Chemical: Drug
trimethoprim

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


Annotated Labels

  1. FDA Label for sulfamethoxazole,trimethoprim and G6PD
  2. HCSC Label for sulfamethoxazole,trimethoprim and G6PD

last updated 09/01/2016

1. FDA Label for sulfamethoxazole,trimethoprim and G6PD

Actionable PGx
Full label available at DailyMed

Genes and/or phenotypes found in this label

  • Bronchitis, Chronic
    • Indications & usage section
    • source: U.S. Food and Drug Administration
  • Diarrhea
    • Indications & usage section
    • source: U.S. Food and Drug Administration
  • Dysentery, Bacillary
    • Indications & usage section
    • source: U.S. Food and Drug Administration
  • Otitis Media
    • Indications & usage section
    • source: U.S. Food and Drug Administration
  • Pneumonia, Pneumocystis
    • Indications & usage section
    • source: U.S. Food and Drug Administration
  • Seizures
    • Adverse reactions section
    • source: PHONT
  • Urinary Tract Infections
    • Indications & usage section
    • source: U.S. Food and Drug Administration
  • ABCB1
    • metabolism/PK, Clinical pharmacology section
    • source: U.S. Food and Drug Administration
  • CYP2C8
    • metabolism/PK, Precautions section
    • source: U.S. Food and Drug Administration
  • CYP2C9
    • metabolism/PK, Clinical pharmacology section, Precautions section
    • source: U.S. Food and Drug Administration
  • G6PD
    • toxicity, Precautions section
    • source: U.S. Food and Drug Administration
  • SLC22A1
    • metabolism/PK, Clinical pharmacology section
    • source: U.S. Food and Drug Administration
  • SLC22A2
    • metabolism/PK, Clinical pharmacology section, Precautions section
    • source: U.S. Food and Drug Administration


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.

? = Mouse-over for quick help

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 trimethoprim

Gene ? Variant?
(147)
Alternate Names ? Chemicals ? Alleles ?
(+ chr strand)
Function ? Amino Acid?
Translation
No VIP available CA No VIP available G6PD B (wildtype) N/A N/A N/A
No VIP available CA VA G6PD Canton, Taiwan-Hakka, Gifu-like, Agrigento-like 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 No VIP available VA NAT2 *4 N/A N/A N/A
No VIP available No VIP available 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 *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 *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 *13 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 Clinical Annotations available 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
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
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
No VIP available No Clinical Annotations available VA
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 No Clinical Annotations available 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 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
rs2289669 NC_000017.10:g.19463343G>A, NC_000017.11:g.19560030G>A, NM_018242.2:c.922-158G>A, XM_005256710.1:c.922-158G>A, XM_005256711.1:c.808-158G>A, XM_005256712.1:c.922-158G>A, XM_005256713.1:c.853-158G>A, XM_005256714.1:c.922-158G>A, XR_934310.1:n.1230C>T, rs386563823, rs56528368, rs57126832
G > A
SNP
No VIP available No Clinical Annotations available VA
rs316019 NC_000006.11:g.160670282A>C, NC_000006.12:g.160249250A>C, NM_003058.3:c.808T>G, NP_003049.2:p.Ser270Ala, rs1755917, rs17846267, rs17859289, rs386580336, rs52803175, rs60007366, rs666224
A > C
SNP
S270A
No VIP available No Clinical Annotations available VA
rs45607939 NC_000008.10:g.18258126A>T, NC_000008.11:g.18400616A>T, NG_012246.1:g.14372A>T, NM_000015.2:c.613A>T, NP_000006.2:p.Met205Leu, XM_011544358.1:c.613A>T, XP_011542660.1:p.Met205Leu
A > T
SNP
M205L
No VIP available No Clinical Annotations available VA
rs7284807 NC_000022.10:g.43015387C>G, NC_000022.11:g.42619381C>G, NG_012194.1:g.35019G>C, NM_000398.6:c.*392G>C, NM_001129819.2:c.*392G>C, NM_001171660.1:c.*392G>C, NM_001171661.1:c.*392G>C, NM_007326.4:c.*392G>C, rs58086521
C > G
SNP
No VIP available No Clinical Annotations available VA
rs75160992 NC_000018.10:g.74291863A>C, NC_000018.9:g.71959098A>C, NG_023211.1:g.5124T>G, NM_001190807.2:c.13T>G, NM_001914.3:c.13T>G, NM_148923.3:c.13T>G, NP_001177736.1:p.Ser5Ala, NP_001905.1:p.Ser5Ala, NP_683725.1:p.Ser5Ala, XM_011525835.1:c.13T>G, XP_011524137.1:p.Ser5Ala, XR_245456.1:n.154T>G
A > C
SNP
S5A
No VIP available No Clinical Annotations available VA
rs76458556 NC_000022.10:g.43015795C>T, NC_000022.11:g.42619789C>T, NG_012194.1:g.34611G>A, NM_000398.6:c.890G>A, NM_001129819.2:c.821G>A, NM_001171660.1:c.989G>A, NM_001171661.1:c.821G>A, NM_007326.4:c.821G>A, NP_000389.1:p.Arg297His, NP_001123291.1:p.Arg274His, NP_001165131.1:p.Arg330His, NP_001165132.1:p.Arg274His, NP_015565.1:p.Arg274His
C > T
SNP
R297H
No VIP available No Clinical Annotations available VA
rs7663179 NC_000004.11:g.25092357T>C, NC_000004.12:g.25090735T>C
T > C
SNP
No VIP available No Clinical Annotations available VA
rs77005399 NC_000018.10:g.74292264C>T, NC_000018.9:g.71959499C>T, NG_023211.1:g.4723G>A, NM_001190807.2:c.-389G>A, NM_001914.3:c.-389G>A, NM_148923.3:c.-389G>A, XM_011525835.1:c.-389G>A, XR_245456.1:n.-248G>A
C > T
SNP
No VIP available No Clinical Annotations available VA
rs77499608 NC_000022.10:g.43014916A>G, NC_000022.11:g.42618910A>G, NG_012194.1:g.35490T>C, NM_000398.6:c.*863T>C, NM_001129819.2:c.*863T>C, NM_001171660.1:c.*863T>C, NM_001171661.1:c.*863T>C, NM_007326.4:c.*863T>C
A > G
SNP
No VIP available No Clinical Annotations available VA
rs8190370 NC_000022.10:g.43045295G>A, NC_000022.11:g.42649289G>A, NG_012194.1:g.5111C>T, NM_000398.6:c.21+6C>T
G > A
SNP
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 147

