Chemical: Drug
atazanavir

last updated 09/15/2016

1. CPIC Guideline for atazanavir and UGT1A1

Summary

The CPIC dosing guideline recommends considering advising individuals who carry two decreased function UGT1A1 alleles about a substantial likelihood of developing jaundice, which may cause non-adherence. The dosing guideline recommends that alternative agents be considered if the risk of non-adherence due to jaundice is high. The risk of discontinuation is low and very low for individuals carrying one, or no decreased function UGT1A1 alleles, respectively.

Annotation

April 2016

Advance online publication September 2015

  • Guidelines regarding the use of pharmacogenomic tests in determining whether atazanavir treatment should be undertaken have been published in Clinical Pharmacology and Therapeutics by the Clinical Pharmacogenetics Implementation Consortium (CPIC).

  • These guidelines are applicable to:

    • Adults
    • At the time of this writing there are no pediatric data regarding associations between UGT1A1 genotypes and likelihood of bilirubin-related discontinuation of atazanavir. However, UGT1A1 genotypes are expected to affect atazanavir-related hyperbilirubinemia similarly in adults and children. Therefore, recommendations for adults may be directly adapted to pediatric patients.
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Table 1: Recommended therapeutic use of atazanavir based on UGT1A1 genotype

Adapted from Tables 1 and 2 of the 2015 guideline manuscript.

Likely phenotypeGenotypesExamples of diplotypesImplications for phenotypic measuresRecommendations for atazanavir therapyClassification of recommendation for atazanavir therapy
Extensive MetabolizerAn individual carrying 2 reference b function and/or increased function alleles; or individuals of genotype CC at rs887829*1/*1; *1/*36; *36/*36; rs887829 CCReference c UGT1A1 activity; very low likelihood of bilirubin-related discontinuation of atazanavir.There is no need to avoid prescribing of atazanavir based on UGT1A1 genetic test result.Strong
Intermediate MetabolizerAn individual carrying one reference b function (*1) c or increased function allele (*36) plus one decreased function allele (*6, *28, *37). Alternatively identified by heterozygosity for rs887829 C/T.*1/*28; *1/*37; *36/*28; *36/*37; rs887829 C/T, *1/*6Somewhat decreased UGT1A1 activity; low likelihood of bilirubin-related discontinuation of atazanavir.There is no need to avoid prescribing of atazanavir based on UGT1A1 genetic test result. Inform the patient that some patients stop atazanavir because of jaundice (yellow eyes and skin), but that this patient’s genotype makes this unlikelyStrong
Poor MetabolizerAn individual carrying two decreased function alleles (*6, *28, *37). Alternatively identified by homozygosity for rs887829 T/T (*80/*80)*28/*28; *28/*37; *37/*37; rs887829 T/T (*80/*80), *6/*6 aMarkedly decreased UGT1A1 activity; high likelihood of bilirubin-related discontinuation of atazanavir.Consider an alternative agent particularly where jaundice would be of concern to the patient.Strong

a Homozygosity for UGT1A1*6, which occurs almost exclusively in individuals of Asian descent, is associated with Gilbert syndrome. However, at this time, it is unclear if patients with this diplotype are at increased risk of severe atazanavir-associated hyperbilirubinemia.

b “reference” function refers to the UGT1A1 alleles to which other alleles are compared.

c The reference function *1 allele is a fully functional refers to the rs8175347 TA6 allele.



Annotated Labels

  1. EMA Label for atazanavir and CYP2C19
  2. HCSC Label for atazanavir and CYP2C19

last updated 09/16/2014

1. EMA Label for atazanavir and CYP2C19

Genetic testing recommended

Genes and/or phenotypes found in this label

  • HIV
    • efficacy, Indications & usage section, Dosage & administration section, Drug interactions section, Adverse reactions section, Pregnancy section, Pharmacodynamics section, Pharmacokinetics section, Warnings and precautions section
    • source: European Medicines Agency
  • CYP2C19
    • toxicity, metabolism/PK, Warnings and precautions section
    • source: European Medicines Agency
  • CYP3A4
    • metabolism/PK, Contraindications section, Drug interactions section, Warnings and precautions section
    • source: European Medicines Agency


Clinical Variants that meet the highest level of criteria, manually curated by PharmGKB, are shown below.

To see more Clinical Variants with lower levels of criteria, click the button at the bottom of the page.

Disclaimer: The PharmGKB's clinical annotations reflect expert consensus based on clinical evidence and peer-reviewed literature available at the time they are written and are intended only to assist clinicians in decision-making and to identify questions for further research. New evidence may have emerged since the time an annotation was submitted to the PharmGKB. The annotations are limited in scope and are not applicable to interventions or diseases that are not specifically identified.

The annotations do not account for individual variations among patients, and cannot be considered inclusive of all proper methods of care or exclusive of other treatments. It remains the responsibility of the health-care provider to determine the best course of treatment for a patient. Adherence to any guideline is voluntary, with the ultimate determination regarding its application to be made solely by the clinician and the patient. PharmGKB assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the PharmGKB clinical annotations, or for any errors or omissions.

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The table below contains information about pharmacogenomic variants on PharmGKB. Please follow the link in the "Variant" column for more information about a particular variant. Each link in the "Variant" column leads to the corresponding PharmGKB Variant Page. The Variant Page contains summary data, including PharmGKB manually curated information about variant-drug pairs based on individual PubMed publications. The PMIDs for these PubMed publications can be found on the Variant Page.

The tags in the first column of the table indicate what type of information can be found on the corresponding Variant Page.

Links in the "Gene" column lead to PharmGKB Gene Pages.

