susceptible to interactions with antiretroviral drugs. Methadone clearance and drug interactions have been attributed to cytochrome P4503A4 (CYP3A4), but actual mechanisms are unknown. Drug interactions can be clinically and mechanistically informative. This investigation assessed effects of the protease inhibitor indinavir on methadone pharmacokinetics and pharmacodynamics, hepatic and intestinal CYP3A4/5 activity (using alfentanil), and intestinal transporter activity (using fexofenadine). Methods Twelve healthy volunteers unde

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7

De Wit, S., M. Debier, M. De Smet, et al. "Effect of Fluconazole on Indinavir Pharmacokinetics in Human Immunodeficiency Virus-Infected Patients." Antimicrobial Agents and Chemotherapy 42, no. 2 (1998): 223–27. http://dx.doi.org/10.1128/aac.42.2.223.

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ABSTRACT To evaluate a potential pharmacokinetic interaction of coadministration of fluconazole, and indinavir, a human immunodeficiency virus (HIV) protease inhibitor, 13 patients were enrolled in a multiple-dose, three-period, placebo-controlled, crossover study. Patients were randomly assigned to receive indinavir at 1,000 mg every 8 h for 7 1 3 days (with fluconazole placebo), fluconazole at 400 mg once daily for 8 days (with indinavir placebo), and indinavir with fluconazole in combination. The pharmacokinetics of both drugs were measured on day 8 of each treatment period. The peak concen

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8

Bergshoeff, A. S., P. L. A. Fraaij, A. M. C. van Rossum, et al. "Pharmacokinetics of Indinavir Combined with Low-Dose Ritonavir in Human Immunodeficiency Virus Type 1-Infected Children." Antimicrobial Agents and Chemotherapy 48, no. 5 (2004): 1904–7. http://dx.doi.org/10.1128/aac.48.5.1904-1907.2004.

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ABSTRACT So far, no pediatric doses for indinavir combined with ritonavir have been defined. This study evaluated the pharmacokinetics of 400 mg of indinavir/m2 combined with 125 mg of ritonavir/m2 every 12 h (q12h) in 14 human immunodeficiency virus type 1-infected children. The area under the concentration-time curve from 0 to 24 h and the minimum concentration of drug in serum for indinavir were similar to those for 800 mg of indinavir-100 mg of ritonavir q12h in adults, while the maximum concentration of drug in serum was slightly decreased, with geometric mean ratios (90% confidence inter

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Ross, Natasha, Nicolette Hendricks-Leukes, Rachel Fanelwa Ajayi, Priscilla Baker, and Emmanuel I. Iwuoha. "Conductive Composite Biosensor System for Electrochemical Indinavir Drug Detection." Journal of Chemistry 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/630408.

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Indinavir is a protease inhibitor antiretroviral (ARV) drug, which forms part of the highly active antiretroviral therapy during the treatment of HIV/AIDS. Indinavir undergoes first-pass metabolism through the cytochrome P450 (CYP) enzymes in the human liver, of which CYP3A4 is the most influential isoenzyme. Multidrug combination therapy and, as such, therapeutic drug monitoring (TDM) during HIV/AIDS treatment are therefore critical, to prevent adverse interactions. The conventional sensitive and specific assays available for quantifying ARV drugs, however, suffer from distinct disadvantages.

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Snyder, Stuart, D. Z. D'Argenio, Owen Weislow, John A. Bilello, and G. L. Drusano. "The Triple Combination Indinavir-Zidovudine-Lamivudine Is Highly Synergistic." Antimicrobial Agents and Chemotherapy 44, no. 4 (2000): 1051–58. http://dx.doi.org/10.1128/aac.44.4.1051-1058.2000.

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ABSTRACT Administration of the combination of indinavir-zidovudine-lamivudine has been demonstrated to cause a large fraction of treated patients to have a decline in human immunodeficiency virus type 1 (HIV-1) copy number to below the detectability of sensitive assays. A recent investigation (G. L. Drusano, J. A. Bilello, D. S. Stein, M. Nessly, A. Meibohm, E. A. Emini, P. Deutsch, J. Condra, J. Chodakewitz, and D. J. Holder, J. Infect. Dis. 178:360–367, 1998) demonstrated that the durability of the antiviral effect was affected by combination chemotherapy. Zidovudine-lamivudine-indinavir dif

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DiCenzo, Robert, Alan Forrest, Margaret A. Fischl, et al. "Pharmacokinetics of Indinavir and Nelfinavir in Treatment-Naive, Human Immunodeficiency Virus-Infected Subjects." Antimicrobial Agents and Chemotherapy 48, no. 3 (2004): 918–23. http://dx.doi.org/10.1128/aac.48.3.918-923.2004.

