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Indinavir

Brand Name: Crixivan Other Names: IDV, indinavir sulfate Drug Class: Protease Inhibitors

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indinavir sulfate

indinavir sulfate

Molecular Weight: 711.876

Drug Description


Indinavir sulfate, the salt form of the active drug indinavir, is a synthetic antiretroviral agent and a peptidomimetic protease inhibitor (PI). [1]


References

[1] AHFS Drug Information 2008; p. 648

HIV/AIDS-Related Uses


Indinavir sulfate was approved by the FDA on March 13, 1996, for use in combination with other antiretroviral agents or as monotherapy for the treatment of HIV infection. [1] Evidence suggests that use of a three-drug regimen that includes indinavir and two nucleoside reverse transcriptase inhibitors (NRTIs) can increase CD4 cell counts and decrease plasma HIV-1 RNA levels in pediatric patients who previously received long-term therapy with NRTIs, especially if the three-drug regimen includes NRTIs not used in previous regimens. [2]

Indinavir sulfate is also used in conjunction with other antiretroviral agents for postexposure prophylaxis of HIV infection in healthcare workers and others who have had occupational exposure to HIV. [3]


References

[1] Wolters Kluwer Health, Inc. Indinavir Sulfate, Facts and Comparisons 4.0. Available at: http://online.factsandcomparisons.com. Accessed 10/25/08.

[2] AHFS Drug Information 2008; p. 648

[3] AHFS Drug Information 2008; p. 649

Dosing Information


Mode of Delivery

Oral. [1]

Dosage Form

Capsules containing indinavir 100, 200, and 400 mg. [2] [3]

The recommended dosage of indinavir is 800 mg (two 400-mg capsules) every 8 hours. In patients with mild to moderate hepatic insufficiency because of cirrhosis, the dose of indinavir should be reduced to 600 mg every 8 hours. The prescribing information provided by the manufacturer details specific dosing adjustments when indinavir is coadministered with delavirdine, didanosine, efavirenz, itraconazole, ketoconazole, and rifabutin. [4]

Storage

Store at room temperature, 15 C to 30 C (59 F to 86 F), in a tightly closed container. Indinavir sulfate capsules are sensitive to moisture and should be dispensed and stored in the original container with a desiccant. Store unit-dose packages at 15 C to 30 C (59 F to 86 F). Protect from moisture. [5]


References

[1] FDA Crixivan Capsules Prescribing Information, April 2008, p. 27. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[2] FDA Crixivan Capsules Prescribing Information, April 2008, p. 27. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[3] AHFS Drug Information 2008; p. 656

[4] FDA Crixivan Capsules Prescribing Information, April 2008, pp. 27-8. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[5] FDA Crixivan Capsules Prescribing Information, April 2008, p. 28. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

Pharmacology


Indinavir is a selective, competitive, reversible inhibitor of HIV protease, an enzyme that plays an essential role in HIV replication in the formation of infectious virus. Indinavir is a structural analogue of the HIV Phe-Pro protease cleavage site. The drug's structure inhibits the function of HIV protease, blocking virus maturation and causing the formation of immature, noninfectious virions. Indinavir is active in both acutely and chronically infected cells; chronically infected cells are not affected by nucleoside reverse transcriptase inhibitors (NRTIs). Although indinavir does not affect early stages of the HIV replication cycle, it does interfere with the production of infectious HIV, limiting further infectious spread of the virus. [1] Indinavir is active against HIV-1 and -2. [2]

Indinavir is rapidly absorbed from the gastrointestinal (GI) tract, with a peak plasma concentration (Cmax) of the drug generally occurring in less than 1 hour and averaging 0.8 hours in fasting adults. Presence of food in the GI tract can substantially decrease the extent of absorption of oral indinavir. [3]

Distribution of indinavir into body tissues and fluids has not been fully characterized. Indinavir has been detected in low concentrations in the cerebrospinal fluid of adults and children receiving the drug. [4]