List of all variant annotations for atazanavir

Gene ? Variant?
(147)
Alternate Names ? Chemicals ? Alleles ?
(+ chr strand)
Function ? Amino Acid?
Translation
No VIP available CA VA ABCB1 *1 N/A N/A N/A
No VIP available CA VA ABCB1 *2 (PMID: 11503014) N/A N/A N/A
No VIP available CA VA CYP3A5 *1A N/A N/A N/A
No VIP available CA VA CYP3A5 *3A N/A N/A N/A
No VIP available CA VA CYP3A5 *6 N/A N/A N/A
No VIP available CA VA CYP3A5 *7 N/A N/A N/A
No VIP available No VIP available VA UGT1A1 *1 N/A N/A N/A
No VIP available No VIP available VA UGT1A1 *6 N/A N/A N/A
No VIP available No VIP available VA UGT1A1 *28 N/A N/A N/A
No VIP available No Clinical Annotations available VA
CYP3A5 deficiency N/A N/A N/A
No VIP available CA VA
rs1042640 NC_000002.11:g.234681544G>C, NC_000002.12:g.233772898G>C, NG_002601.2:g.188155G>C, NG_033238.1:g.17626G>C, NM_000463.2:c.*339G>C, NM_001072.3:c.*339G>C, NM_007120.2:c.*339G>C, NM_019075.2:c.*339G>C, NM_019076.4:c.*339G>C, NM_019077.2:c.*339G>C, NM_019078.1:c.*339G>C, NM_019093.2:c.*339G>C, NM_021027.2:c.*339G>C, NM_205862.1:c.*339G>C, XR_241238.1:n.2134G>C, rs17190748, rs35909575, rs61636700
G > C
SNP
rs1045642 NC_000007.13:g.87138645A>G, NC_000007.14:g.87509329A>G, NG_011513.1:g.208920T>C, NM_000927.4:c.3435T>C, NP_000918.2:p.Ile1145=, rs10239679, rs11568726, rs117328163, rs17210003, rs2229108, rs386513066, rs60023214, rs9690664
A > G
SNP
I1145I
No VIP available CA VA
rs10929303 NC_000002.11:g.234681416T>C, NC_000002.12:g.233772770T>C, NG_002601.2:g.188027T>C, NG_033238.1:g.17498T>C, NM_000463.2:c.*211T>C, NM_001072.3:c.*211T>C, NM_007120.2:c.*211T>C, NM_019075.2:c.*211T>C, NM_019076.4:c.*211T>C, NM_019077.2:c.*211T>C, NM_019078.1:c.*211T>C, NM_019093.2:c.*211T>C, NM_021027.2:c.*211T>C, NM_205862.1:c.*211T>C, XR_241238.1:n.2006T>C, XR_241239.1:n.1969T>C, XR_241240.1:n.2105T>C, XR_241241.1:n.2024T>C, rs35926297, rs59599681
T > C
SNP
No VIP available No Clinical Annotations available VA
rs1128503 NC_000007.13:g.87179601A>G, NC_000007.14:g.87550285A>G, NG_011513.1:g.167964T>C, NM_000927.4:c.1236T>C, NP_000918.2:p.Gly412=, rs116989428, rs17276907, rs2032587, rs2229105, rs28365046, rs386518005, rs58257317
A > G
SNP
G412G
No VIP available No Clinical Annotations available VA
rs1523127 NC_000003.11:g.119501039C>A, NC_000003.12:g.119782192C>A, NG_011856.1:g.6709C>A, NM_003889.3:c.-131C>A, NM_022002.2:c.-566C>A, NM_033013.2:c.-131C>A, XM_005247866.1:c.-296C>A, rs58645792
C > A
SNP
No VIP available No Clinical Annotations available VA
rs1523130 NC_000003.11:g.119499507T>C, NC_000003.12:g.119780660T>C, NG_011856.1:g.5177T>C, NM_003889.3:c.-1663T>C, NM_033013.2:c.-1663T>C, XM_005247866.1:c.-1828T>C, rs118196528, rs3814054, rs59854583, rs61314694
T > C
SNP
No VIP available No Clinical Annotations available VA
rs15524 NC_000007.13:g.99245914A>G, NC_000007.14:g.99648291A>G, NG_007938.1:g.36708T>C, NM_000777.4:c.*14T>C, NM_001291829.1:c.*14T>C, NM_001291830.1:c.*14T>C, NR_033807.2:n.3257T>C, NR_033808.1:n.2125T>C, NR_033809.1:n.1885T>C, XM_005250169.1:c.*14T>C, XM_005250170.1:c.*14T>C, XM_005250171.1:c.*14T>C, XM_005250172.1:c.*14T>C, XM_005250173.1:c.*14T>C, XM_005250197.1:c.*768A>G, XM_005250198.1:c.805+24111A>G, XM_011515843.1:c.*14T>C, XM_011515844.1:c.*14T>C, XM_011515845.1:c.*14T>C, XM_011515846.1:c.*14T>C, XM_011515847.1:c.*14T>C, XM_011515909.1:c.806-20804A>G, XM_011515910.1:c.*768A>G, XR_927402.1:n.1466+24111A>G, rs10372852, rs17161789, rs3173576, rs59358441
A > -
A > G
SNP
No VIP available CA VA
rs17863778 NC_000002.11:g.234590974C>A, NC_000002.12:g.233682328C>A, NG_002601.2:g.97585C>A, NM_019075.2:c.855+44951C>A, NM_019076.4:c.855+63766C>A, NM_019077.2:c.391C>A, NM_021027.2:c.855+9539C>A, NP_061950.2:p.Arg131=, XM_005246081.1:c.391C>A, XP_005246138.1:p.Arg131=, XR_241241.1:n.941+9539C>A
C > A
SNP
R131R
No VIP available CA VA
rs17868323 NC_000002.11:g.234590970T>G, NC_000002.12:g.233682324T>G, NG_002601.2:g.97581T>G, NM_019075.2:c.855+44947T>G, NM_019076.4:c.855+63762T>G, NM_019077.2:c.387T>G, NM_021027.2:c.855+9535T>G, NP_061950.2:p.Asn129Lys, XM_005246081.1:c.387T>G, XP_005246138.1:p.Asn129Lys, XR_241241.1:n.941+9535T>G
T > G
SNP
N129K
No VIP available No Clinical Annotations available VA
rs2032582 NC_000007.13:g.87160618A>C, NC_000007.13:g.87160618A>T, NC_000007.14:g.87531302A>C, NC_000007.14:g.87531302A>T, NG_011513.1:g.186947T>A, NG_011513.1:g.186947T>G, NM_000927.4:c.2677T>A, NM_000927.4:c.2677T>G, NP_000918.2:p.Ser893Ala, NP_000918.2:p.Ser893Thr, rs10228331, rs2229106, rs386553610, rs57135550, rs9641018
A > C
SNP
S893A
No VIP available No Clinical Annotations available VA
rs2306283 NC_000012.11:g.21329738A>G, NC_000012.12:g.21176804A>G, NG_011745.1:g.50611A>G, NM_006446.4:c.388A>G, NP_006437.3:p.Asn130Asp, rs17389242, rs52832430, rs60767041
A > G
SNP
N130D
No VIP available CA VA
rs2472677 NC_000003.11:g.119518417C>T, NC_000003.12:g.119799570C>T, NG_011856.1:g.24087C>T, NM_003889.3:c.-22-7659C>T, NM_022002.2:c.96-7659C>T, NM_033013.2:c.-22-7659C>T, XM_005247866.1:c.-187-7659C>T, rs57813967
C > T
SNP
No VIP available No Clinical Annotations available VA
rs3213619 NC_000007.13:g.87230193A>G, NC_000007.14:g.87600877A>G, NG_011513.1:g.117372T>C, NM_000927.4:c.-129T>C, rs17249446, rs60679736
A > G
SNP
No VIP available No Clinical Annotations available VA
