Chemical: Drug
isoniazid

PharmGKB contains no dosing guidelines for this . To report known genotype-based dosing guidelines, or if you are interested in developing guidelines, click here.


last updated 09/01/2016

1. FDA Label for isoniazid,pyrazinamide,rifampin and NAT2

Informative PGx

Genes and/or phenotypes found in this label

  • Hepatitis, Toxic
    • Indications & usage section, Contraindications section, Warnings section, Precautions section
    • source: PHONT
  • HIV
    • Indications & usage section
    • source: PHONT
  • Leukemia
    • Indications & usage section, Precautions section
    • source: PHONT
  • Toxic liver disease
    • Adverse reactions section, Precautions section
    • source: PHONT
  • Tuberculosis
    • Indications & usage section, Warnings section, Precautions section
    • source: PHONT

PharmGKB contains no Clinical Variants that meet the highest level of criteria.

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 isoniazid

Gene ? Variant?
(147)
Alternate Names ? Chemicals ? Alleles ?
(+ chr strand)
Function ? Amino Acid?
Translation
No VIP available No VIP available VA CYP2E1 *1A N/A N/A N/A
No VIP available No VIP available VA CYP2E1 *5B N/A N/A N/A
No VIP available No VIP available VA CYP2E1 *6 N/A N/A N/A
No VIP available CA No VIP available GSTM1 non-null N/A N/A N/A
No VIP available CA VA GSTM1 null N/A N/A N/A
No VIP available CA No VIP available GSTT1 non-null N/A N/A N/A
No VIP available CA VA GSTT1 null N/A N/A N/A
No VIP available No VIP available VA HLA-DQA1 *01:02:01:01 N/A N/A N/A
No VIP available No VIP available VA HLA-DQB1 *02:01:01 N/A N/A N/A
No VIP available CA VA NAT2 *4 N/A N/A N/A
No VIP available CA VA NAT2 *5 N/A N/A N/A
No VIP available No VIP available VA NAT2 *5A N/A N/A N/A
No VIP available No VIP available VA NAT2 *5B N/A N/A N/A
No VIP available No VIP available VA NAT2 *5C N/A N/A N/A
No VIP available No VIP available VA NAT2 *5D N/A N/A N/A
No VIP available CA VA NAT2 *6 N/A N/A N/A
No VIP available No VIP available VA NAT2 *6A N/A N/A N/A
No VIP available No VIP available VA NAT2 *6B N/A N/A N/A
No VIP available No VIP available VA NAT2 *6J N/A N/A N/A
No VIP available No VIP available VA NAT2 *6O N/A N/A N/A
No VIP available CA VA NAT2 *7 N/A N/A N/A
No VIP available No VIP available VA NAT2 *7A N/A N/A N/A
No VIP available No VIP available VA NAT2 *7B N/A N/A N/A
No VIP available No VIP available VA NAT2 *7G N/A N/A N/A
No VIP available CA No VIP available NAT2 *12 N/A N/A N/A
No VIP available No VIP available VA NAT2 *12A N/A N/A N/A
No VIP available CA VA NAT2 *13 N/A N/A N/A
No VIP available No VIP available VA NAT2 *13A N/A N/A N/A
No VIP available CA VA NAT2 *14 N/A N/A N/A
No VIP available No VIP available VA NAT2 *14A N/A N/A N/A
No VIP available No VIP available VA NAT2 *14B N/A N/A N/A
No VIP available No VIP available VA NAT2 *19 N/A N/A N/A
No VIP available CA VA STAT3 CTA N/A N/A N/A
No VIP available CA VA STAT3 TCG N/A N/A N/A
No VIP available CA VA STAT3 TTA N/A N/A N/A
No VIP available No Clinical Annotations available VA
NAT2 slow acetylator N/A N/A N/A
No VIP available CA VA
rs1041983 NC_000008.10:g.18257795C>T, NC_000008.11:g.18400285C>T, NG_012246.1:g.14041C>T, NM_000015.2:c.282C>T, NP_000006.2:p.Tyr94=, XM_011544358.1:c.282C>T, XP_011542660.1:p.Tyr94=, rs17845484, rs17858364, rs59855457
C > T
SNP
Y94Y
No VIP available No Clinical Annotations available VA
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 No Clinical Annotations available VA
rs1057910 NC_000010.10:g.96741053A=, NC_000010.10:g.96741053A>C, NC_000010.11:g.94981296A=, NC_000010.11:g.94981296A>C, NG_008385.1:g.47639A=, NG_008385.1:g.47639A>C, NM_000771.3:c.1075A=, NM_000771.3:c.1075A>C, NP_000762.2:p.Ile359=, NP_000762.2:p.Ile359Leu, XM_005269575.1:c.1075A=, XM_005269575.1:c.1075A>C, XP_005269632.1:p.Ile359=, XP_005269632.1:p.Ile359Leu, rs17847042, rs3198471, rs61212474
A > C
SNP
I359L
No VIP available No Clinical Annotations available VA
rs1080983 NC_000022.10:g.42528568T=, NC_000022.10:g.42528568T>C, NC_000022.11:g.42132561C=, NC_000022.11:g.42132561C>T, NG_008376.3:g.2431G=, NG_008376.3:g.2431G>A, NM_000106.5:c.-1770A>G, NM_000106.5:c.-1770G>A, NM_001025161.2:c.-1770A>G, NM_001025161.2:c.-1770G>A, NT_187682.1:g.54907T=, NT_187682.1:g.54907T>C, NW_004504305.1:g.54891C=, NW_004504305.1:g.54891C>T, NW_009646208.1:g.18129C=, NW_009646208.1:g.18129C>T, XM_005278353.1:c.-1773A>G, XM_005278353.1:c.-1773G>A, XM_011529966.1:c.-1770A>G, XM_011529966.1:c.-1770G>A, XM_011529967.1:c.-1045-725A>G, XM_011529967.1:c.-1045-725G>A, XM_011529968.1:c.-1770A>G, XM_011529968.1:c.-1770G>A, XM_011529969.1:c.-1228A>G, XM_011529969.1:c.-1228G>A, XM_011529970.1:c.-1770A>G, XM_011529970.1:c.-1770G>A, XM_011529971.1:c.-1228A>G, XM_011529971.1:c.-1228G>A, XM_011529972.1:c.-1770A>G, XM_011529972.1:c.-1770G>A, XM_011547750.1:c.-1233A>G, XM_011547750.1:c.-1233G>A, XM_011547756.1:c.42+2343C>T, XM_011547756.1:c.42+2343T>C, XR_430455.2:n.836C>T, XR_430455.2:n.836T>C, XR_952536.1:n.122C=, XR_952536.1:n.122C>T, XR_952537.1:n.122C=, XR_952537.1:n.122C>T, XR_952538.1:n.122C=, XR_952538.1:n.122C>T, XR_952539.1:n.40+371C>T, XR_952539.1:n.40+371T>C, XR_952540.1:n.-1213C>T, XR_952540.1:n.-1213T>C, XR_952745.1:n.-618A>G, XR_952745.1:n.-618G>A, rs57121857
T > C
SNP
No VIP available No Clinical Annotations available VA
rs1080989 NC_000022.10:g.42527793C=, NC_000022.10:g.42527793C>T, NC_000022.11:g.42131791C=, NC_000022.11:g.42131791C>T, NG_008376.3:g.3201G=, NG_008376.3:g.3201G>A, NM_000106.5:c.-1000A>G, NM_000106.5:c.-1000G>A, NM_001025161.2:c.-1000A>G, NM_001025161.2:c.-1000G>A, NT_187682.1:g.54132C=, NT_187682.1:g.54132C>T, NW_004504305.1:g.54118T=, NW_004504305.1:g.54118T>C, NW_009646208.1:g.17357T=, NW_009646208.1:g.17357T>C, XM_005278353.1:c.-1000A>G, XM_005278353.1:c.-1000G>A, XM_011529966.1:c.-1000G=, XM_011529966.1:c.-1000G>A, XM_011529967.1:c.-1000G=, XM_011529967.1:c.-1000G>A, XM_011529968.1:c.-1000G=, XM_011529968.1:c.-1000G>A, XM_011529969.1:c.-458G=, XM_011529969.1:c.-458G>A, XM_011529970.1:c.-1000G=, XM_011529970.1:c.-1000G>A, XM_011529971.1:c.-458G=, XM_011529971.1:c.-458G>A, XM_011529972.1:c.-1000G=, XM_011529972.1:c.-1000G>A, XM_011547750.1:c.-458G=, XM_011547750.1:c.-458G>A, XM_011547756.1:c.42+1568C>T, XM_011547756.1:c.42+1568T>C, XR_430455.2:n.329-263C>T, XR_430455.2:n.329-263T>C, XR_952536.1:n.-652C>T, XR_952536.1:n.-652T>C, XR_952537.1:n.-652C>T, XR_952537.1:n.-652T>C, XR_952538.1:n.-652C>T, XR_952538.1:n.-652T>C, XR_952539.1:n.-363C>T, XR_952539.1:n.-363T>C, XR_952540.1:n.-1986C>T, XR_952540.1:n.-1986T>C, XR_952745.1:n.158G=, XR_952745.1:n.158G>A
C > T
SNP
No VIP available CA VA
rs11080344 NC_000017.10:g.26104511T>C, NC_000017.11:g.27777485T>C, NG_011470.1:g.28045A>G, NM_000625.4:c.1281+1205A>G, XM_011524859.1:c.1281+1205A>G, XM_011524860.1:c.1278+1205A>G, XM_011524861.1:c.1281+1205A>G, XM_011524862.1:c.615+1205A>G, rs58212720
T > C
SNP
No VIP available No Clinical Annotations available VA
rs11125883 NC_000002.11:g.61710573A>C, NC_000002.12:g.61483438A>C, NM_003400.3:c.2678-347T>G, XM_005264544.1:c.2633-347T>G, XM_005264545.1:c.2480-347T>G, XM_005264546.1:c.2285-347T>G, XM_006712094.2:c.2678-347T>G, XM_011533097.1:c.2678-347T>G, XM_011533098.1:c.2543-347T>G, XM_011533099.1:c.2480-347T>G, rs58222853
A > C
SNP
VIP No Clinical Annotations available No Variant Annotations available
rs1208 NC_000008.10:g.18258316G=, NC_000008.10:g.18258316G>A, NC_000008.11:g.18400806G=, NC_000008.11:g.18400806G>A, NG_012246.1:g.14562G=, NG_012246.1:g.14562G>A, NM_000015.2:c.803G=, NM_000015.2:c.803G>A, NP_000006.2:p.Arg268=, NP_000006.2:p.Arg268Lys, XM_011544358.1:c.803G=, XM_011544358.1:c.803G>A, XP_011542660.1:p.Arg268=, XP_011542660.1:p.Arg268Lys, rs17126586, rs17845485, rs17858365, rs3181478, rs52821724, rs56599719, rs58999469