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ABSTRACT AIDS Clinical Trials Group protocol 388 was designed to compare a three-drug regimen (indinavir with dual nucleosides) to a four-drug regimen (indinavir plus nelfinavir or indinavir plus efavirenz with dual nucleosides). Blood samples from patients taking indinavir and nelfinavir were collected over 8 to 12 h following a specified dose and were analyzed with high-performance liquid chromatography. Pharmacokinetic data were derived by using noncompartmental analysis. Following administration of indinavir every 8 h in the absence of nelfinavir (n = 8), the median predose indinavir conce

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Jann, Michael W., Vicky Spratlin, Kathryn Momary, et al. "Lack of a pharmacokinetic drug-drug interaction with venlafaxine extended-release/indinavir and desvenlafaxine extended-release/indinavir." European Journal of Clinical Pharmacology 68, no. 5 (2011): 715–21. http://dx.doi.org/10.1007/s00228-011-1180-7.

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13

Sohraby, Farzin, and Hassan Aryapour. "Comparative analysis of the unbinding pathways of antiviral drug Indinavir from HIV and HTLV1 proteases by supervised molecular dynamics simulation." PLOS ONE 16, no. 9 (2021): e0257916. http://dx.doi.org/10.1371/journal.pone.0257916.

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Determining the unbinding pathways of potential small molecule compounds from their target proteins is of great significance for designing efficacious treatment solutions. One of these potential compounds is the approved HIV-1 protease inhibitor, Indinavir, which has a weak effect on the HTLV-1 protease. In this work, by employing the SuMD method, we reconstructed the unbinding pathways of Indinavir from HIV and HTLV-1 proteases to compare and understand the mechanism of the unbinding and to discover the reasons for the lack of inhibitory activity of Indinavir against the HTLV-1 protease. We a

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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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15

Kelly, Deborah V., Lizanne C. Béïque, and M. Ian Bowmer. "Extrapyramidal Symptoms with Ritonavir/Indinavir Plus Risperidone." Annals of Pharmacotherapy 36, no. 5 (2002): 827–30. http://dx.doi.org/10.1345/aph.1a335.

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OBJECTIVE: To report a case of suspected extrapyramidal symptoms (EPS) in a patient initiated on ritonavir and indinavir while taking risperidone for a tic disorder. CASE SUMMARY: A 35-year-old white man with AIDS received risperidone 2 mg twice daily for treatment of a Tourette's-like tic disorder. Ritonavir and indinavir were initiated, and 1 week later, he experienced significantly impaired swallowing, speaking, and breathing, and worsening of his existing tremors. Ritonavir and indinavir were discontinued. On the same day, the patient increased the risperidone dosage to 3 mg twice daily. S

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Shulman, Nancy, Andrew Zolopa, Diane Havlir, et al. "Virtual Inhibitory Quotient Predicts Response to Ritonavir Boosting of Indinavir-Based Therapy in Human Immunodeficiency Virus-Infected Patients with Ongoing Viremia." Antimicrobial Agents and Chemotherapy 46, no. 12 (2002): 3907–16. http://dx.doi.org/10.1128/aac.46.12.3907-3916.2002.

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ABSTRACT Depending on the degree of underlying resistance present, optimization of the pharmacokinetics of protease inhibitors may result in improved virologic suppression. Thirty-seven human immunodeficiency virus (HIV)-infected subjects who had chronic detectable viremia and who were receiving 800 mg of indinavir three times a day (TID) were switched to 400 mg of indinavir BID with 400 mg of ritonavir two times a day (BID) for 48 weeks. Full pharmacokinetic evaluations were obtained for 12 subjects before the switch and 3 weeks after the switch. Combination therapy increased the indinavir pr

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Giorgio, Audrey Farèse-Di, Marielle Rouquayrol, Jacques Greiner, Anne-Marie Aubertin, Pierre Vierling, and Roger Guedj. "Synthesis and Anti-HIV Activity of Prodrugs Derived from Saquinavir and Indinavir." Antiviral Chemistry and Chemotherapy 11, no. 2 (2000): 97–110. http://dx.doi.org/10.1177/095632020001100202.