rs3732359 NC_000003.11:g.119536429G>A, NC_000003.12:g.119817582G>A, NG_011856.1:g.42099G>A, NM_003889.3:c.*370G>A, NM_022002.2:c.*370G>A, NM_033013.2:c.*370G>A, XM_005247866.1:c.995+1751G>A, rs56590291, rs57193083
G > A
SNP
No VIP available No Clinical Annotations available VA
rs3732360 NC_000003.11:g.119536581C>T, NC_000003.12:g.119817734C>T, NG_011856.1:g.42251C>T, NM_003889.3:c.*522C>T, NM_022002.2:c.*522C>T, NM_033013.2:c.*522C>T, XM_005247866.1:c.995+1903C>T, rs386584908, rs57419996
C > T
SNP
No VIP available CA VA
rs3806596 NC_000002.11:g.234637707T>C, NC_000002.12:g.233729061T>C, NG_002601.2:g.144318T>C, NM_001072.3:c.861+35196T>C, NM_007120.2:c.867+9374T>C, NM_019075.2:c.856-37973T>C, NM_019076.4:c.856-37973T>C, NM_019077.2:c.856-37973T>C, NM_019078.1:c.867+15203T>C, NM_019093.2:c.-66T>C, NM_021027.2:c.856-37973T>C, NM_205862.1:c.60+35196T>C, XR_241238.1:n.923+9374T>C, XR_241240.1:n.1022+35196T>C, XR_241241.1:n.942-37973T>C, rs17864456, rs56448245, rs57616406
T > C
SNP
No VIP available No Clinical Annotations available VA
rs3814057 NC_000003.11:g.119537254A>C, NC_000003.12:g.119818407A>C, NG_011856.1:g.42924A>C, NM_003889.3:c.*1195A>C, NM_022002.2:c.*1195A>C, NM_033013.2:c.*1195A>C, XM_005247866.1:c.995+2576A>C
A > C
SNP
No VIP available No Clinical Annotations available VA
rs3814058 NC_000003.11:g.119537291T>C, NC_000003.12:g.119818444T>C, NG_011856.1:g.42961T>C, NM_003889.3:c.*1232T>C, NM_022002.2:c.*1232T>C, NM_033013.2:c.*1232T>C, XM_005247866.1:c.995+2613T>C, rs60918337
T > C
SNP
No VIP available No Clinical Annotations available VA
rs3842 NC_000007.13:g.87133366T>C, NC_000007.14:g.87504050T>C, NG_011513.1:g.214199A>G, NM_000927.4:c.*193A>G, rs3747805, rs60395104
T > C
SNP
No VIP available No Clinical Annotations available VA
rs4148323 NC_000002.11:g.234669144G>A, NC_000002.12:g.233760498G>A, NG_002601.2:g.175755G>A, NG_033238.1:g.5226G>A, NM_000463.2:c.211G>A, NM_001072.3:c.862-6536G>A, NM_007120.2:c.868-6536G>A, NM_019075.2:c.856-6536G>A, NM_019076.4:c.856-6536G>A, NM_019077.2:c.856-6536G>A, NM_019078.1:c.868-6536G>A, NM_019093.2:c.868-6536G>A, NM_021027.2:c.856-6536G>A, NM_205862.1:c.61-6536G>A, NP_000454.1:p.Gly71Arg, XR_241238.1:n.924-6536G>A, XR_241239.1:n.233G>A, XR_241240.1:n.1023-6536G>A, XR_241241.1:n.942-6536G>A, rs113525835, rs34360183, rs58105808, rs58585123
G > A
SNP
G71R
No VIP available No Clinical Annotations available VA
rs4149056 NC_000012.11:g.21331549T>C, NC_000012.12:g.21178615T>C, NG_011745.1:g.52422T>C, NM_006446.4:c.521T>C, NP_006437.3:p.Val174Ala, rs52816141, rs60037639
T > C
SNP
V174A
No VIP available CA VA
rs717620 NC_000010.10:g.101542578C>T, NC_000010.11:g.99782821C>T, NG_011798.1:g.5116C>T, NM_000392.4:c.-24C>T, XM_005269536.1:c.-24C>T, XM_006717631.2:c.-24C>T, XM_011539291.1:c.-24C>T, XR_945604.1:n.166C>T, XR_945605.1:n.168C>T, rs17216163, rs386485129, rs58371376
C > T
SNP
No VIP available No Clinical Annotations available VA
rs72554665 NC_000023.10:g.153760484C>A, NC_000023.10:g.153760484C>G, NC_000023.11:g.154532269C>A, NC_000023.11:g.154532269C>G, NG_009015.2:g.20304G>C, NG_009015.2:g.20304G>T, NM_000402.4:c.1466G>C, NM_000402.4:c.1466G>T, NM_001042351.2:c.1376G>C, NM_001042351.2:c.1376G>T, NP_000393.4:p.Arg489Leu, NP_000393.4:p.Arg489Pro, NP_001035810.1:p.Arg459Leu, NP_001035810.1:p.Arg459Pro, NW_003871103.3:g.1966248C>A, NW_003871103.3:g.1966248C>G, XM_005274657.1:c.1469G>C, XM_005274657.1:c.1469G>T, XM_005274657.2:c.1469G>C, XM_005274657.2:c.1469G>T, XM_005274658.1:c.1379G>C, XM_005274658.1:c.1379G>T, XM_005274658.2:c.1379G>C, XM_005274658.2:c.1379G>T, XM_005277833.1:c.1469G>C, XM_005277833.1:c.1469G>T, XM_005277834.1:c.1379G>C, XM_005277834.1:c.1379G>T, XM_011531132.1:c.*498G>C, XM_011531132.1:c.*498G>T, XP_005274714.1:p.Arg490Leu, XP_005274714.1:p.Arg490Pro, XP_005274715.1:p.Arg460Leu, XP_005274715.1:p.Arg460Pro, XP_005277890.1:p.Arg490Leu, XP_005277890.1:p.Arg490Pro, XP_005277891.1:p.Arg460Leu, XP_005277891.1:p.Arg460Pro
C > A
SNP
R489L
No VIP available CA VA
rs7586110 NC_000002.11:g.234590527T>G, NC_000002.12:g.233681881T>G, NG_002601.2:g.97138T>G, NM_019075.2:c.855+44504T>G, NM_019076.4:c.855+63319T>G, NM_019077.2:c.-57T>G, NM_021027.2:c.855+9092T>G, XM_005246081.1:c.-57T>G, XR_241241.1:n.941+9092T>G, rs60348498
T > G
SNP
rs8175347
(TA)6 > (TA)5
(TA)6 > (TA)7
(TA)6 > (TA)8
microsatellite
No VIP available CA VA
rs8330 NC_000002.11:g.234681645G>C, NC_000002.12:g.233772999G>C, NG_002601.2:g.188256G>C, NG_033238.1:g.17727G>C, NM_000463.2:c.*440G>C, NM_001072.3:c.*440G>C, NM_007120.2:c.*440G>C, NM_019075.2:c.*440G>C, NM_019076.4:c.*440G>C, NM_019077.2:c.*440G>C, NM_019078.1:c.*440G>C, NM_019093.2:c.*440G>C, NM_021027.2:c.*440G>C, NM_205862.1:c.*440G>C, XR_241238.1:n.2235G>C, rs3182134, rs35609787, rs386496306, rs57500970
G > C
SNP
No VIP available CA VA
rs887829 NC_000002.11:g.234668570C>T, NC_000002.12:g.233759924C>T, NG_002601.2:g.175181C>T, NG_033238.1:g.4652C>T, NM_000463.2:c.-364C>T, NM_001072.3:c.862-7110C>T, NM_007120.2:c.868-7110C>T, NM_019075.2:c.856-7110C>T, NM_019076.4:c.856-7110C>T, NM_019077.2:c.856-7110C>T, NM_019078.1:c.868-7110C>T, NM_019093.2:c.868-7110C>T, NM_021027.2:c.856-7110C>T, NM_205862.1:c.61-7110C>T, XR_241238.1:n.924-7110C>T, XR_241239.1:n.-342C>T, XR_241240.1:n.1023-7110C>T, XR_241241.1:n.942-7110C>T, rs12990609, rs34790730, rs36207722, rs386619532, rs61315639
C > T
SNP
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 147