G > A
SNP
R268K
rs1495741 NC_000008.10:g.18272881G>A, NC_000008.11:g.18415371G>A, rs57451543
G > A
SNP
No VIP available No Clinical Annotations available VA
rs1524107 NC_000007.13:g.22768219C>T, NC_000007.14:g.22728600C>T, NG_011640.1:g.6454C>T, NM_000600.4:c.211-93C>T, NM_001318095.1:c.-18-93C>T, NR_131935.1:n.-980G>A, XM_005249745.1:c.373-93C>T, XM_005249745.3:c.373-93C>T, XM_005249746.1:c.-18-93C>T, XM_011515390.1:c.211-93C>T, XM_011515391.1:c.-18-93C>T
C > T
SNP
No VIP available CA VA
rs1695 NC_000011.10:g.67585218A>G, NC_000011.9:g.67352689A>G, NG_012075.1:g.6624A>G, NM_000852.3:c.313A>G, NP_000843.1:p.Ile105Val, XM_005273958.1:c.313A>G, XP_005274015.1:p.Ile105Val, rs1138257, rs11553891, rs17353321, rs17856342, rs2230827, rs4609, rs56971933, rs947894
A > G
SNP
I105V
No VIP available No Clinical Annotations available VA
rs1799929 NC_000008.10:g.18257994C>T, NC_000008.11:g.18400484C>T, NG_012246.1:g.14240C>T, NM_000015.2:c.481C>T, NP_000006.2:p.Leu161=, XM_011544358.1:c.481C>T, XP_011542660.1:p.Leu161=, rs17595342, rs4646268, rs58882350, rs60310310
C > T
SNP
L161L
rs1799930 NC_000008.10:g.18258103G>A, NC_000008.11:g.18400593G>A, NG_012246.1:g.14349G>A, NM_000015.2:c.590G>A, NP_000006.2:p.Arg197Gln, XM_011544358.1:c.590G>A, XP_011542660.1:p.Arg197Gln, rs17517027, rs17856496, rs4646269, rs60190029, rs61467963
G > A
SNP
R197Q
No VIP available CA VA
rs1799931 NC_000008.10:g.18258370G>A, NC_000008.11:g.18400860G>A, NG_012246.1:g.14616G>A, NM_000015.2:c.857G>A, NP_000006.2:p.Gly286Glu, XM_011544358.1:c.857G>A, XP_011542660.1:p.Gly286Glu, rs17693862, rs4646270, rs52802193, rs58803786
G > A
SNP
G286E
No VIP available CA VA
rs1800629 NC_000006.11:g.31543031G=, NC_000006.11:g.31543031G>A, NC_000006.12:g.31575254G=, NC_000006.12:g.31575254G>A, NG_007462.1:g.4682G=, NG_007462.1:g.4682G>A, NG_012010.1:g.8156G=, NG_012010.1:g.8156G>A, NM_000594.3:c.-488A>G, NM_000594.3:c.-488G>A, NT_113891.2:g.3052647A=, NT_113891.2:g.3052647A>G, NT_113891.3:g.3052541A=, NT_113891.3:g.3052541A>G, NT_167245.1:g.2828572G=, NT_167245.1:g.2828572G>A, NT_167245.2:g.2822987G=, NT_167245.2:g.2822987G>A, NT_167246.1:g.2885915G=, NT_167246.1:g.2885915G>A, NT_167246.2:g.2880295G=, NT_167246.2:g.2880295G>A, NT_167247.1:g.2922737G=, NT_167247.1:g.2922737G>A, NT_167247.2:g.2917152G=, NT_167247.2:g.2917152G>A, NT_167248.1:g.2836669G=, NT_167248.1:g.2836669G>A, NT_167248.2:g.2831073G=, NT_167248.2:g.2831073G>A, NT_167249.1:g.2873832G=, NT_167249.1:g.2873832G>A, NT_167249.2:g.2874534G=, NT_167249.2:g.2874534G>A, rs116610137, rs117441802, rs148958203, rs3091256, rs36205298, rs4134777, rs59729336
G > A
SNP
No VIP available No Clinical Annotations available VA
rs1801280 NC_000008.10:g.18257854T>C, NC_000008.11:g.18400344T>C, NG_012246.1:g.14100T>C, NM_000015.2:c.341T>C, NP_000006.2:p.Ile114Thr, XM_011544358.1:c.341T>C, XP_011542660.1:p.Ile114Thr, rs4134724, rs56935242
T > C
SNP
I114T
No VIP available No Clinical Annotations available VA
rs2003569 NC_000002.11:g.234667937G>A, NC_000002.12:g.233759291G>A, NG_002601.2:g.174548G>A, NG_033238.1:g.4019G>A, NM_000463.2:c.-997G>A, NM_001072.3:c.862-7743G>A, NM_007120.2:c.868-7743G>A, NM_019075.2:c.856-7743G>A, NM_019076.4:c.856-7743G>A, NM_019077.2:c.856-7743G>A, NM_019078.1:c.868-7743G>A, NM_019093.2:c.868-7743G>A, NM_021027.2:c.856-7743G>A, NM_205862.1:c.61-7743G>A, XR_241238.1:n.924-7743G>A, XR_241239.1:n.-975G>A, XR_241240.1:n.1023-7743G>A, XR_241241.1:n.942-7743G>A, rs17286591
G > A
SNP
No VIP available No Clinical Annotations available VA
rs2008584 NC_000002.11:g.234637015A>G, NC_000002.12:g.233728369A>G, NG_002601.2:g.143626A>G, NM_001072.3:c.861+34504A>G, NM_007120.2:c.867+8682A>G, NM_019075.2:c.856-38665A>G, NM_019076.4:c.856-38665A>G, NM_019077.2:c.856-38665A>G, NM_019078.1:c.867+14511A>G, NM_019093.2:c.-758A>G, NM_021027.2:c.856-38665A>G, NM_205862.1:c.60+34504A>G, XR_241238.1:n.923+8682A>G, XR_241240.1:n.1022+34504A>G, XR_241241.1:n.942-38665A>G, rs16849646, rs17869157, rs55772651, rs60783229, rs62191914
A > G
SNP
No VIP available No Clinical Annotations available VA
rs2031920 NC_000010.10:g.135339845C>T, NC_000010.11:g.133526341C>T, NG_008383.1:g.3979C>T, NM_000773.3:c.-1055C>T, XM_005252665.1:c.-512C>T, rs3813868
C > T
SNP
No VIP available No Clinical Annotations available VA
rs2066992 NC_000007.13:g.22768249G>T, NC_000007.14:g.22728630G>T, NG_011640.1:g.6484G>T, NM_000600.4:c.211-63G>T, NM_001318095.1:c.-18-63G>T, NR_131935.1:n.-1010C>A, XM_005249745.1:c.373-63G>T, XM_005249745.3:c.373-63G>T, XM_005249746.1:c.-18-63G>T, XM_011515390.1:c.211-63G>T, XM_011515391.1:c.-18-63G>T, rs17147236, rs58064907
G > T
SNP
No VIP available No Clinical Annotations available VA
rs2069837 NC_000007.13:g.22768027A>G, NC_000007.14:g.22728408A>G, NG_011640.1:g.6262A>G, NM_000600.4:c.211-285A>G, NM_001318095.1:c.-18-285A>G, NR_131935.1:n.-788T>C, XM_005249745.1:c.373-285A>G, XM_005249745.3:c.373-285A>G, XM_005249746.1:c.-18-285A>G, XM_011515390.1:c.211-285A>G, XM_011515391.1:c.-18-285A>G, rs111176548, rs16873259, rs3779040, rs56908115
A > G
SNP
No VIP available No Clinical Annotations available VA
rs2070401 NC_000021.8:g.30715485A>G, NC_000021.9:g.29343164A>G, NG_029658.1:g.49266A>G, NM_001186.3:c.*331A>G, NM_206866.2:c.*331A>G, NR_027655.2:n.1956-8470A>G, XM_005261012.1:c.*331A>G, XM_005261013.1:c.*331A>G, XM_005261014.1:c.*331A>G, XR_244286.1:n.2072-8470A>G
A > G
SNP
No VIP available No Clinical Annotations available VA
rs2070672 NC_000010.10:g.135340548A>G, NC_000010.11:g.133527044A>G, NG_008383.1:g.4682A>G, NM_000773.3:c.-352A>G, XM_005252665.1:c.21+171A>G, rs58043512
A > G
SNP
No VIP available No Clinical Annotations available VA
rs2070673 NC_000010.10:g.135340567A>T, NC_000010.11:g.133527063A>T, NG_008383.1:g.4701A>T, NM_000773.3:c.-333A>T, XM_005252665.1:c.21+190A>T
A > T
SNP
No VIP available No Clinical Annotations available VA
rs2227956 NC_000006.11:g.31778272G=, NC_000006.11:g.31778272G>A, NC_000006.12:g.31810495G=, NC_000006.12:g.31810495G>A, NG_011855.1:g.9564C=, NG_011855.1:g.9564C>T, NM_005527.3:c.1478C=, NM_005527.3:c.1478C>T, NP_005518.3:p.Thr493=, NP_005518.3:p.Thr493Met, NT_113891.2:g.3287853A=, NT_113891.2:g.3287853A>G, NT_113891.3:g.3287747A=, NT_113891.3:g.3287747A>G, NT_167244.1:g.3093033A=, NT_167244.1:g.3093033A>G, NT_167244.2:g.3143117A=, NT_167244.2:g.3143117A>G, NT_167245.1:g.3063859G=, NT_167245.1:g.3063859G>A, NT_167245.2:g.3058274G=, NT_167245.2:g.3058274G>A, NT_167248.1:g.3071920A=, NT_167248.1:g.3071920A>G, NT_167248.2:g.3066324A=, NT_167248.2:g.3066324A>G, XM_005249070.1:c.1670C=, XM_005249070.1:c.1670C>T, XM_005249070.3:c.1670C=, XM_005249070.3:c.1670C>T, XM_005249071.1:c.1478C=, XM_005249071.1:c.1478C>T, XM_005249072.1:c.1478C=, XM_005249072.1:c.1478C>T, XM_005249073.1:c.1478C=, XM_005249073.1:c.1478C>T, XM_005249073.2:c.1478C=, XM_005249073.2:c.1478C>T, XM_005249074.1:c.1478C=, XM_005249074.1:c.1478C>T, XM_005272813.1:c.1670T=, XM_005272813.1:c.1670T>C, XM_005272814.1:c.1478T=, XM_005272814.1:c.1478T>C, XM_005272815.1:c.1478T=, XM_005272815.1:c.1478T>C, XM_005272816.1:c.1478T=, XM_005272816.1:c.1478T>C, XM_005272816.2:c.1478T=, XM_005272816.2:c.1478T>C, XM_005272817.1:c.1478T=, XM_005272817.1:c.1478T>C, XM_005274858.1:c.1478T=, XM_005274858.1:c.1478T>C, XM_005274859.1:c.1670T=, XM_005274859.1:c.1670T>C, XM_005274859.3:c.1670T=, XM_005274859.3:c.1670T>C, XM_005274860.1:c.1478T=, XM_005274860.1:c.1478T>C, XM_005274861.1:c.1478T=, XM_005274861.1:c.1478T>C, XM_005274861.2:c.1478T=, XM_005274861.2:c.1478T>C, XM_005274862.1:c.1478T=, XM_005274862.1:c.1478T>C, XM_005274970.1:c.1670C=, XM_005274970.1:c.1670C>T, XM_005274970.