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With a view to improving the pharmacological properties, safety and pharmacokinetic profiles of current protease inhibitors, the synthesis of various acyl-substituted saquinavir and indinavir prodrugs, their in vitro stability with respect to hydrolysis and their anti-HIV (LAI and HTLV IIIB) activity and cytotoxicity in CEM-SS and MT4 cells have been investigated. Hydrolysis of the ester bond and liberation of the active free drug was found to be crucial for HIV inhibition: the faster the hydrolysis, the closer the anti-HIV activity was to that of the respective parent drug. This is the case f

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Yeh, Kuang C., Paul J. Deutsch, Heidi Haddix, et al. "Single-Dose Pharmacokinetics of Indinavir and the Effect of Food." Antimicrobial Agents and Chemotherapy 42, no. 2 (1998): 332–38. http://dx.doi.org/10.1128/aac.42.2.332.

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ABSTRACT Indinavir sulfate is a human immunodeficiency virus type 1 (HIV-1) protease inhibitor indicated for treatment of HIV infection and AIDS in adults. The purpose of this report is to summarize single-dose studies which characterized the pharmacokinetics of the drug and the effect of food in healthy volunteers. Indinavir concentrations in plasma and urine were obtained by high-pressure liquid chromatography and UV detection assay methods. The results indicate that indinavir was rapidly absorbed in the fasting state, with the time to the maximum concentration in plasma occurring at ∼0.8 h

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Shankar, Sudha S., Robert V. Considine, J. Christopher Gorski, and Helmut O. Steinberg. "Insulin sensitivity is preserved despite disrupted endothelial function." American Journal of Physiology-Endocrinology and Metabolism 291, no. 4 (2006): E691—E696. http://dx.doi.org/10.1152/ajpendo.00006.2006.

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It is well established that endothelial dysfunction and insulin resistance go hand in hand. However, it is unclear whether endothelial dysfunction per se is sufficient to impair insulin-mediated glucose uptake. We have previously reported that 4 wk of administration of the human immunodeficiency virus (HIV)-1 protease inhibitor indinavir to HIV-negative subjects induces endothelial dysfunction. Hence, we hypothesized that indinavir-induced endothelial dysfunction was associated with impaired insulin-mediated glucose disposal. We measured insulin-mediated glucose disposal at the level of the wh

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Gatti, Giorgio, Alessandra Vigano', Natascia Sala, et al. "Indinavir Pharmacokinetics and Parmacodynamics in Children with Human Immunodeficiency Virus Infection." Antimicrobial Agents and Chemotherapy 44, no. 3 (2000): 752–55. http://dx.doi.org/10.1128/aac.44.3.752-755.2000.

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ABSTRACT The indinavir dosage regimen currently used for human immunodeficiency virus (HIV)-infected children is not based on pharmacokinetic data obtained in the target patient population. The purpose of our study was to characterize indinavir pharmacokinetics and pharmacodynamics in HIV-infected children. Eleven children (age range, 9.0 to 13.6 years; weight range, 21.7 to 56.0 kg) receiving indinavir (500 mg/m2 every 8 h) in combination with lamivudine and stavudine were studied. The correlation of indinavir pharmacokinetic parameters and demographic parameters was evaluated. Also, the phar

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Kraft, Walter K., Jacqueline B. McCrea, Gregory A. Winchell, et al. "Indinavir and Rifabutin Drug Interactions in Healthy Volunteers." Journal of Clinical Pharmacology 44, no. 3 (2004): 305–13. http://dx.doi.org/10.1177/0091270003262807.

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Damle, Bharat D., Vanaja Mummaneni, Sanjeev Kaul, and Catherine Knupp. "Lack of Effect of Simultaneously Administered Didanosine Encapsulated Enteric Bead Formulation (Videx EC) on Oral Absorption of Indinavir, Ketoconazole, or Ciprofloxacin." Antimicrobial Agents and Chemotherapy 46, no. 2 (2002): 385–91. http://dx.doi.org/10.1128/aac.46.2.385-391.2002.