Overview

Generic Names
  • ATV
  • ATZ
  • Atazanavir sulfate
  • BMS-232632
  • atazanavir
Trade Names
  • Latazanavir
  • Reyataz
  • Zrivada
Brand Mixture Names

PharmGKB Accession Id

PA10251

Type(s):

Drug

Description

Atazanavir (formerly known as BMS-232632) is an antiretroviral drug of the protease inhibitor (PI) class. Like other antiretrovirals, it is used to treat infection of human immunodeficiency virus (HIV). Atazanavir is distinguished from other PIs in that it can be given once-daily (rather than requiring multiple doses per day) and has lesser effects on the patient's lipid profile (the amounts of cholesterol and other fatty substances in the blood). Like other protease inhibitors, it is used only in combination with other HIV medications. The U.S. Food and Drug Administration (FDA) approved atazanavir on June 20, 2003. Wikipedia

Source: Drug Bank

Indication

Used in combination with other antiretroviral agents for the treatment of HIV-1 infection, as well as postexposure prophylaxis of HIV infection in individuals who have had occupational or nonoccupational exposure to potentially infectious body fluids of a person known to be infected with HIV when that exposure represents a substantial risk for HIV transmission.

Source: Drug Bank

Other Vocabularies

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Atazanavir selectively inhibits the virus-specific processing of viral Gag and Gag-Pol polyproteins in HIV-1 infected cells by binding to the active site of HIV-1 protease, thus preventing the formation of mature virions. Atazanavir is not active against HIV-2.

Source: Drug Bank

Pharmacology

Atazanavir (ATV) is an azapeptide HIV-1 protease inhibitor (PI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). HIV-1 protease is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV-1. Atazanavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature non-infectious viral particles. Protease inhibitors are almost always used in combination with at least two other anti-HIV drugs. Atazanivir is pharmacologically related but structurally different from other protease inhibitors and other currently available antiretrovirals.

Source: Drug Bank

Food Interaction

Administration with food reduces pharmacokinetic variability.|Food increases product absorption.

Source: Drug Bank

Absorption, Distribution, Metabolism, Elimination & Toxicity

Biotransformation

Atazanavir is extensively metabolized in humans, primarily by the liver. The major biotransformation pathways of atazanavir in humans consisted of monooxygenation and dioxygenation. Other minor biotransformation pathways for atazanavir or its metabolites consisted of glucuronidation, N-dealkylation, hydrolysis, and oxygenation with dehydrogenation. In vitro studies using human liver microsomes suggested that atazanavir is metabolized by CYP3A.

Source: Drug Bank

Protein Binding

86% bound to human serum proteins (alpha-1-acid glycoprotein and albumin). Protein binding is independent of concentration.

Source: Drug Bank

Absorption

Atazanavir is rapidly absorbed with a T max of approximately 2.5 hours. Administration of atazanavir with food enhances bioavailability and reduces pharmacokinetic variability. Oral bioavailability is 60-68%.

Source: Drug Bank

Half-Life

Elimination half-life in adults (healthy and HIV infected) is approximately 7 hours (following a 400 mg daily dose with a light meal). Elimination half-life in hepatically impaired is 12.1 hours (following a single 400 mg dose).

Source: Drug Bank

Chemical Properties

Chemical Formula

C38H52N6O7

Source: Drug Bank

Isomeric SMILES

CC(C)(C)[C@@H](C(=O)N[C@@H](CC1=CC=CC=C1)[C@H](CN(CC2=CC=C(C=C2)C3=CC=CC=N3)NC(=O)[C@H](C(C)(C)C)NC(=O)OC)O)NC(=O)OC

Source: Drug Bank

COC(=O)N[C@H](C(=O)N[C@@H](CC1=CC=CC=C1)[C@@H](O)CN(CC1=CC=C(C=C1)C1=NC=CC=C1)NC(=O)[C@@H](NC(=O)OC)C(C)(C)C)C(C)(C)C

Source: Drug Bank

Canonical SMILES

COC(=O)N[C@H](C(=O)N[C@@H]

Source: Drug Bank

Average Molecular Weight

704.8555

Source: Drug Bank

Monoisotopic Molecular Weight

704.389748048

Source: Drug Bank

SMILES

COC(=O)N[C@H](C(=O)N[C@@H](CC1=CC=CC=C1)[C@@H](O)CN(CC1=CC=C(C=C1)C1=CC=CC=N1)NC(=O)[C@@H](NC(=O)OC)C(C)(C)C)C(C)(C)C

Source: Drug Bank

InChI String

InChI=1S/C38H52N6O7/c1-37(2,3)31(41-35(48)50-7)33(46)40-29(22-25-14-10-9-11-15-25)30(45)24-44(43-34(47)32(38(4,5)6)42-36(49)51-8)23-26-17-19-27(20-18-26)28-16-12-13-21-39-28/h9-21,29-32,45H,22-24H2,1-8H3,(H,40,46)(H,41,48)(H,42,49)(H,43,47)/t29-,30-,31+,32+/m0/s1

Source: Drug Bank

Genes that are associated with this drug in PharmGKB's database based on (1) variant annotations, (2) literature review, (3) pathways or (4) information automatically retrieved from DrugBank, depending on the "evidence" and "source" listed below.

Curated Information ?

Drug Targets

Gene Description
ABCB1 (source: Drug Bank )

Curated Information ?

EvidenceDrug
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
bilirubin
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
raltegravir