3:c.1670C=, XM_005274970.3:c.1670C>T, XM_005274971.1:c.1478C=, XM_005274971.1:c.1478C>T, XM_005274972.1:c.1478C=, XM_005274972.1:c.1478C>T, XM_005274973.1:c.1478C=, XM_005274973.1:c.1478C>T, XM_005274973.2:c.1478C=, XM_005274973.2:c.1478C>T, XM_005274974.1:c.1478C=, XM_005274974.1:c.1478C>T, XM_005275398.1:c.1478T=, XM_005275398.1:c.1478T>C, XM_005275399.1:c.1670T=, XM_005275399.1:c.1670T>C, XM_005275400.1:c.1478T=, XM_005275400.1:c.1478T>C, XM_005275401.1:c.1478T=, XM_005275401.1:c.1478T>C, XM_005275401.2:c.1478T=, XM_005275401.2:c.1478T>C, XM_005275402.1:c.1478T=, XM_005275402.1:c.1478T>C, XM_011514566.1:c.1478C=, XM_011514566.1:c.1478C>T, XM_011546311.1:c.1478T=, XM_011546311.1:c.1478T>C, XM_011547246.1:c.1478T=, XM_011547246.1:c.1478T>C, XM_011547247.1:c.1670T=, XM_011547247.1:c.1670T>C, XM_011547652.1:c.1478C=, XM_011547652.1:c.1478C>T, XM_011548238.1:c.1478T=, XM_011548238.1:c.1478T>C, XM_011548239.1:c.1670T=, XM_011548239.1:c.1670T>C, XP_005249127.1:p.Thr557=, XP_005249127.1:p.Thr557Met, XP_005249128.1:p.Thr493=, XP_005249128.1:p.Thr493Met, XP_005249129.1:p.Thr493=, XP_005249129.1:p.Thr493Met, XP_005249130.1:p.Thr493=, XP_005249130.1:p.Thr493Met, XP_005249131.1:p.Thr493=, XP_005249131.1:p.Thr493Met, XP_005272870.1:p.Met557=, XP_005272870.1:p.Met557Thr, XP_005272871.1:p.Met493=, XP_005272871.1:p.Met493Thr, XP_005272872.1:p.Met493=, XP_005272872.1:p.Met493Thr, XP_005272873.1:p.Met493=, XP_005272873.1:p.Met493Thr, XP_005272874.1:p.Met493=, XP_005272874.1:p.Met493Thr, XP_005274915.1:p.Met493=, XP_005274915.1:p.Met493Thr, XP_005274916.1:p.Met557=, XP_005274916.1:p.Met557Thr, XP_005274917.1:p.Met493=, XP_005274917.1:p.Met493Thr, XP_005274918.1:p.Met493=, XP_005274918.1:p.Met493Thr, XP_005274919.1:p.Met493=, XP_005274919.1:p.Met493Thr, XP_005275027.1:p.Thr557=, XP_005275027.1:p.Thr557Met, XP_005275028.1:p.Thr493=, XP_005275028.1:p.Thr493Met, XP_005275029.1:p.Thr493=, XP_005275029.1:p.Thr493Met, XP_005275030.1:p.Thr493=, XP_005275030.1:p.Thr493Met, XP_005275031.1:p.Thr493=, XP_005275031.1:p.Thr493Met, XP_005275455.1:p.Met493=, XP_005275455.1:p.Met493Thr, XP_005275456.1:p.Met557=, XP_005275456.1:p.Met557Thr, XP_005275457.1:p.Met493=, XP_005275457.1:p.Met493Thr, XP_005275458.1:p.Met493=, XP_005275458.1:p.Met493Thr, XP_005275459.1:p.Met493=, XP_005275459.1:p.Met493Thr, XP_011512868.1:p.Thr493=, XP_011512868.1:p.Thr493Met, XP_011544613.1:p.Met493=, XP_011544613.1:p.Met493Thr, XP_011545548.1:p.Met493=, XP_011545548.1:p.Met493Thr, XP_011545549.1:p.Met557=, XP_011545549.1:p.Met557Thr, XP_011545954.1:p.Thr493=, XP_011545954.1:p.Thr493Met, XP_011546540.1:p.Met493=, XP_011546540.1:p.Met493Thr, XP_011546541.1:p.Met557=, XP_011546541.1:p.Met557Thr, rs116591280, rs117465227, rs148468928, rs35842419, rs386561656, rs52829371, rs57160046
G > A
SNP
T493M
No VIP available No Clinical Annotations available VA
rs3755319 NC_000002.11:g.234667582A=, NC_000002.11:g.234667582A>C, NC_000002.12:g.233758936A=, NC_000002.12:g.233758936A>C, NG_002601.2:g.174193A=, NG_002601.2:g.174193A>C, NG_033238.1:g.3664A=, NG_033238.1:g.3664A>C, NM_000463.2:c.-1352A=, NM_000463.2:c.-1352A>C, NM_001072.3:c.862-8098A=, NM_001072.3:c.862-8098A>C, NM_007120.2:c.868-8098A=, NM_007120.2:c.868-8098A>C, NM_019075.2:c.856-8098A=, NM_019075.2:c.856-8098A>C, NM_019076.4:c.856-8098A=, NM_019076.4:c.856-8098A>C, NM_019077.2:c.856-8098A=, NM_019077.2:c.856-8098A>C, NM_019078.1:c.868-8098A=, NM_019078.1:c.868-8098A>C, NM_019093.2:c.868-8098A=, NM_019093.2:c.868-8098A>C, NM_021027.2:c.856-8098A=, NM_021027.2:c.856-8098A>C, NM_205862.1:c.61-8098A=, NM_205862.1:c.61-8098A>C, XR_241238.1:n.924-8098A=, XR_241238.1:n.924-8098A>C, XR_241239.1:n.-1330A=, XR_241239.1:n.-1330A>C, XR_241240.1:n.1023-8098A=, XR_241240.1:n.1023-8098A>C, XR_241241.1:n.942-8098A=, XR_241241.1:n.942-8098A>C, rs35208194, rs36208045, rs57256426
A > C
SNP
No VIP available No Clinical Annotations available VA
rs3813867 NC_000010.10:g.135339605G>C, NC_000010.11:g.133526101G>C, NG_008383.1:g.3739G>C, NM_000773.3:c.-1295G>C, XM_005252665.1:c.-752G>C, rs57822387
G > C
SNP
No VIP available No Clinical Annotations available VA
rs3814637 NC_000010.10:g.96521045C>T, NC_000010.11:g.94761288C>T, NG_008384.2:g.3583C>T, NM_000769.2:c.-1418C>T, rs11565103, rs117910415, rs17878465, rs58858251
C > G
C > T
SNP
No VIP available No Clinical Annotations available VA
rs3815583 NC_000016.10:g.55833130A=, NC_000016.10:g.55833130A>C, NC_000016.9:g.55867042A=, NC_000016.9:g.55867042A>C, NG_012057.1:g.5034T=, NG_012057.1:g.5034T>G, NM_001025194.1:c.-75T=, NM_001025194.1:c.-75T>G, NM_001025195.1:c.-75T=, NM_001025195.1:c.-75T>G, NM_001266.4:c.-75T=, NM_001266.4:c.-75T>G, NW_003315945.1:g.57035C=, NW_003315945.1:g.57035C>A, XM_005255774.1:c.-75T=, XM_005255774.1:c.-75T>G, XM_005276867.1:c.-75G=, XM_005276867.1:c.-75G>T, XM_011522816.1:c.-75T=, XM_011522816.1:c.-75T>G, XM_011546995.1:c.-75G=, XM_011546995.1:c.-75G>T, rs11076115, rs118051681
A > C
SNP
No VIP available No Clinical Annotations available VA
rs4147581
C > G
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
rs4149032 NC_000012.11:g.21317791C>T, NC_000012.12:g.21164857C>T, NG_011745.1:g.38664C>T, NM_006446.4:c.85-7793C>T, rs57192307
C > T
SNP
rs4646244 NC_000008.10:g.18247718T>A, NC_000008.11:g.18390208T>A, NG_012246.1:g.3964T>A, NM_000015.2:c.-1144T>A, rs17595300
T > A
SNP
No VIP available No Clinical Annotations available VA
rs4646267 NC_000008.10:g.18247913A>G, NC_000008.11:g.18390403A>G, NG_012246.1:g.4159A>G, NM_000015.2:c.-949A>G
A > G
SNP
No VIP available No Clinical Annotations available VA
rs4646903 NC_000015.10:g.74719300A>G, NC_000015.9:g.75011641A>G, NG_008431.1:g.1759A>G, NM_000499.3:c.*1189T>C, NM_000499.4:c.*1189T>C, NM_000499.4:c.*947+242T>C, NM_001319216.1:c.*1189T>C, NM_001319216.1:c.*947+242T>C, NM_001319217.1:c.*1189T>C, NM_001319217.1:c.*947+242T>C, XM_005254185.1:c.*1189T>C, XM_005254186.1:c.*1189T>C, XM_005254187.1:c.*1189T>C, XM_005254188.1:c.*1189T>C, XM_005254189.1:c.*1189T>C, rs116877783, rs17861083, rs5030838
A > G
A > T
SNP
No VIP available No Clinical Annotations available VA
rs4720833 NC_000007.13:g.1574403A>G, NC_000007.14:g.1534767A>G, NM_002360.3:c.-45+3869A>G, XM_005249851.1:c.-2609A>G, XR_108727.1:n.114T>C, rs10359168, rs57926061
A > G
SNP
No VIP available No Clinical Annotations available VA
rs4918758 NC_000010.10:g.96697252T>C, NC_000010.11:g.94937495T>C, NG_008385.1:g.3838T>C, NM_000771.3:c.-1188T>C, XM_005269575.1:c.-1188T>C, rs17110346
T > C
SNP
No VIP available No Clinical Annotations available VA
rs4986893 NC_000010.10:g.96540410G>A, NC_000010.11:g.94780653G>A, NG_008384.2:g.22948G>A, NM_000769.2:c.636G>A, NP_000760.1:p.Trp212Ter, rs52827375, rs57081121
G > A
SNP
W212*
No VIP available No Clinical Annotations available VA
rs6413432 NC_000010.10:g.135348544T>A, NC_000010.11:g.133535040T>A, NG_008383.1:g.12678T>A, NM_000773.3:c.967+1143T>A, XM_005252665.1:c.1027+1143T>A
T > A
SNP
No VIP available No Clinical Annotations available VA
rs6431625 NC_000002.11:g.234637912T>C, NC_000002.12:g.233729266T>C, NG_002601.2:g.144523T>C, NM_001072.3:c.861+35401T>C, NM_007120.2:c.867+9579T>C, NM_019075.2:c.856-37768T>C, NM_019076.4:c.856-37768T>C, NM_019077.2:c.856-37768T>C, NM_019078.1:c.867+15408T>C, NM_019093.2:c.140T>C, NM_021027.2:c.856-37768T>C, NM_205862.1:c.60+35401T>C, NP_061966.1:p.Val47Ala, XR_241238.1:n.923+9579T>C, XR_241240.1:n.1022+35401T>C, XR_241241.1:n.942-37768T>C, rs17864457, rs61313666
T > C
SNP
V47A
No VIP available No Clinical Annotations available VA
rs9332096 NC_000010.10:g.96696875C>T, NC_000010.11:g.94937118C>T, NG_008385.1:g.3461C>T, NM_000771.3:c.-1565C>T, XM_005269575.1:c.-1565C>T
C > T
SNP
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 147