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ABSTRACT Didanosine formulation that contains a buffer to prevent it from acid-mediated degradation can result in a significant decrease in the oral absorption of certain drugs because of interactions with antacids. An enteric formulation of didanosine is unlikely to cause such drug interactions because it lacks antacids. This study was undertaken to determine whether the enteric bead formulation of didanosine (Videx EC) influences the bioavailability of indinavir, ketoconazole, and ciprofloxacin, three drugs that are representative of a broader class of drugs affected by interaction with anta

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Cott, Jerry M. "Herb-Drug Interactions: Focus on Pharmacokinetics." CNS Spectrums 6, no. 10 (2001): 827–32. http://dx.doi.org/10.1017/s1092852900001644.

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ABSTRACTRecent literature regarding drug-drug, herb-drug, and food-drug interactions must not be ignored; nor can they always be taken at face value. Studies have shown that St. John's wort (SJW)(Hypericum perforatum) can reduce plasma levels of indinavir, cyclosporin, digoxin, and possibly other drugs as well. Current knowledge regarding the metabolism of these medications suggests that the cytochrome P450 (CYP) drug metabolizing enzyme systems cannot account for all these effects. It has been reported that the P-glycoprotein (Pgp) transmembrane pump is also induced by SJW. Medications that a

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Feleni, Usisipho, Rachel Fanelwa Ajayi, Abongile Jijana, et al. "Tin Selenide Quantum Dots Electrochemical Biotransducer for the Determination of Indinavir - A Protease Inhibitor Anti-Retroviral Drug." Journal of Nano Research 44 (November 2016): 196–207. http://dx.doi.org/10.4028/www.scientific.net/jnanor.44.196.

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Biocompatibility of tin selenide quantum dots was achieved by the incorporation of 3-mercaptopropionic acid (3-MPA) as a capping agent, which also improved the stability and the solubility of the material. The UV-Vis spectrophotometric analysis of the quantum dots revealed a broad absorption band at ~ 330 nm (with a corresponding band gap, Eg, value of 3.75 eV), which is within the range of values expected for quantum dots materials. The 3-mercaptopropionic acid-capped tin selenide (3-MPA-SnSe) quantum dots were used to develop an electrochemical biosensor for indinavir, which is a protease in

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Feleni, Usisipho, Rachel Fanelwa Ajayi, Abongile Jijana, et al. "Tin Selenide Quantum Dots Electrochemical Biotransducer for the Determination of Indinavir - A Protease Inhibitor Anti-Retroviral Drug." Journal of Nano Research 45 (January 2017): 12–24. http://dx.doi.org/10.4028/www.scientific.net/jnanor.45.12.

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Biocompatibility of tin selenide quantum dots was achieved by the incorporation of 3-mercaptopropionic acid (3-MPA) as a capping agent, which also improved the stability and the solubility of the material. The UV-Vis spectrophotometric analysis of the quantum dots revealed a broad absorption band at ~ 330 nm (with a corresponding band gap, Eg, value of 3.75 eV), which is within the range of values expected for quantum dots materials. The 3-mercaptopropionic acid-capped tin selenide (3-MPA-SnSe) quantum dots were used to develop an electrochemical biosensor for indinavir, which is a protease in

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Skvortsov, V. S., D. S. Druzhilovskiy, and A. V. Veselovsky. "Potential inhibitors of protease 3CLpro virus COVID-19: drug reposition." Biomedical Chemistry: Research and Methods 3, no. 1 (2020): e00124. http://dx.doi.org/10.18097/bmcrm00124.

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Pneumonia caused by the COVID-19 virus has led to quick search of drugs that would able to block the spread of this virus. A standard way of drug development is a long process. One approach that can significantly accelerate drug development is drug reposition. In this study a virtual screening of the database of approved drugs has been used for search inhibitors against 3СLpro COVID-19, the main protease of COVID-19. Molecular docking, simulation of molecular dynamics and binding energy estimation by MM-GBSA method allowed to select several compounds for further experimental testing. The most

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Ferry, James J., Beth D. Herman, Barbara J. Carel, Glenn F. Carlson, and Donald H. Batts. "Pharmacokinetic Drug-Drug Interaction Study of Delavirdine and Indinavir in Healthy Volunteers." Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology 18, no. 3 (1998): 252–59. http://dx.doi.org/10.1097/00042560-199807010-00009.