Overview

Generic Names
Trade Names
  • Abacin
  • Abaprim
  • Alprim
  • Apo-Sulfatrim
  • Bactin
  • Bactramin
  • Bactrim
  • Bactrim DS
  • Bactrim Pediatric
  • Baktar
  • Chemotrim
  • Comox
  • Cotrim
  • Cotrim D.S.
  • Drylin
  • Eusaprim
  • Fectrim
  • Gantaprim
  • Gantrim
  • Idotrim
  • Imexim
  • Instalac
  • Ipral
  • Kepinol
  • Laratrim
  • Lidaprim
  • Linaris
  • Methoprim
  • Microtrim
  • Monoprim
  • Monotrim
  • Monotrimin
  • Nopil
  • Oraprim
  • Priloprim
  • Primosept
  • Primsol
  • Proloprim
  • Septra
  • Septra DS
  • Septra Grape
  • Septrin
  • Sigaprim
  • Sulfamethoprim
  • Sulfamethoprim-DS
  • Sulfamethoxazole & Trimethoprim
  • Sulfatrim
  • Sulfatrim Pediatric
  • Sulfatrim-DS
  • Sulfatrim-SS
  • Sulfotrim
  • Sulmeprim
  • Sulmeprim Pediatric
  • Sulprim
  • Sumetrolim
  • Supracombin
  • Suprim
  • Syraprim
  • Teleprim
  • Thiocuran
  • Tiempe
  • Tmp-Ratiopharm
  • Trigonyl
  • Trimanyl
  • Trimesulf
  • Trimeth/Sulfa
  • Trimethioprim
  • Trimethopriom
  • Trimetoprim
  • Trimexazole
  • Trimogal
  • Trimopan
  • Trimpex
  • Trimpex 200
  • Triprim
  • Unitrim
  • Uretrim
  • Uro-Septra
  • Uroplus
  • Uroplus DS
  • Uroplus SS
  • Wellcoprim
Brand Mixture Names

PharmGKB Accession Id

PA451788

Type(s):

Drug

Description

A pyrimidine inhibitor of dihydrofolate reductase, it is an antibacterial related to pyrimethamine. The interference with folic acid metabolism may cause a depression of hematopoiesis. It is potentiated by sulfonamides and the trimethoprim-sulfamethoxazole combination is the form most often used. It is sometimes used alone as an antimalarial. Trimethoprim resistance has been reported.