Overview

Generic Names
  • HIA
  • Hydrazid
  • Hydrazide
  • INH
  • Isohydrazide
  • Isonicotinhydrazid
  • Isonicotinic acid hydrazide
  • Isonicotinic hydrazide
  • Isonicotinohydrazide
  • Isonicotinoyl hydrazide
  • Isonicotinyl hydrazide
  • Isonicotinyl hydrazine
  • Isonicotinylhydrazine
Trade Names
  • Andrazide
  • Antimicina
  • Antituberkulosum
  • Armacide
  • Armazid
  • Armazide
  • Atcotibine
  • Azuren
  • Bacillin
  • Cedin
  • Cemidon
  • Chemiazid
  • Chemidon
  • Cortinazine
  • Cotinazin
  • Cotinizin
  • Defonin
  • Dibutin
  • Diforin
  • Dinacrin
  • Ditubin
  • Ebidene
  • Eralon
  • Ertuban
  • Eutizon
  • Evalon
  • FSR 3
  • Fimalene
  • GINK
  • Hidranizil
  • Hidrasonil
  • Hidrulta
  • Hidrun
  • Hycozid
  • Hyozid
  • Hyzyd
  • Ido-tebin
  • Idrazil
  • Inah
  • Inizid
  • Iscotin
  • Isidrina
  • Ismazide
  • Isobicina
  • Isocid
  • Isocidene
  • Isocotin
  • Isolyn
  • Isonerit
  • Isonex
  • Isoniacid
  • Isoniazid SA
  • Isoniazide
  • Isonicazide
  • Isonicid
  • Isonico
  • Isonicotan
  • Isonicotil
  • Isonide
  • Isonidrin
  • Isonikazid
  • Isonilex
  • Isonin
  • Isonindon
  • Isonirit
  • Isoniton
  • Isonizide
  • Isopyrin
  • Isotamine
  • Isotebe
  • Isotebezid
  • Isotinyl
  • Isozide
  • Isozyd
  • Laniazid
  • Laniozid
  • Mybasan
  • Neo-Tizide
  • Neoteben
  • Neoxin
  • Neumandin
  • Nevin
  • Niadrin
  • Nicazide
  • Nicetal
  • Nicizina
  • Niconyl
  • Nicotibina
  • Nicotibine
  • Nicotisan
  • Nicozide
  • Nidaton
  • Nidrazid
  • Nikozid
  • Niplen
  • Nitadon
  • Nydrazid
  • Nyscozid
  • Pelazid
  • Percin
  • Phthisen
  • Pycazide
  • Pyreazid
  • Pyricidin
  • Pyridicin
  • Pyrizidin
  • Raumanon
  • Razide
  • Retozide
  • Rifamate
  • Rimicid
  • Rimifon
  • Rimiphone
  • Rimitsid
  • Robiselin
  • Robisellin
  • Roxifen
  • Sanohidrazina
  • Sauterazid
  • Sauterzid
  • Stanozide
  • TB-Phlogin
  • TB-Razide
  • TB-Vis
  • Tebecid
  • Tebenic
  • Tebexin
  • Tebilon
  • Tebos
  • Teebaconin
  • Tekazin
  • Tibazide
  • Tibemid
  • Tibison
  • Tibivis
  • Tibusan
  • Tubazid
  • Tubazide
  • Tubeco
  • Tubecotubercid
  • Tuberian
  • Tubicon
  • Tubilysin
  • Tubomel
  • Tyvid
  • Unicocyde
  • Unicozyde
  • Vazadrine
  • Vederon
  • Zidafimia
  • Zinadon
  • Zonazide
Brand Mixture Names
  • Isotamine B 300 (Isoniazid + Pyridoxine Hydrochloride)
  • Rifater (Isoniazid + Pyrazinamide + Rifampin)