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LERNER, LORI B., MARC CENDRON, and STEPHEN N. ROUS. "NEPHROLITHIASIS FROM INDINAVIR, A NEW HUMAN IMMUNODEFICIENCY VIRUS DRUG." Journal of Urology 159, no. 6 (1998): 2074–75. http://dx.doi.org/10.1016/s0022-5347(01)63253-1.

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Vera, Trinity, Joey P. Granger, and David E. Stec. "Inhibition of bilirubin metabolism induces moderate hyperbilirubinemia and attenuates ANG II-dependent hypertension in mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 3 (2009): R738—R743. http://dx.doi.org/10.1152/ajpregu.90889.2008.

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Population studies indicate that moderate hyperbilirubinemia is associated with reduced incidence of cardiovascular diseases, including hypertension. Despite this correlative evidence, no studies have directly tested the hypothesis that moderate increases in plasma bilirubin levels can attenuate the development of hypertension. This hypothesis was tested by treating mice with Indinavir, a drug that competes with bilirubin for metabolism by UDP-glucuronosyltransferase 1A1 (UGT1A1). Treatment of mice with Indinavir (500 mg·kg−1·day−1, gavage) resulted in a twofold increase in plasma unconjugated

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Clay, Patrick G., and Molly M. Adams. "Pseudo-Parkinson Disease Secondary to Ritonavir–Buspirone Interaction." Annals of Pharmacotherapy 37, no. 2 (2003): 202–5. http://dx.doi.org/10.1177/106002800303700207.

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OBJECTIVE: To report a case of Parkinson-like symptoms appearing in a patient after introduction of ritonavir to buspirone therapy. CASE SUMMARY: A 54-year-old HIV-positive white man presented to the clinic with a 2-week history of ataxia, shuffling gait, cogwheel rigidity, resting tremor, and sad affect with masked features. This patient had been receiving high-dose buspirone (40 mg every morning and 30 mg every evening) for 2 years prior to the introduction of ritonavir/indinavir combination therapy (400 mg/400 mg twice daily) 6 weeks prior to initiation of the above symptoms. Buspirone was

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Melnick, Laurence, Shiow-Shong Yang, Rick Rossi, Charlie Zepp, and Donald Heefner. "An Escherichia coli Expression Assay and Screen for Human Immunodeficiency Virus Protease Variants with Decreased Susceptibility to Indinavir." Antimicrobial Agents and Chemotherapy 42, no. 12 (1998): 3256–65. http://dx.doi.org/10.1128/aac.42.12.3256.

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ABSTRACT We have developed a recombinant Escherichia coliscreening system for the rapid detection and identification of amino acid substitutions in the human immunodeficiency virus (HIV) protease associated with decreased susceptibility to the protease inhibitor indinavir (MK-639; Merck & Co.). The assay depends upon the correct processing of a segment of the HIV-1 HXB2 gag-polpolyprotein followed by detection of HIV reverse transcriptase activity by a highly sensitive, colorimetric enzyme-linked immunosorbent assay. The highly sensitive system detects the contributions of single substitut

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Csajka, Chantal, Catia Marzolini, Karin Fattinger, et al. "Population Pharmacokinetics of Indinavir in Patients Infected with Human Immunodeficiency Virus." Antimicrobial Agents and Chemotherapy 48, no. 9 (2004): 3226–32. http://dx.doi.org/10.1128/aac.48.9.3226-3232.2004.

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ABSTRACT Indinavir is currently used at a fixed dose of 800 mg either three times a day or twice a day in combination with 100 mg of ritonavir. Dosage individualization based on plasma concentration monitoring might, however, be indicated. This study aimed to assess the pharmacokinetic profile of indinavir in patients infected with human immunodeficiency virus to characterize interpatient and intrapatient variability and to build up a Bayesian approach for dosage adaptation. A population analysis was performed with the NONMEM computer program with 569 plasma samples from a cohort of 239 unsele

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Kakuda, Thomas N., Linda M. Page, Peter L. Anderson, et al. "Pharmacological Basis for Concentration-Controlled Therapy with Zidovudine, Lamivudine, and Indinavir." Antimicrobial Agents and Chemotherapy 45, no. 1 (2001): 236–42. http://dx.doi.org/10.1128/aac.45.1.236-242.2001.