Source: Drug Bank

Indication

For the treatment of urinary tract infections, uncomplicated pyelonephritis (with sulfamethoxazole) and mild acute prostatitis. May be used as pericoital (with sulfamethoxazole) or continuous prophylaxis in females with recurrent cystitis. May be used as an alternative to treat asymptomatic bacteriuria during pregnancy (only before the last 6 weeks of pregnancy). Other uses include: alternative agent in respiratory tract infections (otitis, sinusitus, bronchitis and pneumonia), treatment of Pneumocystis jirovecii pneumonia (acute or prophylaxis), Nocardia infections, and traveller's diarrhea.

Source: Drug Bank

Other Vocabularies

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Trimethoprim binds to dihydrofolate reductase and inhibits the reduction of dihydrofolic acid (DHF) to tetrahydrofolic acid (THF). THF is an essential precursor in the thymidine synthesis pathway and interference with this pathway inhibits bacterial DNA synthesis. Trimethoprim's affinity for bacterial dihydrofolate reductase is several thousand times greater than its affinity for human dihydrofolate reductase. Sulfamethoxazole inhibits dihydrofolate synthetase (aka dihydropteroate synthetase), an enzyme involved further upstream in the same pathway. Trimethoprim and sulfamethoxazole are commonly used in combination due to their synergistic effects. This drug combination also reduces the development of resistance that is seen when either drug is used alone.

Source: Drug Bank

Pharmacology

Trimethoprim is a pyrimidine analogue that disrupts folate synthesis, an essential part of the thymidine synthesis pathway. Inhibition of the enzyme starves the bacteria of nucleotides necessary for DNA replication.The drug, therefore, exhibits bactericidal activity.

Source: Drug Bank

Food Interaction

Do not take calcium, aluminium, magnesium or iron supplements within 2 hours of taking this medication.|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

Hepatic metabolism to oxide and hydroxylated metabolites.

Source: Drug Bank

Protein Binding

42-46% bound to plasma proteins

Source: Drug Bank

Absorption

Readily and almost completely absorbed in the GI tract with peak serum concentrations attained 1-4 hours after oral administration. Widely distributed to tissues and fluids including kidney, lung, seminal fluid, aqueous humour, middle ear fluid, sputum, vaginal secretions, bile, bone and CSF.

Source: Drug Bank

Half-Life

8-11 hours in adults with normal renal function

Source: Drug Bank

Toxicity

LD 50=4850 (orally in mice)

Source: Drug Bank

Route of Elimination

Ten to twenty percent of trimethoprim is metabolized, primarily in the liver; the remainder is excreted unchanged in the urine.
After oral administration, 50% to 60% of trimethoprim is excreted in the urine within 24 hours, approximately 80% of this being unmetabolized trimethoprim. Trimethoprim also passes the placental barrier and is excreted in human milk.

Source: Drug Bank

Chemical Properties

Chemical Formula

C14H18N4O3

Source: Drug Bank

Isomeric SMILES

COc1cc(cc(c1OC)OC)Cc2cnc(nc2N)N

Source: OpenEye

Canonical SMILES

COC1=CC(CC2=CN=C(N)N=C2N)=CC(OC)=C1OC

Source: Drug Bank

Average Molecular Weight

290.3177

Source: Drug Bank

Monoisotopic Molecular Weight

290.137890462

Source: Drug Bank

SMILES

COC1=CC(CC2=CN=C(N)N=C2N)=CC(OC)=C1OC

Source: Drug Bank

InChI String

InChI=1S/C14H18N4O3/c1-19-10-5-8(6-11(20-2)12(10)21-3)4-9-7-17-14(16)18-13(9)15/h5-7H,4H2,1-3H3,(H4,15,16,17,18)

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
DHFR (source: Drug Bank )
TYMS (source: Drug Bank )