PharmGKB Accession Id

PA450112

Type(s):

Drug

Description

Antibacterial agent used primarily as a tuberculostatic. It remains the treatment of choice for tuberculosis.

Source: Drug Bank

Indication

For the treatment of all forms of tuberculosis in which organisms are susceptible.

Source: Drug Bank

Other Vocabularies

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Isoniazid is a prodrug and must be activated by bacterial catalase. Specficially, activation is associated with reduction of the mycobacterial ferric KatG catalase-peroxidase by hydrazine and reaction with oxygen to form an oxyferrous enzyme complex. Once activated, isoniazid inhibits the synthesis of mycoloic acids, an essential component of the bacterial cell wall. At therapeutic levels isoniazid is bacteriocidal against actively growing intracellular and extracellular Mycobacterium tuberculosis organisms. Specifically isoniazid inhibits InhA, the enoyl reductase from Mycobacterium tuberculosis, by forming a covalent adduct with the NAD cofactor. It is the INH-NAD adduct that acts as a slow, tight-binding competitive inhibitor of InhA.

Source: Drug Bank

Pharmacology

Isoniazid is a bactericidal agent active against organisms of the genus Mycobacterium, specifically M. tuberculosis, M. bovis and M. kansasii. It is a highly specific agent, ineffective against other microorganisms. Isoniazid is bactericidal to rapidly-dividing mycobacteria, but is bacteriostatic if the mycobacterium is slow-growing.

Source: Drug Bank

Food Interaction

Avoid alcohol.|Avoid aged foods (cheese, red wine), pickled foods, cured foods (bacon/ham), chocolate, fava beans, beer, unless approved by your physician.|Do not take calcium, aluminum, magnesium or Iron supplements within 2 hours of taking this medication.|Increase dietary intake of magnesium, folate, vitamin B6, B12, and/or consider taking a multivitamin.|Take on empty stomach: 1 hour before or 2 hours after meals.|Take with a full glass of water.

Source: Drug Bank

Absorption, Distribution, Metabolism, Elimination & Toxicity

Biotransformation

Primarily hepatic. Isoniazid is acetylated by N -acetyl transferase to N -acetylisoniazid; it is then biotransformed to isonicotinic acid and monoacetylhydrazine. Monoacetylhydrazine is associated with hepatotoxicity via formation of a reactive intermediate metabolite when N-hydroxylated by the cytochrome P450 mixed oxidase system. The rate of acetylation is genetically determined. Slow acetylators are characterized by a relative lack of hepatic N -acetyltransferase.

Source: Drug Bank

Protein Binding

Very low (0-10%)

Source: Drug Bank

Absorption

Readily absorbed following oral administration; however, may undergo significant first pass metabolism. Absorption and bioavailability are reduced when isoniazid is administered with food.

Source: Drug Bank

Half-Life

Fast acetylators: 0.5 to 1.6 hours. Slow acetylators: 2 to 5 hours.

Source: Drug Bank

Toxicity

LD 50 100 mg/kg (Human, oral). Adverse reactions include rash, abnormal liver function tests, hepatitis, peripheral neuropathy, mild central nervous system (CNS) effects. In vivo, Isoniazid reacts with pyridoxal to form a hydrazone, and thus inhibits generation of pyridoxal phosphate. Isoniazid also combines with pyridoxal phosphate; high doses interfere with the coenzyme function of the latter.

Source: Drug Bank

Route of Elimination

From 50 to 70 percent of a dose of isoniazid is excreted in the urine within 24 hours.

Source: Drug Bank

Chemical Properties

Chemical Formula

C6H7N3O

Source: Drug Bank

Isomeric SMILES

c1cnccc1C(=O)NN

Source: OpenEye

Canonical SMILES

NNC(=O)C1=CC=NC=C1

Source: Drug Bank

Average Molecular Weight

137.1393

Source: Drug Bank

Monoisotopic Molecular Weight

137.058911861

Source: Drug Bank

SMILES

NNC(=O)C1=CC=NC=C1

Source: Drug Bank

InChI String

InChI=1S/C6H7N3O/c7-9-6(10)5-1-3-8-4-2-5/h1-4H,7H2,(H,9,10)

Source: Drug Bank

PharmGKB Curated Pathways

Pathways created internally by PharmGKB based primarily on literature evidence.

  1. Acetaminophen Pathway (therapeutic doses), Pharmacokinetics
    Stylized diagram showing acetaminophen metabolism and transport in the liver.

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
ABAT (source: Drug Bank )