Drug Interactions

Interaction Description
amiodarone - atazanavir Increased risk of cardiotoxicity/arrhythmias (source: Drug Bank )
amiodarone - atazanavir Increased risk of cardiotoxicity/arrhythmias (source: Drug Bank )
amitriptyline - atazanavir Atazanavir increases the effect and toxicity of tricyclics (source: Drug Bank )
amitriptyline - atazanavir Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
amoxapine - atazanavir Atazanavir increases the efect and toxicity of tricyclics (source: Drug Bank )
amoxapine - atazanavir Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, amoxapine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amoxapine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
atazanavir - acenocoumarol The protease inhibitor increase the anticoagulant effect (source: Drug Bank )
atazanavir - acenocoumarol The protease inhibitor, atazanavir, may increase the anticoagulant effect of acenocoumarol. (source: Drug Bank )
atazanavir - aluminium This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - amiodarone Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
atazanavir - amiodarone Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
atazanavir - amitriptyline Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - amitriptyline Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
atazanavir - amoxapine Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - amoxapine Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, amoxapine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amoxapine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
atazanavir - anisindione The protease inhibitor, atazanavir, may increase the anticoagulant effect of anisindione. (source: Drug Bank )
atazanavir - atorvastatin Increases the effect and toxicity of the statin (source: Drug Bank )
atazanavir - atorvastatin Increases the effect and toxicity of the statin (source: Drug Bank )
atazanavir - bepridil Increases the effect and toxicity of bepridil (source: Drug Bank )
atazanavir - calcium This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - calcium This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - cimetidine This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - cimetidine This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - cisapride Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
atazanavir - cisapride Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
atazanavir - clarithromycin Increases levels of clarithromycin (source: Drug Bank )
atazanavir - clarithromycin Increases levels of clarithromycin (source: Drug Bank )
atazanavir - clomipramine Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - clomipramine Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
atazanavir - cyclosporine Increases the effect and toxicity of immunosuppressant (source: Drug Bank )
atazanavir - cyclosporine Increases the effect and toxicity of immunosuppressant (source: Drug Bank )
atazanavir - desipramine Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - desipramine Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, desipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
atazanavir - dicumarol The protease inhibitor increases the anticoagulant effect (source: Drug Bank )
atazanavir - dicumarol The protease inhibitor, atazanavir, may increase the anticoagulant effect of dicumarol. (source: Drug Bank )
atazanavir - dihydroergotamine Increases the effect and toxicity of ergot derivative (source: Drug Bank )
atazanavir - dihydroxyaluminium This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - diltiazem Increases the effect and toxicity of diltiazem (source: Drug Bank )
atazanavir - diltiazem Increases the effect and toxicity of diltiazem (source: Drug Bank )
atazanavir - doxepin Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - doxepin Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, doxepin, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of doxepin if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
atazanavir - efavirenz Efavirenz decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - efavirenz Efavirenz decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - ergotamine Increases the effect and toxicity of ergot derivative (source: Drug Bank )
atazanavir - erlotinib This CYP3A4 inhibitor increases levels/toxicity of erlotinib (source: Drug Bank )
atazanavir - erlotinib This CYP3A4 inhibitor increases levels/toxicity of erlotinib (source: Drug Bank )
atazanavir - esomeprazole This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - esomeprazole This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - famotidine This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - famotidine This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - imipramine Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - imipramine Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
atazanavir - indinavir Increased risk of hyperbilirubinemia with this association (source: Drug Bank )
atazanavir - indinavir Increased risk of hyperbilirubinemia with this association (source: Drug Bank )
atazanavir - irinotecan Increases levels/effect of irinotecan (source: Drug Bank )
atazanavir - irinotecan Increases levels/effect of irinotecan (source: Drug Bank )
atazanavir - lansoprazole This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - lansoprazole This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - lidocaine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
atazanavir - lidocaine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
atazanavir - lovastatin Increased risk of myopathy/rhabdomyolysis (source: Drug Bank )
atazanavir - lovastatin Increased risk of myopathy/rhabdomyolysis (source: Drug Bank )
atazanavir - Magnesium This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - Magnesium This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - magnesium oxide This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - magnesium sulfate This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - methylergonovine Increases the effect and toxicity of ergot derivative (source: Drug Bank )
atazanavir - methylergonovine Increases the effect and toxicity of ergot derivative (source: Drug Bank )
atazanavir - midazolam Increases the effect and toxicity of benzodiazepine (source: Drug Bank )
atazanavir - midazolam Increases the effect and toxicity of benzodiazepine (source: Drug Bank )
atazanavir - nevirapine Nevirapine decreases levels/effect of atazanavir (source: Drug Bank )
atazanavir - nevirapine Nevirapine decreases levels/effect of atazanavir (source: Drug Bank )
atazanavir - nizatidine This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - nortriptyline Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - nortriptyline Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, nortriptyline, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of nortriptyline if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
atazanavir - omeprazole This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - omeprazole This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - pantoprazole This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - pantoprazole This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - pimozide The protease inhibitor increases the effect and toxicity of pimozide (source: Drug Bank )
atazanavir - pimozide The protease inhibitor, atazanavir, may increase the effect and toxicity of pimozide. (source: Drug Bank )
atazanavir - protriptyline Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - protriptyline Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, protriptyline, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of protriptyline if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
atazanavir - quinidine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
atazanavir - quinidine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
atazanavir - rabeprazole This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - rabeprazole This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - ranitidine This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - ranitidine This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - ranolazine Increased levels of ranolazine- risk of toxicity (source: Drug Bank )
atazanavir - rifabutin Increases levels/toxicity of rifabutin (source: Drug Bank )
atazanavir - rifabutin Increases levels/toxicity of rifabutin (source: Drug Bank )
atazanavir - rifampin Rifampin reduces levels and efficacy of atazanavir (source: Drug Bank )
atazanavir - rifampin Rifampin reduces levels and efficacy of atazanavir (source: Drug Bank )
atazanavir - ritonavir Association with dose adjustment (source: Drug Bank )
atazanavir - ritonavir Association with dose adjustment (source: Drug Bank )
atazanavir - sildenafil Increases the effect and toxicity of sildenafil (source: Drug Bank )
atazanavir - sildenafil Increases the effect and toxicity of sildenafil (source: Drug Bank )
atazanavir - simvastatin Increased risk of myopathy/rhabdomyolysis (source: Drug Bank )
atazanavir - simvastatin Increased risk of myopathy/rhabdomyolysis (source: Drug Bank )
atazanavir - sirolimus Increases the effect and toxicity of immunosuppressant (source: Drug Bank )
atazanavir - sirolimus Increases the effect and toxicity of immunosuppressant (source: Drug Bank )
atazanavir - sodium This gastric pH modifier decreases the levels/effect of atazanavir (source: Drug Bank )
atazanavir - sodium bicarbonate This gastric pH modifier decreases the levels/effect of atazanavir (source: Drug Bank )
atazanavir - sunitinib Possible increase in sunitinib levels (source: Drug Bank )
atazanavir - sunitinib Possible increase in sunitinib levels (source: Drug Bank )
atazanavir - tacrolimus Increases the effect and toxicity of immunosuppressant (source: Drug Bank )
atazanavir - tacrolimus Increases the effect and toxicity of immunosuppressant (source: Drug Bank )
atazanavir - tenofovir Tenofovir decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - tenofovir Tenofovir decreases the levels/effects of atazanavir (source: Drug Bank )
atazanavir - triazolam Increases the effect and toxicity of benzodiazepine (source: Drug Bank )
atazanavir - triazolam Increases the effect and toxicity of benzodiazepine (source: Drug Bank )
atazanavir - trimipramine Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - trimipramine Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, trimipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of trimipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
atazanavir - warfarin The protease inhibitor increases the anticoagulant effect (source: Drug Bank )
atazanavir - warfarin The protease inhibitor, atazanavir, may increase the anticoagulant effect of warfarin. (source: Drug Bank )
atorvastatin - atazanavir Atazanavir increases the effect and toxicity of the statin (source: Drug Bank )
atorvastatin - atazanavir Atazanavir increases the effect and toxicity of the statin (source: Drug Bank )
bepridil - atazanavir Atazanavir increases the effect and toxicity of bepridil (source: Drug Bank )
bepridil - atazanavir Atazanavir increases the effect and toxicity of bepridil (source: Drug Bank )
bromazepam - atazanavir Atazanavir, a strong CYP3A4 inhibitor, may increase the serum concentration of bromazepam by decreasing its metabolism. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of bromazepam if atazanavir is initiated, discontinued or dose changed. Dosage adjustments may be required. (source: Drug Bank )
cimetidine - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
cimetidine - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