Indinavir sulfate is in FDA Pregnancy Category C. Adequate and well-controlled studies have not been done in pregnant women. The optimal dosing regimen for pregnant patients has not been established. A dose of indinavir, 800 mg three times daily, with zidovudine and lamivudine has been studied in 16 HIV infected pregnant patients enrolled at 14 to 28 weeks gestation. The mean area under the concentration-time curve (AUC) at 30 to 32 weeks gestation was 74% lower than at 6 weeks postpartum. The mean trough plasma concentration (Cmin) in 55% of these patients was below assay threshold for quantification. Based on the substantially lower drug exposures and the limited data in HIV infected pregnant patients, indinavir use is not recommended. [5]

It is not known whether indinavir crosses the placenta in humans; it does cross the placenta in laboratory animals. [6] Hyperbilirubinemia has occurred in patients receiving indinavir sulfate, but it is unknown whether drug administered during pregnancy will exacerbate hyperbilirubinemia in neonates. [7]

Indinavir sulfate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. An Antiretroviral Pregnancy Registry has been established to monitor the outcomes of pregnant women exposed to indinavir. Physicians may register patients by calling 1-800-258-4263 or online at http://www.APRegistry.com. Although it is not known whether indinavir is excreted in human milk, there exists the potential for adverse effects from indinavir in nursing infants. Mothers should be instructed to discontinue nursing if they are receiving indinavir. [8]

Protein binding of indinavir is moderate and approximately 60% over a range of 0.05 to 10 mcg/ml. [9]

The metabolic fate of indinavir has not been fully determined, but the drug is metabolized in the liver. Systemic clearance of indinavir is rapid; the plasma half-life of indinavir averages 1.8 hours in adults and 1.1 hours in children. Indinavir is metabolized to at least seven metabolites, including one glucuronide conjugate and six oxidative metabolites. In vitro studies indicate that cytochrome P450 (CYP) 3A4 is the major enzyme involved in the formation of the oxidative metabolites. Indinavir is excreted primarily in the feces both as unabsorbed drug and as metabolites. Following a 400-mg oral dose, 83% was recovered in feces (19.1% as unchanged drug) and 19% was recovered in urine (9.4% as unchanged drug). It is not known if indinavir is removed by hemodialysis or peritoneal dialysis. [10]

Although the complete mechanisms of resistance or reduced susceptibility to indinavir have not been fully determined to date, acquisition of multiple HIV protease mutations appears to be necessary for high-level resistance to the drug. In vitro studies indicate that the antiretroviral effects of indinavir and some NRTIs are additive or synergistic against HIV-1, and there is evidence from clinical studies that antiretroviral regimens that include indinavir and one or two nucleoside agents can suppress in vivo viral replication to a greater extent than monotherapy. There is also evidence that use of regimens that suppress HIV replication to levels that cannot be detected by sensitive plasma HIV-1 RNA assays is associated with a lower viral mutation rate and may delay or prevent the emergence of resistance. Several studies indicate that the incidence of HIV protease mutations and HIV reverse transcriptase mutations associated with indinavir or zidovudine resistance, respectively, is lower in isolates obtained from patients receiving indinavir/zidovudine combination therapy than in isolates obtained from patients receiving monotherapy with these drugs. [11]

Some degree of cross resistance can occur among the various PIs. Further study is needed to more fully evaluate the extent and clinical implications of cross resistance among the drugs and to determine whether administration of one PI has an effect on subsequent therapy with any other PI. [12] [13] Cross resistance between indinavir and reverse transcriptase inhibitors is thought to be unlikely because they affect different enzyme target sites; however, cross resistance was observed between indinavir and ritonavir, another PI. Varying degrees of resistance have been noted between indinavir and other PIs. [14]


References

[1] AHFS Drug Information 2008; pp. 654-5

[2] AHFS Drug Information 2008; p. 654

[3] AHFS Drug Information 2008; p. 656

[4] AHFS Drug Information 2008; p. 656

[5] FDA Crixivan Capsules Prescribing Information, April 2008, pp. 6, 22-3. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[6] AHFS Drug Information 2008; p. 652