Drug Interactions

Interaction Description
acetaminophen - isoniazid Risk of hepatotoxicity (source: Drug Bank )
aminophylline - isoniazid Isoniazid increases the effect and toxicity of theophhylline (source: Drug Bank )
bromazepam - isoniazid Isoniazid, 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 isoniazid is initiated, discontinued or dose changed. Dosage adjustments may be required. (source: Drug Bank )
carbamazepine - isoniazid Carbamazepine effect is increased as is isoniazid toxicity (source: Drug Bank )
carbamazepine - isoniazid Carbamazepine effect is increased as is isoniazid toxicity (source: Drug Bank )
dantrolene - isoniazid Isoniazid 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 isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
disulfiram - isoniazid Increased risk of CNS adverse efects (source: Drug Bank )
disulfiram - isoniazid Increased risk of CNS adverse efects (source: Drug Bank )
fosphenytoin - isoniazid Isoniazid increases the effect of phenytoin (source: Drug Bank )
isoniazid - acenocoumarol The agent increases the effect of anticoagulant (source: Drug Bank )
isoniazid - acenocoumarol Isoniazid may increase the anticoagulant effect of acenocoumarol. (source: Drug Bank )
isoniazid - acetaminophen Risk of hepatotoxicity (source: Drug Bank )
isoniazid - acetaminophen Risk of hepatotoxicity (source: Drug Bank )
isoniazid - aminophylline Increases the effect and toxicity of theophylline (source: Drug Bank )
isoniazid - anisindione Isoniazid may increase the anticoagulant effect of anisindione. (source: Drug Bank )
isoniazid - carbamazepine Carbamazepine effect is increased as is isoniazid toxicity (source: Drug Bank )
isoniazid - carbamazepine Carbamazepine effect is increased as is isoniazid toxicity (source: Drug Bank )
isoniazid - dicumarol The agent increases the effect of anticoagulant (source: Drug Bank )
isoniazid - dicumarol Isoniazid may increase the anticoagulant effect of dicumarol. (source: Drug Bank )
isoniazid - disulfiram Increased risk of CNS adverse effects (source: Drug Bank )
isoniazid - disulfiram Increased risk of CNS adverse effects (source: Drug Bank )
isoniazid - dyphylline Increases the effect and toxicity of theophylline (source: Drug Bank )
isoniazid - ethotoin Isoniazid increases the effect of phenytoin in 20% of patients (source: Drug Bank )
isoniazid - fosphenytoin Isoniazid increases the effect of phenytoin in 20% of patients (source: Drug Bank )
isoniazid - ketoconazole Isoniazid decreases the effect of ketoconazole (source: Drug Bank )
isoniazid - ketoconazole Isoniazid decreases the effect of ketoconazole (source: Drug Bank )
isoniazid - meperidine Possible episodes of hypotension (source: Drug Bank )
isoniazid - meperidine Possible episodes of hypotension (source: Drug Bank )
isoniazid - mephenytoin Isoniazid increases the effect of phenytoin in 20% of patients (source: Drug Bank )
isoniazid - mephenytoin Isoniazid increases the effect of phenytoin in 20% of patients (source: Drug Bank )
isoniazid - oxtriphylline Increases the effect and toxicity of theophylline (source: Drug Bank )
isoniazid - phenytoin Isoniazid increases the effect of phenytoin in 20% of patients (source: Drug Bank )
isoniazid - phenytoin Isoniazid increases the effect of phenytoin in 20% of patients (source: Drug Bank )
isoniazid - theophylline Increases the effect and toxicity of theophylline (source: Drug Bank )
isoniazid - theophylline Increases the effect and toxicity of theophylline (source: Drug Bank )
isoniazid - warfarin The agent increases the effect of anticoagulant (source: Drug Bank )
isoniazid - warfarin Isoniazid may increase the anticoagulant effect of warfarin. (source: Drug Bank )
ketoconazole - isoniazid Isoniazid decreases the effect of ketoconazole (source: Drug Bank )
ketoconazole - isoniazid Isoniazid decreases the effect of ketoconazole (source: Drug Bank )
meperidine - isoniazid Possible episodes of hypotension (source: Drug Bank )
meperidine - isoniazid Possible episodes of hypotension (source: Drug Bank )
oxtriphylline - isoniazid Isoniazid increases the effect and toxicity of theophylline (source: Drug Bank )
phenytoin - isoniazid Isoniazid increases the effect of phenytoin in 20% of patients (source: Drug Bank )
phenytoin - isoniazid Isoniazid increases the effect of phenytoin in 20% of patients (source: Drug Bank )
tadalafil - isoniazid Isoniazid may reduce the metabolism of Tadalafil. Concomitant therapy should be avoided if possible due to high risk of Tadalafil toxicity. (source: Drug Bank )
tamoxifen - isoniazid Isoniazid may increase the serum concentration of Tamoxifen by decreasing its metabolism and clearance. Isoniazid may also decrease the therapeutic effect of Tamoxifen by decreasing active metabolite production. Monitor for changes in the therapeutic/adverse effects of Tamoxifen if Isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
tamoxifen - isoniazid Isoniazid may increase the serum concentration of Tamoxifen by decreasing its metabolism and clearance. Isoniazid may also decrease the therapeutic effect of Tamoxifen by decreasing active metabolite production. Monitor for changes in the therapeutic/adverse effects of Tamoxifen if Isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
tamsulosin - isoniazid Isoniazid, a CYP3A4/2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP3A4/2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Isoniazid is initiated, discontinued, or dose changed. (source: Drug Bank )
tamsulosin - isoniazid Isoniazid, a CYP3A4/2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP3A4/2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Isoniazid is initiated, discontinued, or dose changed. (source: Drug Bank )
telithromycin - isoniazid Isoniazid may increase the plasma concentration of Telithromycin. Consider alternate therapy or monitor therapeutic/adverse effects. (source: Drug Bank )
teniposide - isoniazid The strong CYP3A4 inhibitor, Isoniazid, 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 Isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
theophylline - isoniazid Isoniazid increases the effect and toxicity of theophylline (source: Drug Bank )
theophylline - isoniazid Isoniazid increases the effect and toxicity of theophylline (source: Drug Bank )
tiagabine - isoniazid The strong CYP3A4 inhibitor, Isoniazid, 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 Isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
tolterodine - isoniazid Isoniazid may decrease the metabolism and clearance of Tolterodine. Adjust Tolterodine dose and monitor for efficacy and toxicity. (source: Drug Bank )
tolterodine - isoniazid Isoniazid may decrease the metabolism and clearance of Tolterodine. Adjust Tolterodine dose and monitor for efficacy and toxicity. (source: Drug Bank )
tramadol - isoniazid Isoniazid may increase Tramadol toxicity by decreasing Tramadol metabolism and clearance. Isoniazid may decrease the effect of Tramadol by decreasing active metabolite production. (source: Drug Bank )
trazodone - isoniazid The CYP3A4 inhibitor, Isoniazid, may increase Trazodone efficacy/toxicity by decreasing Trazodone metabolism and clearance. Consider alternate therapy or monitor for changes in Trazodone efficacy/toxicity if Isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
trazodone - isoniazid The CYP3A4 inhibitor, Isoniazid, may increase Trazodone efficacy/toxicity by decreasing Trazodone metabolism and clearance. Consider alternate therapy or monitor for changes in Trazodone efficacy/toxicity if Isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - isoniazid The strong CYP3A4/CYP2C19 inhibitor, Isoniazide, may decrease the metabolism and clearance of Trimipramine, a CYP3A4/CYP2C19 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
vardenafil - isoniazid Isoniazid, 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 - isoniazid Isoniazid, a CYP3A4 inhibitor, may decrease the metabolism and clearance of Venlafaxine, a CYP3A4 substrate. Monitor for changes in therapeutic/adverse effects of Venlafaxine if Isoniazid is initiated, discontinued, or dose changed. (source: Drug Bank )
verapamil - isoniazid Isoniazid, 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 Isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
vincristine - isoniazid Isoniazid, 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 Isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
vinorelbine - isoniazid Isoniazid, 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 Isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
zolpidem - isoniazid Isoniazid, 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 isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
zonisamide - isoniazid Isoniazid, 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 isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
zopiclone - isoniazid Isoniazid, 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 isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )

Curated Information ?

Relationships from National Drug File - Reference Terminology (NDF-RT)