Drug Interactions

Interaction Description
dapsone - trimethoprim Increased toxicity of both products (source: Drug Bank )
dapsone - trimethoprim Increased toxicity of both products (source: Drug Bank )
fosphenytoin - trimethoprim Trimethoprim increases the effect of hydantoin (source: Drug Bank )
methotrexate - trimethoprim Timethoprim increases methotrexate toxicity (source: Drug Bank )
methotrexate - trimethoprim Timethoprim increases methotrexate toxicity (source: Drug Bank )
phenytoin - trimethoprim Trimethoprim increases the effect of hydantoin (source: Drug Bank )
phenytoin - trimethoprim Trimethoprim increases the effect of hydantoin (source: Drug Bank )
procainamide - trimethoprim Trimethoprim increases serum levels of procainamide (source: Drug Bank )
procainamide - trimethoprim Trimethoprim increases serum levels of procainamide (source: Drug Bank )
rifampin - trimethoprim Rifampin decreases the effect of trimethoprim (source: Drug Bank )
rifampin - trimethoprim Rifampin decreases the effect of trimethoprim (source: Drug Bank )
tolbutamide - trimethoprim Tolbutamide, a strong CYP2C9 inhibitor, may decrease the metabolism and clearance of Trimethoprim. Consider alternate therapy or monitor for changes in Trimethoprim therapeutic and adverse effects if Tolbutamide is initiated, discontinued or dose changed. (source: Drug Bank )
tolbutamide - trimethoprim Tolbutamide, a strong CYP2C9 inhibitor, may decrease the metabolism and clearance of Trimethoprim. Consider alternate therapy or monitor for changes in Trimethoprim therapeutic and adverse effects if Tolbutamide is initiated, discontinued or dose changed. (source: Drug Bank )
trandolapril - trimethoprim Increased risk of hyperkalemia. Monitor serum potassium levels. (source: Drug Bank )
trimethoprim - capecitabine The strong CYP2C9 inhibitor, Capecitabine, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Capecitabine is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - delavirdine The strong CYP2C9 inhibitor, Delavirdine, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Delavirdine is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - dofetilide Trimethoprim may significantly reduced the clearance of Dofetilide. Trimethoprim is a cation transport inhibitor and may interfere with renal excretion of Dofetilide. Concomitant use is contraindicated. (source: Drug Bank )
trimethoprim - dofetilide Trimethoprim may significantly reduced the clearance of Dofetilide. Trimethoprim is a cation transport inhibitor and may interfere with renal excretion of Dofetilide. Concomitant use is contraindicated. (source: Drug Bank )
trimethoprim - floxuridine The strong CYP2C9 inhibitor, Floxuridine, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Floxuridine is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - fluconazole The strong CYP2C9 inhibitor, Fluconazole, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Fluconazole is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - fluorouracil The strong CYP2C9 inhibitor, Fluorouracil, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Fluorouracil is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - flurbiprofen The strong CYP2C9 inhibitor, Flurbiprofen, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Flurbiprofen is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - gemfibrozil The strong CYP2C9 inhibitor, Gemfibrozil, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Gemfibrozil is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - ibuprofen The strong CYP2C9 inhibitor, Ibuprofen, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Ibuprofen is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - indomethacin The strong CYP2C9 inhibitor, Indomethacine, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Indomethacine is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - ketoconazole The strong CYP2C9 inhibitor, Ketoconazole, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Ketoconazole is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - leucovorin The efficacy of Trimethoprim may be reduced by Leucovorin (folinic acid). The antibiotic, Trimethoprim, acts by blocking bacterial folic acid metabolism. Leucovorin may reduce the efficacy of Trimethoprim by providing an alternate source of folic acid. The therapeutic effect of Trimethoprim should be closely monitored. (source: Drug Bank )
trimethoprim - leucovorin The efficacy of Trimethoprim may be reduced by Leucovorin (folinic acid). The antibiotic, Trimethoprim, acts by blocking bacterial folic acid metabolism. Leucovorin may reduce the efficacy of Trimethoprim by providing an alternate source of folic acid. The therapeutic effect of Trimethoprim should be closely monitored. (source: Drug Bank )
trimethoprim - methotrexate Trimethoprim may increase the adverse/toxic effects of Methotrexate (e.g. bone marrow suppression). Concomitant use should be avoided or closely monitored for Methotrexate toxicity. (source: Drug Bank )
trimethoprim - methotrexate Trimethoprim may increase the adverse/toxic effects of Methotrexate (e.g. bone marrow suppression). Concomitant use should be avoided or closely monitored for Methotrexate toxicity. (source: Drug Bank )
trimethoprim - miconazole The strong CYP2C9 inhibitor, Miconazole, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Miconazole is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - nicardipine The strong CYP2C9 inhibitor, Nicardipine, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Nicardipine is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - piroxicam The strong CYP2C9 inhibitor, Piroxicam, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Piroxicam is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - procainamide Trimethoprim may reduce the clearance of Procainamide. Alternative treatments should be considered. If Trimethoprim is initiated or the dose is increased, monitor for increased toxicity of Procainamide (e.g. QTc intervals, EKG, serum drug concentrations). If Trimethoprim is discontinued or the dose decreased, monitor for reduced effects of Procainamide. (source: Drug Bank )
trimethoprim - procainamide Trimethoprim may reduce the clearance of Procainamide. Alternative treatments should be considered. If Trimethoprim is initiated or the dose is increased, monitor for increased toxicity of Procainamide (e.g. QTc intervals, EKG, serum drug concentrations). If Trimethoprim is discontinued or the dose decreased, monitor for reduced effects of Procainamide. (source: Drug Bank )
trimethoprim - sulfadiazine The strong CYP2C9 inhibitor, Sulfadiazine, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Sulfadiazine is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - sulfisoxazole The strong CYP2C9 inhibitor, Sulfisoxazole, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Sulfisoxazole is initiated, discontinued or dose changed. (source: Drug Bank )
trimethoprim - tolbutamide The strong CYP2C9 inhibitor, Tolbutamide, may decrease the metabolism and clearance of Trimethoprim, a CYP2C9 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimethoprim if Tolbutamide is initiated, discontinued or dose changed. (source: Drug Bank )