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ABSTRACT Conventional antiretroviral therapy involves administration of standard fixed doses to adults and adolescents. This approach ignores interindividual variability in pharmacokinetics and results in substantial differences in systemic concentrations among patients. Thus, variability in systemic concentrations contributes to variability in response to therapy. This study was designed to evaluate the feasibility and safety of a regimen of zidovudine, lamivudine, and indinavir designed to achieve select target concentrations versus standard dose therapy. Twenty-four antiretroviral-naı̈ve su

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Burger, David M., Annemarie M. C. van Rossum, Patricia W. H. Hugen, et al. "Pharmacokinetics of the Protease Inhibitor Indinavir in Human Immunodeficiency Virus Type 1-Infected Children." Antimicrobial Agents and Chemotherapy 45, no. 3 (2001): 701–5. http://dx.doi.org/10.1128/aac.45.3.701-705.2001.

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ABSTRACT The objective of this study was to evaluate the pharmacokinetics of indinavir in human immunodeficiency virus-infected children as part of a prospective, open, uncontrolled, multicenter study in The Netherlands. Human immunodeficiency virus type 1-infected children were monitored over 6 months of treatment with zidovudine (120 mg/m2 every 8 h [q8h]), lamivudine (4 mg/kg of body weight q12h), and indinavir (33mg/kg of metabolic weight [MW] q8h). Four weeks after the start of treatment, the steady-state pharmacokinetics of indinavir were determined by high-pressure liquid chromatography

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Sarvagalla, Sailu, Chun Hei Antonio Cheung, Ju-Ya Tsai, Hsing Pang Hsieh, and Mohane Selvaraj Coumar. "Disruption of protein–protein interactions: hot spot detection, structure-based virtual screening and in vitro testing for the anti-cancer drug target – survivin." RSC Advances 6, no. 38 (2016): 31947–59. http://dx.doi.org/10.1039/c5ra22927h.

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Ignaszak, A., N. Hendricks, T. Waryo, et al. "Novel therapeutic biosensor for indinavir—A protease inhibitor antiretroviral drug." Journal of Pharmaceutical and Biomedical Analysis 49, no. 2 (2009): 498–501. http://dx.doi.org/10.1016/j.jpba.2008.10.025.

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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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Moyer, Thomas P., Zelalem Temesgen, Robert Enger, et al. "Drug Monitoring of Antiretroviral Therapy for HIV-1 Infection: Method Validation and Results of a Pilot Study." Clinical Chemistry 45, no. 9 (1999): 1465–76. http://dx.doi.org/10.1093/clinchem/45.9.1465.

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Abstract Background: Antiretroviral therapy for HIV-1 infection has become increasingly complex. The availability of new and potent drugs and progress in understanding the pathogenesis of HIV-1 infection have led to the establishment of new treatment paradigms. The varying dosing regimens, associated toxicities, and the potential for drug-drug and food-drug interactions further complicate treatment. This complexity contributes to patient nonadherence. Because clinicians have no tools to monitor adherence or drug-drug interactions and because response requires that therapy exceed the known inhi

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Leowattana, Wattana. "Antiviral Drugs and Acute Kidney Injury (AKI)." Infectious Disorders - Drug Targets 19, no. 4 (2019): 375–82. http://dx.doi.org/10.2174/1871526519666190617154137.

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The introduction of more efficient antiviral drugs are common cause drug-induced acute kidney injury (AKI). The true prevalence of antiviral drugs induced nephrotoxicity is hardly determined. It causes AKI by many mechanisms including acute tubular necrosis (ATN), allergic interstitial nephritis (AIN), and crystal nephropathy. ATN has been described with a few kinds of antiviral drugs such as cidofovir, adefovir and tenofovir with unique effects on transporter defects, apoptosis, and mitochondrial injury. AIN from atazanavir is a rapid onset of AKI and usually nonoliguric but dialytic therapy

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Sadler, Brian M., Catherine Gillotin, Yu Lou, et al. "Pharmacokinetic Study of Human Immunodeficiency Virus Protease Inhibitors Used in Combination with Amprenavir." Antimicrobial Agents and Chemotherapy 45, no. 12 (2001): 3663–68. http://dx.doi.org/10.1128/aac.45.12.3663-3668.2001.