[7] FDA Crixivan Capsules Prescribing Information, April 2008, p. 23. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[8] FDA Crixivan Capsules Prescribing Information, April 2008, p. 23. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[9] AHFS Drug Information 2008; p. 656

[10] AHFS Drug Information 2008; p. 656

[11] AHFS Drug Information 2008; p. 655

[12] AHFS Drug Information 2008; p. 655

[13] AHFS Drug Information 2008; p. 655

[14] AHFS Drug Information 2008; p. 655

Adverse Events/Toxicity


Adverse effects commonly observed with indinavir use include nephrolithiasis/urolithiasis, jaundice, diabetes or hyperglycemia, ketoacidosis, asthenia, GI disturbances (abdominal or stomach pain, nausea, diarrhea, vomiting), headache, insomnia, taste perversion, acid regurgitation, anorexia, appetite increase, cough, dizziness, fever, rash, and somnolence. [1]

The most frequently clinically reported serious adverse effect of indinavir sulfate is nephrolithiasis/urolithiasis. This effect appears to be dose related, occurring more frequently in patients receiving more than 2.4 grams daily, and is significantly more frequent in pediatric patients. If symptoms of nephrolithiasis/urolithiasis (flank pain with or without hematuria) occur, temporary interruption or discontinuation of indinavir sulfate therapy may be considered. [2] To ensure adequate hydration, which reduces the risk of developing nephrolithiasis, the manufacturer recommends that adults receiving indinavir sulfate drink at least 1.5 liters of water per day. [3]

Some patients receiving indinavir sulfate have developed acute hemolytic anemia, with some cases resulting in death. Hepatitis, including cases resulting in hepatic failure and death, has been reported in patients treated with indinavir, though a causal relationship between indinavir use and these events has not been established. Administration of PIs such as indinavir may cause new onset of diabetes mellitus or exacerbation of pre-existing diabetes mellitus and hyperglycemia, but a causal relationship has not been established between PI therapy and these events. [4]


References

[1] Wolters Kluwer Health, Inc. Indinavir Sulfate, Facts and Comparisons 4.0. Available at: http://online.factsandcomparisons.com. Accessed 10/25/08.

[2] FDA Crixivan Capsules Prescribing Information, April 2008, pp. 23-4. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[3] FDA Crixivan Capsules Prescribing Information, April 2008, p. 27. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[4] FDA Crixivan Capsules Prescribing Information, April 2008, pp. 16-7. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

Drug and Food Interactions


Presence of food in the GI tract substantially decreases absorption of indinavir. In clinical studies, administration with a meal high in calories, fat, and protein resulted in a 77% AUC reduction and an 84% reduction in Cmax. Administration with lighter meals resulted in little or no change in the indinavir AUC, Cmax, and Cmin. [1] For optimum absorption, indinavir should be administered with water 1 hour before or 2 hours after a meal. [2]

Both indinavir and atazanavir are associated with indirect hyperbilirubinemia. Combinations of these drugs have not been adequately studied, and coadministration of indinavir and atazanavir is not recommended. [3] Delavirdine inhibits the metabolism of indinavir such that coadministration of indinavir 400 mg or 600 mg three times daily with delavirdine 400 mg three times daily alters indinavir AUC, Cmax, and Cmin. Conversely, indinavir had no effect on delavirdine pharmacokinetics. [4] In a small, volunteer-based study, twice-daily coadministration of indinavir 800 mg with ritonavir with food for 2 weeks resulted in a 2.7-fold increase in daily indinavir AUC, a 1.6-fold increase in indinavir Cmax, and an 11-fold increase in indinavir Cmin for a ritonavir 100 mg dose. With a ritonavir 200 mg dose, there was a 3.6-fold increase of daily indinavir AUC, a 1.8-fold increase in indinavir Cmax, and a 24-fold increase in indinavir Cmin. In the same study, twice-daily coadminstration of indinavir with ritonavir (100 or 200 mg) resulted in daily ritonavir AUC increases not observed in people who received the same doses of ritonavir alone. [5]