cisapride - atazanavir Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
cisapride - atazanavir Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clarithromycin - atazanavir Atazanavir increases levels of clarithromycin (source: Drug Bank )
clarithromycin - atazanavir Atazanavir increases levels of clarithromycin (source: Drug Bank )
clomipramine - atazanavir Atazanavir increases the effect and toxicity of tricyclics (source: Drug Bank )
clomipramine - atazanavir Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
cyclosporine - atazanavir Atazanavir increases the effect and toxicity of immunosuppressant (source: Drug Bank )
cyclosporine - atazanavir Atazanavir increases the effect and toxicity of immunosuppressant (source: Drug Bank )
dantrolene - atazanavir Atazanavir may increase the serum concentration of dantrolene by decreasing its metabolism. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of dantrolene if atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
desipramine - atazanavir Atazanavir increases the effect and toxicity of tricyclics (source: Drug Bank )
desipramine - atazanavir Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, desipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
dihydroergotamine - atazanavir Atazanavir increases the effect and toxicity of ergot derivative (source: Drug Bank )
dihydroergotamine - atazanavir Atazanavir increases the effect and toxicity of ergot derivative (source: Drug Bank )
diltiazem - atazanavir Atazanavir increases the effect and toxicity of diltiazem (source: Drug Bank )
diltiazem - atazanavir Atazanavir increases the effect and toxicity of diltiazem (source: Drug Bank )
doxepin - atazanavir Atazanavir increases the effect and toxicity of tricyclics (source: Drug Bank )
doxepin - atazanavir Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, doxepin, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of doxepin if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
ergotamine - atazanavir Atazanavir increases the effect and toxicity of ergot derivative (source: Drug Bank )
ergotamine - atazanavir Atazanavir increases the effect and toxicity of ergot derivative (source: Drug Bank )
esomeprazole - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
esomeprazole - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
famotidine - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
famotidine - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
imipramine - atazanavir Atazanavir increases the effect and toxicity of tricyclics (source: Drug Bank )
imipramine - atazanavir Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
indinavir - atazanavir Increased risk of hyperbilirubinemia with this association (source: Drug Bank )
indinavir - atazanavir Increased risk of hyperbilirubinemia with this association (source: Drug Bank )
lansoprazole - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
lansoprazole - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
lovastatin - atazanavir Increased risk of myopathy/rhabdomyolysis (source: Drug Bank )
lovastatin - atazanavir Increased risk of myopathy/rhabdomyolysis (source: Drug Bank )
Magnesium - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
midazolam - atazanavir Atazanavir increases the effect and toxicity of benzodiazepine (source: Drug Bank )
midazolam - atazanavir Atazanavir increases the effect and toxicity of benzodiazepine (source: Drug Bank )
nevirapine - atazanavir Decreases levels/effect of atazanavir (source: Drug Bank )
nevirapine - atazanavir Decreases levels/effect of atazanavir (source: Drug Bank )
nizatidine - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
nortriptyline - atazanavir Atazanavir increases the effect and toxicity of tricyclics (source: Drug Bank )
nortriptyline - atazanavir Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, nortriptyline, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of nortriptyline if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
omeprazole - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
omeprazole - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
pantoprazole - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
pantoprazole - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
pimozide - atazanavir The protease inhibitor increases the effect and toxicity of pimozide (source: Drug Bank )
pimozide - atazanavir The protease inhibitor, atazanavir, may increase the effect and toxicity of pimozide. (source: Drug Bank )
quinidine - atazanavir Increased risk of cardiotoxicity/arrhythmias (source: Drug Bank )
quinidine - atazanavir Increased risk of cardiotoxicity/arrhythmias (source: Drug Bank )
rabeprazole - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
rabeprazole - atazanavir This gastric pH modifier decreases the levels/effects of atazanavir (source: Drug Bank )
ramelteon - atazanavir Atazanavir increases levels/toxicity of ramelteon (source: Drug Bank )
ramelteon - atazanavir Atazanavir increases levels/toxicity of ramelteon (source: Drug Bank )
ranitidine - atazanavir This gastric pH modifier decreases the levels/effects of atazanaivr (source: Drug Bank )
ranitidine - atazanavir This gastric pH modifier decreases the levels/effects of atazanaivr (source: Drug Bank )
ranolazine - atazanavir Increased levels of ranolazine - risk of toxicity (source: Drug Bank )
rifabutin - atazanavir Atazanavir increases levels/toxicity of rifabutin (source: Drug Bank )
rifabutin - atazanavir Atazanavir increases levels/toxicity of rifabutin (source: Drug Bank )
rifampin - atazanavir Rifampin reduces levels and efficacy of atazanavir (source: Drug Bank )
rifampin - atazanavir Rifampin reduces levels and efficacy of atazanavir (source: Drug Bank )
tadalafil - atazanavir Atazanavir may reduce the metabolism of Tadalafil. Concomitant therapy should be avoided if possible due to high risk of Tadalafil toxicity. (source: Drug Bank )
tamoxifen - atazanavir Atazanavir may increase the serum concentration of Tamoxifen by decreasing its metabolism. Monitor for increased adverse/toxic effects of Tamoxifen. (source: Drug Bank )
tamoxifen - atazanavir Atazanavir may increase the serum concentration of Tamoxifen by decreasing its metabolism. Monitor for increased adverse/toxic effects of Tamoxifen. (source: Drug Bank )
tamsulosin - atazanavir Atazanvir, a CYP3A4 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP3A4 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Atazanavir is initiated, discontinued, or dose changed. (source: Drug Bank )
tamsulosin - atazanavir Atazanvir, a CYP3A4 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP3A4 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Atazanavir is initiated, discontinued, or dose changed. (source: Drug Bank )
telithromycin - atazanavir Co-administration may result in altered plasma concentrations of Atazanavir and/or Telithromycin. Consider alternate therapy or monitor the therapeutic/adverse effects of both agents. (source: Drug Bank )
teniposide - atazanavir The strong CYP3A4 inhibitor, Atazanavir, may decrease the metabolism and clearance of Teniposide, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Teniposide if Atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
tiagabine - atazanavir The strong CYP3A4 inhibitor, Atazanavir, may decrease the metabolism and clearance of Tiagabine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Tiagabine if Atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
tipranavir - atazanavir Tipranavir, co-administered with Ritonavir, may decrease the plasma concentration of Atazanavir. Consider alternate therapy. (source: Drug Bank )
tolterodine - atazanavir Atazanavir may decrease the metabolism and clearance of Tolterodine. Adjust the Tolterodine dose and monitor for efficacy and toxicity. (source: Drug Bank )
tolterodine - atazanavir Atazanavir may decrease the metabolism and clearance of Tolterodine. Adjust the Tolterodine dose and monitor for efficacy and toxicity. (source: Drug Bank )
tramadol - atazanavir Atazanavir may increase Tramadol toxicity by decreasing Tramadol metabolism and clearance. (source: Drug Bank )
trazodone - atazanavir The protease inhibitor, Atazanavir, may increase the efficacy/toxicity of Trazodone by inhibiting Trazodone metabolism and clearance. Monitor for changes in Trazodone efficacy/toxicity if Atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
trazodone - atazanavir The protease inhibitor, Atazanavir, may increase the efficacy/toxicity of Trazodone by inhibiting Trazodone metabolism and clearance. Monitor for changes in Trazodone efficacy/toxicity if Atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
triazolam - atazanavir Atazanavir increases the effect and toxicity of benzodiazepine (source: Drug Bank )
triazolam - atazanavir Atazanavir increases the effect and toxicity of benzodiazepine (source: Drug Bank )
trimipramine - atazanavir The strong CYP3A4 inhibitor, Atazanavir, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
vardenafil - atazanavir Atazanavir, a strong CYP3A4 inhibitor, may reduce the metabolism and clearance of Vardenafil. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of Vardenafil. (source: Drug Bank )
venlafaxine - atazanavir Atazanavir, a CYP3A4 inhibitor, may decrease the metabolism and clearance of Venlafaxine, a CYP3A4 substrate. Monitor for changes in therapeutic/adverse effects of Venlafaxine if Atazanavir is initiated, discontinued, or dose changed. (source: Drug Bank )
verapamil - atazanavir Atazanavir, a strong CYP3A4 inhibitor, may increase the serum concentration of Veramapil, a CYP3A4 substrate, by decreasing its metabolism and clearance. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Verapamil if Atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
vincristine - atazanavir Atazanavir, a strong CYP3A4 inhibitor, may increase the serum concentration of Vincristine by decreasing its metabolism. Consider alternate therapy to avoid Vincristine toxicity. Monitor for changes in the therapeutic and adverse effects of Vincristine if Atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
vinorelbine - atazanavir Atazanavir, a strong CYP3A4 inhibitor, may increase the serum concentration of Vinorelbine by decreasing its metabolism. Consider alternate therapy to avoid Vinorelbine toxicity. Monitor for changes in the therapeutic and adverse effects of Vinorelbine if Atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
voriconazole - atazanavir Voriconazole, a strong CYP3A4 inhibitor, may increase the serum concentration of atazanavir by decreasing its metabolism. The serum concentration of voriconazole may be increased by atazanavir. Monitor for changes in the therapeutic and adverse effects of both agents if concomitant therapy is initiated, discontinued or if doses are changed. (source: Drug Bank )
zolpidem - atazanavir Atazanavir, a strong CYP3A4 inhibitor, may increase the serum concentration of zolpidem by decreasing its metabolism. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of zolpidem if atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
zonisamide - atazanavir Atazanavir, a strong CYP3A4 inhibitor, may increase the serum concentration of zonisamide by decreasing its metabolism. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of zonisamide if atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
zopiclone - atazanavir Atazanavir, a strong CYP3A4 inhibitor, may increase the serum concentration of zopiclone by decreasing its metabolism. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of zopiclone if atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )

Curated Information ?

Publications related to atazanavir: 53

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Pharmacogenetics of unboosted atazanavir in HIV-infected individuals in resource-limited settings: a sub-study of the AIDS Clinical Trials Group (ACTG) PEARLS study (NWCS 342). The Journal of antimicrobial chemotherapy. 2016. Castillo-Mancilla Jose R, et al. PubMed
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Treatment response to unboosted atazanavir in combination with tenofovir disoproxil fumarate and lamivudine in human immunodeficiency virus-1-infected patients who have achieved virological suppression: A therapeutic drug monitoring and pharmacogenetic study. Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi. 2016. Tsai Mao-Song, et al. PubMed
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Pharmacogenomically actionable medications in a safety net health care system. SAGE open medicine. 2016. Carpenter Janet S, et al. PubMed
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Successful pharmacogenetics-based optimization of unboosted atazanavir plasma exposure in HIV-positive patients: a randomized, controlled, pilot study (the REYAGEN study). The Journal of antimicrobial chemotherapy. 2015. Bonora S, et al. PubMed
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Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for UGT1A1 and Atazanavir Prescribing. Clinical pharmacology and therapeutics. 2015. Gammal Roseann S, et al. PubMed
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Screening for UGT1A1 Genotype in Study A5257 Would Have Markedly Reduced Premature Discontinuation of Atazanavir for Hyperbilirubinemia. Open forum infectious diseases. 2015. Vardhanabhuti Saran, et al. PubMed
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Polymorphisms associated with renal adverse effects of antiretroviral therapy in a Southern Brazilian HIV cohort. Pharmacogenetics and genomics. 2015. da Rocha Ivete M, et al. PubMed
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Pharmacogenetic testing can identify patients taking atazanavir at risk for hyperbilirubinemia. Journal of acquired immune deficiency syndromes (1999). 2015. Avihingsanon Anchalee, et al. PubMed
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Cholelithiasis and Nephrolithiasis in HIV-Positive Patients in the Era of Combination Antiretroviral Therapy. PloS one. 2015. Lin Kuan-Yin, et al. PubMed
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Single-nucleotide polymorphisms in the UDP-glucuronosyltransferase 1A-3' untranslated region are associated with atazanavir-induced nephrolithiasis in patients with HIV-1 infection: a pharmacogenetic study. The Journal of antimicrobial chemotherapy. 2014. Nishijima Takeshi, et al. PubMed
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Voriconazole and atazanavir: a CYP2C19-dependent manageable drug-drug interaction. Pharmacogenomics. 2014. Calcagno Andrea, et al. PubMed
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PharmGKB summary: very important pharmacogene information for UGT1A1. Pharmacogenetics and genomics. 2014. Barbarino Julia M, et al. PubMed
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In vitro OATP1B1 and OATP1B3 inhibition is associated with observations of benign clinical unconjugated hyperbilirubinemia. Xenobiotica; the fate of foreign compounds in biological systems. 2014. Chiou William J, et al. PubMed
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High prevalence of the UGT1A1*28 variant in HIV-infected individuals in Greece. International journal of STD & AIDS. 2014. Panagopoulos P, et al. PubMed
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Genomewide association study of atazanavir pharmacokinetics and hyperbilirubinemia in AIDS Clinical Trials Group protocol A5202. Pharmacogenetics and genomics. 2014. Johnson Daniel H, et al. PubMed
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EMA Initiatives and Perspectives on Pharmacogenomics. British journal of clinical pharmacology. 2014. Ehmann Falk, et al. PubMed
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Extended mathematical model for "in vivo" quantification of the interaction betweeen atazanavir and bilirubin. Journal of clinical pharmacology. 2013. Lozano Roberto, et al. PubMed
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Clinical and pharmacogenetic factors affecting neonatal bilirubinemia following atazanavir treatment of mothers during pregnancy. AIDS research and human retroviruses. 2013. Eley Timothy, et al. PubMed
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Evaluating the in vitro inhibition of UGT1A1, OATP1B1, OATP1B3, MRP2, and BSEP in predicting drug-induced hyperbilirubinemia. Molecular pharmaceutics. 2013. Chang Jae H, et al. PubMed
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TokyoGreen derivatives as specific and practical fluorescent probes for UDP-glucuronosyltransferase (UGT) 1A1. Chemical communications (Cambridge, England). 2013. Terai Takuya, et al. PubMed
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Effect of the UGT1A1*28 allele on unconjugated hyperbilirubinemia in HIV-positive patients receiving Atazanavir: a systematic review. The Annals of pharmacotherapy. 2013. Culley Celia L, et al. PubMed
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Impact of UGT1A1 Gilbert variant on discontinuation of ritonavir-boosted atazanavir in AIDS Clinical Trials Group Study A5202. The Journal of infectious diseases. 2013. Ribaudo Heather J, et al. PubMed
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Predictors of the change in bilirubin levels over twelve weeks of treatment with atazanavir. AIDS research and therapy. 2013. Cotter Aoife G, et al. PubMed
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Cost-effectiveness analysis of UGT1A1 genetic testing to inform antiretroviral prescribing in HIV disease. Antiviral therapy. 2013. Schackman Bruce R, et al. PubMed
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Effect of Adherence as Measured by MEMS, Ritonavir Boosting, and CYP3A5 Genotype on Atazanavir Pharmacokinetics in Treatment-Naive HIV-Infected Patients. Clinical pharmacology and therapeutics. 2012. Savic R M, et al. PubMed
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Short communication: UGT1A1*28 variant allele is a predictor of severe hyperbilirubinemia in HIV-infected patients on HAART in southern Brazil. AIDS research and human retroviruses. 2012. Turatti Lisiane, et al. PubMed
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Switching to unboosted atazanavir reduces bilirubin and triglycerides without compromising treatment efficacy in UGT1A1*28 polymorphism carriers. The Journal of antimicrobial chemotherapy. 2012. Ferraris Laurenzia, et al. PubMed