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ABSTRACT In an open-label, randomized, multicenter, multiple-dose pharmacokinetic study, we determined the steady-state pharmacokinetics of amprenavir with and without coadministration of indinavir, nelfinavir, or saquinavir soft gel formulation in 31 human immunodeficiency virus type 1-infected subjects. The results indicated that amprenavir plasma concentrations were decreased by saquinavir soft gel capsule (by 32% for area under the concentration-time curve at steady state [AUCss] and 37% for peak plasma concentration at steady state [C max,ss]) and increased by indinavir (33% for AUCss). N

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Langmann, P., M. Zilly, B. Weißbrich, S. Desch, T. Väth, and H. Klinker. "Therapeutic Drug Monitoring of Indinavir in HIV-Infected Patients Undergoing HAART." Infection 30, no. 1 (2002): 13–16. http://dx.doi.org/10.1007/s15010-001-1111-0.

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Sidrim, J. J. C., L. V. Perdigão-Neto, R. A. Cordeiro, et al. "Viral protease inhibitors affect the production of virulence factors in Cryptococcus neoformans." Canadian Journal of Microbiology 58, no. 7 (2012): 932–36. http://dx.doi.org/10.1139/w2012-075.

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The effects of the protease inhibitors saquinavir, darunavir, ritonavir, and indinavir on growth inhibition, protease and phospholipase activities, as well as capsule thickness of Cryptococcus neoformans were investigated. Viral protease inhibitors did not reduce fungal growth when tested in concentrations ranging from 0.001 to 1.000 mg/L. A tendency toward increasing phospholipase activity was observed with the highest tested drug concentration in a strain-specific pattern. However, these drugs reduced protease activity as well as capsule production. Our results confirm a previous finding tha

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Prabu-Jeyabalan, Moses, Ellen A. Nalivaika, Nancy M. King, and Celia A. Schiffer. "Viability of a Drug-Resistant Human Immunodeficiency Virus Type 1 Protease Variant: Structural Insights for Better Antiviral Therapy." Journal of Virology 77, no. 2 (2003): 1306–15. http://dx.doi.org/10.1128/jvi.77.2.1306-1315.2003.

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ABSTRACT Under the selective pressure of protease inhibitor therapy, patients infected with human immunodeficiency virus (HIV) often develop drug-resistant HIV strains. One of the first drug-resistant mutations to arise in the protease, particularly in patients receiving indinavir or ritonavir treatment, is V82A, which compromises the binding of these and other inhibitors but allows the virus to remain viable. To probe this drug resistance, we solved the crystal structures of three natural substrates and two commercial drugs in complex with an inactive drug-resistant mutant (D25N/V82A) HIV-1 p

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Schippers, Emile F., Patricia W. H. Hugen, Jan den Hartigh, et al. "No drug–drug interaction between nelfinavir or indinavir and mefloquine in HIV-1-infected patients." AIDS 14, no. 17 (2000): 2794–95. http://dx.doi.org/10.1097/00002030-200012010-00023.

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Remmel, Rory P., Sagar P. Kawle, Dennis Weller, and Courtney V. Fletcher. "Simultaneous HPLC Assay for Quantification of Indinavir, Nelfinavir, Ritonavir, and Saquinavir in Human Plasma." Clinical Chemistry 46, no. 1 (2000): 73–81. http://dx.doi.org/10.1093/clinchem/46.1.73.

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Abstract Background: HIV protease inhibitors are recommended as part of combination antiretroviral therapy. Dual protease inhibitor therapy is also being used clinically. Consequently, a simultaneous assay for indinavir, nelfinavir, ritonavir, and saquinavir was developed. Methods: Indinavir, nelfinavir, ritonavir, and saquinavir were extracted from plasma (250 μL) with methyl-t-butyl ether at basic pH after addition of an internal standard (A-86093). The compounds were separated on a Keystone BetaBasic C4 column (250 × 3 mm i.d.) at 40 °C with a mobile phase of acetonitrile-50 mmol/L ammonium

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Article, Editorial. "Monitoring of Foreign Drug Safety Information." Safety and Risk of Pharmacotherapy 7, no. 4 (2019): 221–26. http://dx.doi.org/10.30895/2312-7821-2019-7-4-221-226.