May Treat
May Prevent
Contraindicated With

Publications related to isoniazid: 110

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NAT2 variants are associated with drug-induced liver injury caused by anti-tuberculosis drugs in Indonesian patients with tuberculosis. Journal of human genetics. 2016. Yuliwulandari Rika, et al. PubMed
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HLA-DQ B1*0201 and A1*0102 Alleles Are Not Responsible for Antituberculosis Drug-Induced Hepatotoxicity Risk in Spanish Population. Frontiers in medicine. 2016. Leiro-Fernández Virginia, et al. PubMed
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Development of a prediction system for anti-tuberculosis drug-induced liver injury in Japanese patients. Human genome variation. 2016. Mushiroda Taisei, et al. PubMed
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Susceptibility of N-acetyltransferase 2 slow acetylators to antituberculosis drug-induced liver injury: a meta-analysis. Pharmacogenomics. 2015. Shi Jing, et al. PubMed
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Genetic Polymorphisms of Glutathione S-Transferase P1 (GSTP1) and the Incidence of Anti-Tuberculosis Drug-Induced Hepatotoxicity. PloS one. 2016. Wu Shouquan, et al. PubMed
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Antidotes to coumarins, isoniazid, methotrexate and thyroxine; toxins that work via metabolic processes. British journal of clinical pharmacology. 2015. Bateman D Nicholas, et al. PubMed
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Serum drug concentrations of INH and RMP predict 2-month sputum culture results in tuberculosis patients. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease. 2015. Mah A, et al. PubMed
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A proposal for an individualized pharmacogenetic-guided isoniazid dosage regimen for patients with tuberculosis. Drug design, development and therapy. 2015. Jung Jin Ah, et al. PubMed
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Analysis of IL-6, STAT3 and HSPA1L Gene Polymorphisms in Anti-Tuberculosis Drug-Induced Hepatitis in a Nested Case-Control Study. PloS one. 2015. Wang Jing, et al. PubMed
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Involvement of cytochrome P450 1A1 and glutathione S-transferase P1 polymorphisms and promoter hypermethylation in the progression of anti-tuberculosis drug-induced liver injury: a case-control study. PloS one. 2015. He Lei, et al. PubMed
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Pharmacogenomics of antimicrobial agents. Pharmacogenomics. 2014. Aung Ar Kar, et al. PubMed
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N-acetyltransferase 2 (NAT2) genotype as a risk factor for development of drug-induced liver injury relating to antituberculosis drug treatment in a mixed-ethnicity patient group. European journal of clinical pharmacology. 2014. Ng Ching-Soon, et al. PubMed
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PharmGKB summary: very important pharmacogene information for N-acetyltransferase 2. Pharmacogenetics and genomics. 2014. McDonagh Ellen M, et al. PubMed
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Association of NAT2, GST and CYP2E1 polymorphisms and anti-tuberculosis drug-induced hepatotoxicity. Tuberculosis (Edinburgh, Scotland). 2014. Singla Neha, et al. PubMed
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Future of pharmacogenetics-based therapy for tuberculosis. Pharmacogenomics. 2014. Matsumoto Tomoshige, et al. PubMed
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Evolution and transmission of drug-resistant tuberculosis in a Russian population. Nature genetics. 2014. Casali Nicola, et al. PubMed
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Single nucleotide polymorphic macrophage cytokine regulation by Mycobacterium tuberculosis and drug treatment. Pharmacogenomics. 2014. Singh Amit K, et al. PubMed
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N-acetyltransferase 2, cytochrome P4502E1 and glutathione S-transferase genotypes in antitubercular treatment-induced hepatotoxicity in North Indians. Journal of clinical pharmacy and therapeutics. 2014. Rana S V, et al. PubMed
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Full-gene sequencing analysis of NAT2 and its relationship with isoniazid pharmacokinetics in Venezuelan children with tuberculosis. Pharmacogenomics. 2014. Verhagen Lilly M, et al. PubMed
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Dependence of efavirenz- and rifampicin-isoniazid-based antituberculosis treatment drug-drug interaction on CYP2B6 and NAT2 genetic polymorphisms: ANRS 12154 study in Cambodia. The Journal of infectious diseases. 2014. Bertrand Julie, et al. PubMed
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The incidence of liver injury in Uyghur patients treated for TB in Xinjiang Uyghur autonomous region, China, and its association with hepatic enzyme polymorphisms nat2, cyp2e1, gstm1 and gstt1. PloS one. 2014. Xiang Yang, et al. PubMed
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Association of N-acetyltransferase 2 and cytochrome P450 2E1 gene polymorphisms with antituberculosis drug-induced hepatotoxicity in Western India. Journal of gastroenterology and hepatology. 2013. Gupta Vinod H, et al. PubMed
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Mycobacterium tuberculosis mutation rate estimates from different lineages predict substantial differences in the emergence of drug-resistant tuberculosis. Nature genetics. 2013. Ford Christopher B, et al. PubMed
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Challenges in pharmacogenetics. European journal of clinical pharmacology. 2013. Cascorbi Ingolf, et al. PubMed
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HLA-DRB1*1501 and VDR polymorphisms and survival of Mycobacterium tuberculosis in human macrophages exposed to inhalable microparticles. Pharmacogenomics. 2013. Singh Amit K, et al. PubMed
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N-acetyl transferase 2 and cytochrome P450 2E1 genes and isoniazid-induced hepatotoxicity in Brazilian patients. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease. 2013. Santos N P C, et al. PubMed
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The NAT2 tag SNP rs1495741 correlates with the susceptibility of antituberculosis drug-induced hepatotoxicity. Pharmacogenetics and genomics. 2013. Ho Hsin-Tien, et al. PubMed
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Relationship of NAT2, CYP2E1 and GSTM1/GSTT1 polymorphisms with mild elevation of liver enzymes in Brazilian individuals under anti-tuberculosis drug therapy. Clinica chimica acta; international journal of clinical chemistry. 2013. Forestiero Francisco Jose, et al. PubMed
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Slow N-acetyltransferase 2 genotype contributes to anti-tuberculosis drug-induced hepatotoxicity: a meta-analysis. Molecular biology reports. 2013. Du Haijian, et al. PubMed
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Correlation of N-acetyltransferase 2 genotype with isoniazid acetylation in polish tuberculosis patients. BioMed research international. 2013. Zabost Anna, et al. PubMed
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The roles of GSTM1 and GSTT1 null genotypes and other predictors in anti-tuberculosis drug-induced liver injury. Journal of clinical pharmacy and therapeutics. 2012. Monteiro T P, et al. PubMed
NAT2 genotype guided regimen reduces isoniazid-induced liver injury and early treatment failure in the 6-month four-drug standard treatment of tuberculosis: A randomized controlled trial for pharmacogenetics-based therapy. European journal of clinical pharmacology. 2012. Azuma Junichi, et al. PubMed
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Sex, ethnicity and slow acetylator profile are the major causes of hepatotoxicity induced by antituberculosis drugs. Journal of gastroenterology and hepatology. 2012. Chamorro Julián G, et al. PubMed
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CYP2E1, GSTM1 and GSTT1 genetic polymorphisms and susceptibility to antituberculosis drug-induced hepatotoxicity: a nested case-control study. Journal of clinical pharmacy and therapeutics. 2012. Tang S-W, et al. PubMed
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Polymorphism of the N-acetyltransferase 2 gene as a susceptibility risk factor for antituberculosis drug-induced hepatotoxicity in Tunisian patients with tuberculosis. Pathologie-biologie. 2012. Ben Mahmoud L, et al. PubMed
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Genetic interaction between NAT2, GSTM1, GSTT1, CYP2E1, and environmental factors is associated with adverse reactions to anti-tuberculosis drugs. Molecular diagnosis & therapy. 2012. Costa Gustavo N O, et al. PubMed
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PharmGKB summary: very important pharmacogene information for GSTT1. Pharmacogenetics and genomics. 2012. Thorn Caroline F, et al. PubMed
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NAT2 and CYP2E1 polymorphisms associated with antituberculosis drug-induced hepatotoxicity in Chinese patients. Clinical and experimental pharmacology & physiology. 2012. An Hui-Ru, et al. PubMed
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TNF-alpha genetic polymorphism -308G/A and antituberculosis drug-induced hepatitis. Liver international : official journal of the International Association for the Study of the Liver. 2012. Kim Sang-Heon, et al. PubMed
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NAT2 polymorphisms and susceptibility to anti-tuberculosis drug-induced liver injury: a meta-analysis. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease. 2012. Wang P-Y, et al. PubMed
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Genetic variants in antioxidant pathway: risk factors for hepatotoxicity in tuberculosis patients. Tuberculosis (Edinburgh, Scotland). 2012. Nanashima Kazutaka, et al. PubMed
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The pharmacogenetics of NAT2 enzyme maturation in perinatally HIV exposed infants receiving isoniazid. Journal of clinical pharmacology. 2012. Zhu Rui, et al. PubMed
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Genetic association studies in drug-induced liver injury. Drug metabolism reviews. 2012. Daly Ann K, et al. PubMed
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A novel metabolite of antituberculosis therapy demonstrates host activation of isoniazid and formation of the isoniazid-NAD+ adduct. Antimicrobial agents and chemotherapy. 2012. Mahapatra Sebabrata, et al. PubMed
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Accuracy of various human NAT2 SNP genotyping panels to infer rapid, intermediate and slow acetylator phenotypes. Pharmacogenomics. 2012. Hein David W, et al. PubMed
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Arylamine N-acetyltransferases--from drug metabolism and pharmacogenetics to identification of novel targets for pharmacological intervention. Advances in pharmacology (San Diego, Calif.). 2012. Sim Edith, et al. PubMed
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NAT2 genetic polymorphisms and anti-tuberculosis drug-induced hepatotoxicity in Chinese community population. Annals of hepatology. 2012. Lv Xiaozhen, et al. PubMed
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Pharmacogenetic study of drug-metabolising enzyme polymorphisms on the risk of anti-tuberculosis drug-induced liver injury: a meta-analysis. PloS one. 2012. Cai Yu, et al. PubMed
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Relationship between CYP2E1 polymorphism and increase of ALT activity during therapy of patients with pulmonary tuberculosis. Bulletin of experimental biology and medicine. 2011. Kudryashov A V, et al. PubMed
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N-acetyltransferase 2 polymorphisms and risk of anti-tuberculosis drug-induced hepatotoxicity in Caucasians. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease. 2011. Leiro-Fernandez V, et al. PubMed
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The SLCO1B1 rs4149032 polymorphism is highly prevalent in South Africans and is associated with reduced rifampin concentrations: dosing implications. Antimicrobial agents and chemotherapy. 2011. Chigutsa Emmanuel, et al. PubMed
Genetic polymorphisms of NAT2, CYP2E1 and GST enzymes and the occurrence of antituberculosis drug-induced hepatitis in Brazilian TB patients. Memórias do Instituto Oswaldo Cruz. 2011. Teixeira Raquel Lima de Figueiredo, et al. PubMed
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Comparison between acetylator phenotype and genotype polymorphism of n-acetyltransferase-2 in tuberculosis patients. Hepatology international. 2011. Rana S V, et al. PubMed
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A fresh look at the mechanism of isoniazid-induced hepatotoxicity. Clinical pharmacology and therapeutics. 2011. Metushi I G, et al. PubMed