If both didanosine and indinavir are part of a treatment regimen, they should be administered at least 1 hour apart on an empty stomach. A normal acidic pH may be necessary for the optimal absorption of indinavir, and didanosine requires a buffer to increase the pH so that acid does not rapidly degrade didanosine in the stomach. [6]

Competition of CYP3A4 substrates by indinavir could inhibit the metabolism of amiodarone, cisapride, ergot derivatives, midazolam, pimozide, and triazolam, resulting in elevated plasma concentrations of these medications. Thus, concurrent administration with indinavir raises the potential for serious and/or life threatening side effects. Concurrent use of ketoconazole and indinavir results in a 68% increase in the AUC of indinavir; a dosage reduction of indinavir to 600 mg every 8 hours is recommended when these medications are coadministered. [7]

Concurrent use of rifabutin and indinavir results in a 32% increase in the AUC of indinavir and a 204% increase in the AUC of rifabutin. Dosage reduction of rifabutin to150 mg once daily or 300 mg three times weekly is necessary when it is coadministered with indinavir. Because rifampin is a potent inducer of CYP3A4, which could significantly decrease the plasma concentration of indinavir, concurrent use with indinavir is not recommended. [8]

Concomitant use of indinavir with lovastatin or simvastatin is contraindicated due to increased risk of myopathy including rhabdomyolysis. Caution should be exercised if indinavir is used concurrently with atorvastatin or rosuvastatin. Titrate the atorvastatin and rosuvastatin doses carefully and use the lowest necessary dose with indinavir. [9]

Concomitant use of indinavir and St. John's wort (Hypericum perforatum) or products containing St. John's wort may substantially decrease indinavir concentrations and may lead to loss of virologic response and possible resistance to indinavir or other PIs. [10]

Coadministration of indinavir and sildenafil, tadalafil, or vardenafil is expected to substantially increase sildenafil, tadalafil, or vardenafil plasma concentrations and the risk of phosphodiesterase type 5 (PDE) inhibitor-associated adverse effects, including hypotension, visual changes, and priapism. Patients receiving a PDE5 inhibitor should report any symptoms to their doctors. [11] Indinavir (800 mg every 8 hours) coadministered with a single 10-mg dose of vardenafil results in a 16-fold increase in vardenafil AUC, a sevenfold increase in vardenafil Cmax, and a twofold increase in vardenafil half-life. [12] People taking PIs should also not be prescribed sildenafil to treat pulmonary arterial hypertension if they have liver or kidney impairment. [13]

Alfuzosin and salmeterol should not be coadministered with any PIs, including indinavir. [14]

Patients already taking indinavir should received 62.5 mg of bosentan taken daily or every other day, based on individual tolerability. For patients beginning treatment with a PI who are already taking bosentan, bosentan should be discontinued at least 36 hours prior to initiation of PI treatment. Bosentan should be resumed at least 10 days after PI initiation at a dosage of 62.5 mg taken daily or every other day, based on individual tolerability. [15]

Patients already taking indinavir should initially received 20 mg of tadalafil daily and then increase to 40 mg daily, based on individual tolerability. For patients beginning treatment with a PI who are already taking tadalafil, tadalafil should be discontinued at least 24 hours prior to initiation of PI treatment. Tadalafil should be resumed at least 1 week later at a dosage of 20 mg daily. This should be increased to 40 mg daily, based on individual tolerability. [16]

Patients receiving colchicine for the treatment of gout flares should take 0.6 mg (1 tablet) x 1 dose, followed by 0.3 mg (half tablet) 1 hour later. The dose should be repeated no earlier than 3 days later. Patients taking a PI without ritonavir should take 1.2 mg (2 tablets) x 1 dose. The dose should be repeated no earlier than 3 days later. [17]