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Analysis of administrative decisions of foreign regulatory authorities on the recoil of medicines and/or the need for changes in the instructions for their medical use due to changes in the safety profile, conducted by experts of the Scientific Centre for Expert Evaluation of Medicinal Products revealed 23 administrative decisions. These decisions contained information on the following medicines registered in Russia: аmitriptyline, duloxetine, quetiapine, lamotrigine, topiramate, phenytoin, articaine, epinephrine, bupivacaine, oxybutynin, dexlansoprazole, pantoprazole, esomeprazole, famotidine

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Verscheijden, Laurens F. M., Jan B. Koenderink, Saskia N. de Wildt, and Frans G. M. Russel. "Differences in P-glycoprotein activity in human and rodent blood–brain barrier assessed by mechanistic modelling." Archives of Toxicology 95, no. 9 (2021): 3015–29. http://dx.doi.org/10.1007/s00204-021-03115-y.

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AbstractVariation in the efficacy and safety of central nervous system drugs between humans and rodents can be explained by physiological differences between species. An important factor could be P-glycoprotein (Pgp) activity in the blood–brain barrier (BBB), as BBB expression of this drug efflux transporter is reportedly lower in humans compared to mouse and rat and subject to an age-dependent increase. This might complicate animal to human extrapolation of brain drug disposition and toxicity, especially in children. In this study, the potential species-specific effect of BBB Pgp activity on

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Patick, A. K., T. J. Boritzki, and L. A. Bloom. "Activities of the human immunodeficiency virus type 1 (HIV-1) protease inhibitor nelfinavir mesylate in combination with reverse transcriptase and protease inhibitors against acute HIV-1 infection in vitro." Antimicrobial Agents and Chemotherapy 41, no. 10 (1997): 2159–64. http://dx.doi.org/10.1128/aac.41.10.2159.

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Nelfinavir mesylate (formerly AG1343) is a potent and selective, nonpeptidic inhibitor of human immunodeficiency virus type 1 (HIV-1) protease that was discovered by protein structure-based design methodologies. We evaluated the antiviral and cytotoxic effects of two-drug combinations of nelfinavir with the clinically approved antiretroviral therapeutics zidovudine (ZDV), lamivudine (3TC), dideoxycytidine (ddC; zalcitabine), stavudine (d4T), didanosine (ddI), indinavir, saquinavir, and ritonavir and a three-drug combination of nelfinavir with ZDV and 3TC against an acute HIV-1 strain RF infect

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van Praag, Rieneke M. E., Sjoerd Repping, Jan W. A. de Vries, Joep M. A. Lange, Richard M. W. Hoetelmans, and Jan M. Prins. "Pharmacokinetic Profiles of Nevirapine and Indinavir in Various Fractions of Seminal Plasma." Antimicrobial Agents and Chemotherapy 45, no. 10 (2001): 2902–7. http://dx.doi.org/10.1128/aac.45.10.2902-2907.2001.

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ABSTRACT Limited data are available on antiretroviral drug concentrations in seminal plasma during a dosing interval. Further, since human ejaculate is composed of fluids originating from the testes, the seminal vesicles, and the prostate, all having different physiological characteristics, drug concentrations in total seminal plasma do not necessarily reflect concentrations in the separate compartments. Five human immunodeficiency virus type 1-infected patients on nevirapine (NVP; 200 mg twice a day [b.i.d.]) and/or indinavir (IDV; 800 mg b.i.d. with ritonavir, 100 mg b.i.d.) regimens used a

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Donnerer, J., M. Kronawetter, A. Kapper, I. Haas, and H. H. Kessler. "Therapeutic Drug Monitoring of the HIV/AIDS Drugs Abacavir, Zidovudine, Efavirenz, Nevirapine, Indinavir, Lopinavir, and Nelfinavir." Pharmacology 69, no. 4 (2003): 197–204. http://dx.doi.org/10.1159/000073664.

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