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The Dual Role of Pharmacogenetics in HIV Treatment: Mutations and Polymorphisms Regulating Antiretroviral Drug Resistance and Disposition. Pharmacological reviews. 2012. Michaud Veronique, et al. PubMed
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Intrapatient and interpatient pharmacokinetic variability of raltegravir in the clinical setting. Therapeutic drug monitoring. 2012. Siccardi Marco, et al. PubMed
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Severe atazanavir-associated hyperbilirubinemia revealing Canton G6PD deficiency in an Asian HIV-infected patient. AIDS (London, England). 2012. Javelle Emilie, et al. PubMed
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Short communication: use of serum bilirubin levels as surrogate marker of early virological response to atazanavir-based antiretroviral therapy. AIDS research and human retroviruses. 2011. Morello Judit, et al. PubMed
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Clinical pharmacology profile of raltegravir, an HIV-1 integrase strand transfer inhibitor. Journal of clinical pharmacology. 2011. Brainard Diana M, et al. PubMed
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Detrimental effect of atazanavir plasma concentrations on total serum bilirubin levels in the presence of UGT1A1 polymorphisms. Journal of acquired immune deficiency syndromes (1999). 2011. Cicconi Paola, et al. PubMed
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Association of pharmacogenetic markers with premature discontinuation of first-line anti-HIV therapy: an observational cohort study. The Journal of infectious diseases. 2011. Lubomirov Rubin, et al. PubMed
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Successful tacrolimus treatment following renal transplant in a HIV-infected patient with raltegravir previously treated with a protease inhibitor based regimen. Drug metabolism and drug interactions. 2011. Cousins Darren, et al. PubMed
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Nuclear receptor-mediated induction of CYP450 by antiretrovirals: functional consequences of NR1I2 (PXR) polymorphisms and differential prevalence in whites and sub-Saharan Africans. Journal of acquired immune deficiency syndromes (1999). 2010. Svärd Jenny, et al. PubMed
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Exposure-related effects of atazanavir on the pharmacokinetics of raltegravir in HIV-1-infected patients. Therapeutic drug monitoring. 2010. Cattaneo Dario, et al. PubMed
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Population Pharmacokinetic modelling of the association between 63396C->T Pregnane-X-Receptor (PXR) polymorphism and unboosted atazanavir clearance. Antimicrobial agents and chemotherapy. 2010. Schipani Alessandro, et al. PubMed
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Incidence of atazanavir-associated hyperbilirubinemia in Korean HIV patients: 30 months follow-up results in a population with low UDP-glucuronosyltransferase1A1*28 allele frequency. Journal of Korean medical science. 2010. Choe Pyoeng Gyun, et al. PubMed
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Genetic factors influencing severe atazanavir-associated hyperbilirubinemia in a population with low UDP-glucuronosyltransferase 1A1*28 allele frequency. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2010. Park Wan Beom, et al. PubMed
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Prediction of adverse drug reactions using decision tree modeling. Clinical pharmacology and therapeutics. 2010. Hammann F, et al. PubMed
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Pharmacogenetics of antiretrovirals. Antiviral research. 2010. Tozzi Valerio. PubMed
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Atazanavir pharmacokinetics in genetically determined CYP3A5 expressors versus non-expressors. The Journal of antimicrobial chemotherapy. 2009. Anderson Peter L, et al. PubMed
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Family 1 uridine-5'-diphosphate glucuronosyltransferases (UGT1A): from Gilbert's syndrome to genetic organization and variability. Archives of toxicology. 2008. Strassburg Christian P, et al. PubMed
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Pharmacogenetics of Gilbert's syndrome. Pharmacogenomics. 2008. Strassburg Christian P. PubMed
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Pharmacogenetics of antiretroviral agents. Current opinion in HIV and AIDS. 2008. Owen Andrew, et al. PubMed
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Diagnosis and management of HIV drug hypersensitivity. The Journal of allergy and clinical immunology. 2008. Davis Carla M, et al. PubMed
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Multidrug resistance 1 polymorphisms and trough concentrations of atazanavir and lopinavir in patients with HIV. Pharmacogenomics. 2007. Ma Qing, et al. PubMed
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Genetic factors influencing atazanavir plasma concentrations and the risk of severe hyperbilirubinemia. AIDS (London, England). 2007. Rodríguez-Nóvoa Sonia, et al. PubMed
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Gilbert's disease and atazanavir: from phenotype to UDP-glucuronosyltransferase haplotype. Hepatology (Baltimore, Md.). 2006. Lankisch Tim O, et al. PubMed
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Overview of the pharmacogenetics of HIV therapy. The pharmacogenomics journal. 2006. Rodríguez-Nóvoa S, et al. PubMed
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In vitro inhibition of UDP glucuronosyltransferases by atazanavir and other HIV protease inhibitors and the relationship of this property to in vivo bilirubin glucuronidation. Drug metabolism and disposition: the biological fate of chemicals. 2005. Zhang Donglu, et al. PubMed
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Gilbert syndrome and the development of antiretroviral therapy-associated hyperbilirubinemia. The Journal of infectious diseases. 2005. Rotger Margalida, et al. PubMed

LinkOuts

Web Resource:
Wikipedia
DrugBank:
DB01072
ChEBI:
37924
KEGG Drug:
D01276
PubChem Compound:
148192
PubChem Substance:
46508504
725881
Drugs Product Database (DPD):
2248610
BindingDB:
13934
ChemSpider:
130642
Therapeutic Targets Database:
DNC000332

Clinical Trials

These are trials that mention atazanavir and are related to either pharmacogenetics or pharmacogenomics.

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Sources for PharmGKB drug information: DrugBank, PubChem.