For the prevention of gout-flares, if the original colchicine regimen was 0.6 mg twice a day, the regimen should be adjusted to 0.3 mg once a day. If the original colchicine regimen was 0.6 mg once a day, the regimen should be adjusted to 0.3 mg once every other day. In patients taking a PI without ritonavir, if the original regimen was 0.6 mg twice a day, the regimen should be adjusted to 0.3 mg twice a day or 0.6 mg once a day. If the original regimen was 0.6 mg once a day, the regimen should be adjusted to 0.3 mg once a day. [18]

For the treatment of familial Mediterranean fever (FMF), the maximum daily dose of colchicine should be 0.6 mg (may be given as 0.3 mg twice a day). In patients taking a PI without ritonavir, the maximum daily dose should be 1.2 mg (may be given as 0.6 mg twice a day). [19]

People taking PIs should not also be prescribed colchicine if they have liver or kidney impairment. [20]

In vitro drug metabolism studies suggest that there is a potential for drug interactions when trazodone is given with CYP3A4 inhibitors. It is likely that indinavir, a CYP3A4 inhibitor, may lead to substantial increases in trazodone plasma concentrations with the potential for adverse effects. If trazodone is used with a potent CYP3A4 inhibitor, a lower dose of trazodone should be considered. [21]

Coadministration of indinavir and efavirenz reduces indinavir levels. Clinical data suggest that when indinavir is used in combination with efavirenz, increasing the dosage of indinavir to 1,000 mg once every 8 hours is not sufficient to compensate for this drug interaction. In a 10-day study investigating indinavir 1,000 mg administered every 8 hours with efavirenz, the indinavir AUC decreased 33% to 46% and the Cmin decreased 39% to 57%. The addition of ritonavir 100 to 200 mg twice daily may help to boost concentrations of indinavir when coadministered with efavirenz, but data on the optimal dosage are not available. [22]


References

[1] FDA Crixivan Capsules Prescribing Information, April 2008, p. 5. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[2] FDA Crixivan Capsules Prescribing Information, April 2008, p. 18. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[3] FDA Crixivan Capsules Prescribing Information, April 2008, p. 17. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[4] FDA Crixivan Capsules Prescribing Information, April 2008, p. 10. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[5] FDA Crixivan Capsules Prescribing Information, April 2008, p. 11. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[6] Pharm GKB The Pharmacogenetics and Pharmacogenomics Knowledge Base - indinavir. Available at: http://www.pharmgkb.org/do/serve?objId=PA449977&objCls=Drug. Accessed 10/25/08.

[7] AHFS Drug Information 2008; p. 652

[8] AHFS Drug Information 2008; p. 652

[9] FDA Crixivan Prescribing Information, February 2012. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2012/020685s075lbl.pdf. Accessed 03/04/12.

[10] FDA Crixivan Capsules Prescribing Information, April 2008, p. 17. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[11] FDA Crixivan Capsules Prescribing Information, April 2008, p. 17. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[12] FDA Crixivan Capsules Prescribing Information, April 2008, p. 11. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2008/020685s068lbl.pdf. Accessed 10/25/08.

[13] FDA. “New label information affecting all approved protease inhibitors for treatment of HIV” April 27, 2010. Available at: http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/HIVandAIDSActivities/ucm209920.htm. Accessed: 04/30/2010.

[14] FDA. “New label information affecting all approved protease inhibitors for treatment of HIV” April 27, 2010. Available at: http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/HIVandAIDSActivities/ucm209920.htm. Accessed: 04/30/2010.

[15] FDA. “New label information affecting all approved protease inhibitors for treatment of HIV” April 27, 2010. Available at: http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/HIVandAIDSActivities/ucm209920.htm. Accessed: 04/30/2010.

[16] FDA. “New label information affecting all approved protease inhibitors for treatment of HIV” April 27, 2010. Available at: http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/HIVandAIDSActivities/ucm209920.htm. Accessed: 04/30/2010.