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A single nucleotide polymorphism tags variation in the arylamine N-acetyltransferase 2 phenotype in populations of European background. Pharmacogenetics and genomics. 2011. García-Closas Montserrat, et al. PubMed
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Association of N-acetyltransferase-2 genotypes and anti-tuberculosis induced liver injury; first case-controlled study from Iran. Current drug safety. 2011. Khalili Hossein, et al. PubMed
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NAT2, CYP2C9, CYP2C19, and CYP2E1 genetic polymorphisms in anti-TB drug-induced maculopapular eruption. European journal of clinical pharmacology. 2011. Kim Sang-Heon, et al. PubMed
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Databases in the area of pharmacogenetics. Human mutation. 2011. Sim Sarah C, et al. PubMed
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Role of polymorphic N-acetyl transferase2 and cytochrome P4502E1 gene in antituberculosis treatment-induced hepatitis. Journal of gastroenterology and hepatology. 2011. Bose Purabi Deka, et al. PubMed
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Association of isoniazid-metabolizing enzyme genotypes and isoniazid-induced hepatotoxicity in tuberculosis patients. In vivo (Athens, Greece). 2011. Sotsuka Takayo, et al. PubMed
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Pharmacogenetic & pharmacokinetic biomarker for efavirenz based ARV and rifampicin based anti-TB drug induced liver injury in TB-HIV infected patients. PloS one. 2011. Yimer Getnet, et al. PubMed
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Genetic variation in carboxylesterase genes and susceptibility to isoniazid-induced hepatotoxicity. The pharmacogenomics journal. 2010. Yamada S, et al. PubMed
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Medications and glucose-6-phosphate dehydrogenase deficiency: an evidence-based review. Drug safety : an international journal of medical toxicology and drug experience. 2010. Youngster Ilan, et al. PubMed
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GSTT1 and GSTM1 gene deletions are not associated with hepatotoxicity caused by antitubercular drugs. Journal of clinical pharmacy and therapeutics. 2010. Chatterjee S, et al. PubMed
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Drug-induced liver injury: past, present and future. Pharmacogenomics. 2010. Daly Ann K. PubMed
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NAT2 and CYP2E1 polymorphisms and susceptibility to first-line anti-tuberculosis drug-induced hepatitis. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease. 2010. Lee S-W, et al. PubMed
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Low N-acetyltransferase 2 activity in isoniazid-associated acute hepatitis requiring liver transplantation. Transplant international : official journal of the European Society for Organ Transplantation. 2010. Cramer Jakob P, et al. PubMed
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GSTT1 and GSTM1 null mutations and adverse reactions induced by antituberculosis drugs in Koreans. Tuberculosis (Edinburgh, Scotland). 2010. Kim Sang-Heon, et al. PubMed
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Genetic polymorphisms of cytochrome P450 and glutathione S-transferase associated with antituberculosis drug-induced hepatotoxicity in Chinese tuberculosis patients. The Journal of international medical research. 2010. Wang T, et al. PubMed
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Genetic polymorphisms of drug-metabolizing enzymes and anti-TB drug-induced hepatitis. Pharmacogenomics. 2009. Kim Sang-Heon, et al. PubMed
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Genetic variations of NAT2 and CYP2E1 and isoniazid hepatotoxicity in a diverse population. Pharmacogenomics. 2009. Yamada So, et al. PubMed
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N-acetyltransferase SNPs: emerging concepts serve as a paradigm for understanding complexities of personalized medicine. Expert opinion on drug metabolism & toxicology. 2009. Hein David W. PubMed
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Arylamine N-acetyltransferases: structural and functional implications of polymorphisms. Toxicology. 2008. Sim Edith, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Drug-metabolising enzyme polymorphisms and predisposition to anti-tuberculosis drug-induced liver injury: a meta-analysis. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease. 2008. Sun F, et al. PubMed
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Structure/function evaluations of single nucleotide polymorphisms in human N-acetyltransferase 2. Current drug metabolism. 2008. Walraven Jason M, et al. PubMed
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Association of slow N-acetyltransferase 2 profile and anti-TB drug-induced hepatotoxicity in patients from Southern Brazil. European journal of clinical pharmacology. 2008. Possuelo L G, et al. PubMed
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Influence of glutathione S-transferase M1 and T1 homozygous null mutations on the risk of antituberculosis drug-induced hepatotoxicity in a Caucasian population. Liver international : official journal of the International Association for the Study of the Liver. 2008. Leiro Virginia, et al. PubMed
Effects of N-acetyltransferase 2 (NAT2), CYP2E1 and Glutathione-S-transferase (GST) genotypes on the serum concentrations of isoniazid and metabolites in tuberculosis patients. The Journal of toxicological sciences. 2008. Fukino Katsumi, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Pharmacogenomics of anti-TB drugs-related hepatotoxicity. Pharmacogenomics. 2008. Roy Puspita Das, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
Antituberculosis drug-induced hepatotoxicity: concise up-to-date review. Journal of gastroenterology and hepatology. 2008. Tostmann Alma, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
Isoniazid: metabolic aspects and toxicological correlates. Current drug metabolism. 2007. Preziosi Paolo. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
New anti-tuberculosis drugs with novel mechanisms of action. Current medicinal chemistry. 2008. Rivers Emma C, et al. PubMed
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Genotype and phenotype of NAT2 and the occurrence of adverse drug reactions in Mexican individuals to an isoniazid-based prophylactic chemotherapy for tuberculosis. Molecular medicine reports. 2008. Díaz-Molina Raúl, et al. PubMed
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Determining the relation between N-acetyltransferase-2 acetylator phenotype and antituberculosis drug induced hepatitis by molecular biologic tests. Tüberküloz ve toraks. 2008. Bozok Cetintaş Vildan, et al. PubMed
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NAT2 6A, a haplotype of the N-acetyltransferase 2 gene, is an important biomarker for risk of anti-tuberculosis drug-induced hepatotoxicity in Japanese patients with tuberculosis. World journal of gastroenterology : WJG. 2007. Higuchi Norihide, et al. PubMed
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Genetic polymorphisms of NAT2 and CYP2E1 associated with antituberculosis drug-induced hepatotoxicity in Korean patients with pulmonary tuberculosis. Tuberculosis (Edinburgh, Scotland). 2007. Cho Hyun-Jung, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Isoniazid bactericidal activity and resistance emergence: integrating pharmacodynamics and pharmacogenomics to predict efficacy in different ethnic populations. Antimicrobial agents and chemotherapy. 2007. Gumbo Tawanda, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Two years review of cutaneous adverse drug reaction from first line anti-tuberculous drugs. The Medical journal of Malaysia. 2007. Tan W C, et al. PubMed
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Analysis of nucleotide diversity of NAT2 coding region reveals homogeneity across Native American populations and high intra-population diversity. The pharmacogenomics journal. 2007. Fuselli S, et al. PubMed
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An official ATS statement: hepatotoxicity of antituberculosis therapy. American journal of respiratory and critical care medicine. 2006. Saukkonen Jussi J, et al. PubMed
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DNA microarray genotyping of N-acetyltransferase 2 polymorphism using carbodiimide as the linker for assessment of isoniazid hepatotoxicity. Tuberculosis (Edinburgh, Scotland). 2006. Shimizu Yasuo, et al. PubMed
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CYP2E1 genotype and isoniazid-induced hepatotoxicity in patients treated for latent tuberculosis. European journal of clinical pharmacology. 2006. Vuilleumier Nicolas, et al. PubMed
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Predisposition of antituberculosis drug induced hepatotoxicity by cytochrome P450 2E1 genotype and haplotype in pediatric patients. Journal of gastroenterology and hepatology. 2006. Roy Bidyut, et al. PubMed
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The influence of NAT2 genotypes on the plasma concentration of isoniazid and acetylisoniazid in Chinese pulmonary tuberculosis patients. Clinica chimica acta; international journal of clinical chemistry. 2006. Chen Bing, et al. PubMed
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Adverse reactions to first-line antituberculosis drugs. Expert opinion on drug safety. 2006. Forget Eric J, et al. PubMed
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Acetylation genotype and phenotype in patients with systemic lupus erythematosus. Pharmacological reports : PR. 2006. Rychlik-Sych Mariola, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Isoniazid pharmacokinetics in children treated for respiratory tuberculosis. Archives of disease in childhood. 2005. Schaaf H S, et al. PubMed
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Should we use N-acetyltransferase type 2 genotyping to personalize isoniazid doses?. Antimicrobial agents and chemotherapy. 2005. Kinzig-Schippers Martina, et al. PubMed
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Lack of association between arylamine N-acetyltransferase 2 (NAT2) polymorphism and systemic sclerosis. European journal of clinical pharmacology. 2005. Skretkowicz K, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Effects of prototypical microsomal enzyme inducers on cytochrome P450 expression in cultured human hepatocytes. Drug metabolism and disposition: the biological fate of chemicals. 2003. Madan Ajay, et al. PubMed
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Cytochrome P450 2E1 genotype and the susceptibility to antituberculosis drug-induced hepatitis. Hepatology (Baltimore, Md.). 2003. Huang Yi-Shin, et al. PubMed
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Polymorphism of the N-acetyltransferase 2 gene as a susceptibility risk factor for antituberculosis drug-induced hepatitis. Hepatology (Baltimore, Md.). 2002. Huang Yi-Shin, et al. PubMed
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Increased risk of antituberculosis drug-induced hepatotoxicity in individuals with glutathione S-transferase M1 'null' mutation. Journal of gastroenterology and hepatology. 2001. Roy B, et al. PubMed
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Slow N-acetyltransferase 2 genotype affects the incidence of isoniazid and rifampicin-induced hepatotoxicity. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease. 2000. Ohno M, et al. PubMed
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Populations and genetic polymorphisms. Molecular diagnosis : a journal devoted to the understanding of human disease through the clinical application of molecular biology. 1999. Weber W W. PubMed
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Meta-analysis of phenotype and genotype of NAT2 deficiency in Chinese populations. Pharmacogenetics. 1997. Xie H G, et al. PubMed
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Human acetyltransferase polymorphisms. Mutation research. 1997. Grant D M, et al. PubMed
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N-acetylation pharmacogenetics. Pharmacological reviews. 1985. Weber W W, et al. PubMed
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Clinical importance of the interaction of phenytoin and isoniazid: a report from the Boston Collaborative Drug Surveillance Program. Chest. 1979. Miller R R, et al. PubMed
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Drug-induced haemolysis in glucose-6-phosphate dehydrogenase deficiency. British medical journal. 1976. Chan T K, et al. PubMed

LinkOuts

Web Resource:
Wikipedia
National Drug Code Directory:
0555-0066-02
DrugBank:
DB00951
PDB:
ISZ
ChEBI:
6030
KEGG Compound:
C07054
KEGG Drug:
D00346
PubChem Compound:
3767
PubChem Substance:
46506039
9266
Drugs Product Database (DPD):
577782
ChemSpider:
3635
HET:
ISZ
Therapeutic Targets Database:
DAP000011
FDA Drug Label at DailyMed:
9499f1cf-2f46-4047-8b71-90aee7dee854

Clinical Trials

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