[17] FDA. “New label information affecting all approved protease inhibitors for treatment of HIV” April 27, 2010. Available at: http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/HIVandAIDSActivities/ucm209920.htm. Accessed: 04/30/2010.

[18] FDA. “New label information affecting all approved protease inhibitors for treatment of HIV” April 27, 2010. Available at: http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/HIVandAIDSActivities/ucm209920.htm. Accessed: 04/30/2010.

[19] FDA. “New label information affecting all approved protease inhibitors for treatment of HIV” April 27, 2010. Available at: http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/HIVandAIDSActivities/ucm209920.htm. Accessed: 04/30/2010.

[20] FDA. “New label information affecting all approved protease inhibitors for treatment of HIV” April 27, 2010. Available at: http://www.fda.gov/ForConsumers/ByAudience/ForPatientAdvocates/HIVandAIDSActivities/ucm209920.htm. Accessed: 04/30/2010.

[21] FDA Desyrel Prescribing Information, September 2003, p. 1. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2005/18207s030lbl.pdf. Accessed 10/25/08.

[22] FDA Sustiva Prescribing Information, March 2008, p. 23. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2009/021360s018,020972s031lbl.pdf. Accessed 10/25/08.

Contraindications


CRIXIVAN is contraindicated in patients with clinically significant hypersensitivity to any of its components.

Inhibition of CYP3A4 by CRIXIVAN can result in elevated plasma concentrations of the following drugs, potentially causing serious or life-threatening reactions:

Drug Interactions With Crixivan: Contraindicated Drugs
- Alpha 1-adrenoreceptor antagonist: alfuzosin.
- Antiarrhythmics: amiodarone.
- Ergot derivatives: dihydroergotamine, ergonovine, ergotamine, methylergonovine.
- GI motility agents: cisapride.
- HMG-CoA Reductase Inhibitors: lovastatin, simvastatin.
- Neuroleptics: pimozide.
- PDE5 Inhibitors: Revatio1 (sildenafil) [for treatment of pulmonary arterial hypertension].
- Sedative/hypnotics: oral midazolam, triazolam, alprazolam.
[1]


References

[1] FDA Crixivan Prescribing Information, February 2012. Available at: http://www.accessdata.fda.gov/drugsatfda_docs/label/2012/020685s075lbl.pdf. Accessed 03/04/12.

Clinical Trials


Click here to search ClinicalTrials.gov for trials that use Indinavir.


Chemistry



Further Reading



Crixivan Capsules Prescribing Information from the FDA Web site [PDF]. A more current version may be available on the manufacturer's Web site.
Boyd MA, Srasuebkul P, Khongphattanayothin M, Ruxrungtham K, Hassink EA, Duncombe CJ, Ubolyam S, Burger DM, Reiss P, Stek M Jr, Lange J, Cooper DA, Phanuphak P. Boosted versus unboosted indinavir with zidovudine and lamivudine in nucleoside pre-treated patients: a randomized, open-label trial with 112 weeks of follow-up (HIV-NAT 005). Antivir Ther. 2006;11(2):223-32.
Boyd M. Indinavir: the forgotten HIV-protease inhibitor. Does it still have a role? Expert Opin Pharmacother. 2007 May;8(7):957-64.
Cressey TR, Plipat N, Fregonese F, Chokephaibulkit K. Indinavir/ritonavir remains an important component of HAART for the treatment of HIV/AIDS, particularly in resource-limited settings. Expert Opin Drug Metab Toxicol. 2007 Jun;3(3):347-361.
Launay O, Duval X, Dalban C, Descamps D, Peytavin G, Certain A, Mouajjah S, Ralaimazava P, Verdon R, Costagliola D, Clavel F; ANRS 109 VISTA Study Group. Lamivudine and indinavir/ritonavir maintenance therapy in highly pretreated HIV-infected patients (Vista ANRS 109). Antivir Ther. 2006;11(7):889-99.


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