Curated Information ?

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

May Treat
Contraindicated With

Publications related to trimethoprim: 34

No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
CYP2B6 genotype-based efavirenz dose recommendations during rifampicin-based antituberculosis cotreatment for a sub-Saharan Africa population. Pharmacogenomics. 2016. Mukonzo Jackson 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
Pharmacogenomics of antimicrobial agents. Pharmacogenomics. 2014. Aung Ar Kar, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Trimethoprim-Metformin Interaction and its Genetic Modulation by OCT2 and MATE1. British journal of clinical pharmacology. 2013. Grün Barbara, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Evaluation of polymorphisms in the sulfonamide detoxification genes NAT2, CYB5A, and CYB5R3 in patients with sulfonamide hypersensitivity. Pharmacogenetics and genomics. 2012. Sacco James C, 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
Influence of NAT2 polymorphisms on sulfamethoxazole pharmacokinetics in renal transplant recipients. Antimicrobial agents and chemotherapy. 2012. Kagaya Hideaki, 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
Genome-wide association study of serious blistering skin rash caused by drugs. The pharmacogenomics journal. 2011. Shen Y, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Prevalence of G6PD deficiency in a large cohort of HIV-infected patients. The Journal of infection. 2010. Serpa Jose A, 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
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
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Aseptic meningitis, hemolytic anemia, hepatitis, and orthostatic hypotension in a patient treated with trimethoprim-sulfamethoxazole. American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists. 2010. Chisholm-Burns Marie A, 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
TNF, LTA, HSPA1L and HLA-DR gene polymorphisms in HIV-positive patients with hypersensitivity to cotrimoxazole. Pharmacogenomics. 2009. Alfirevic Ana, 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
Trimethoprim and the CYP2C8*3 allele have opposite effects on the pharmacokinetics of pioglitazone. Drug metabolism and disposition: the biological fate of chemicals. 2008. Tornio Aleksi, 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
Glucose-6-phosphate dehydrogenase deficiency. Lancet. 2008. Cappellini M D, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Prevalence and significance of G6PD deficiency in patients of an urban HIV clinic. Journal of the International Association of Physicians in AIDS Care (Chicago, Ill. : 2002). 2008. Tungsiripat Marisa, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Pneumocystis carinii pneumonia in Hong Kong: a 10 year retrospective study. Journal of medical microbiology. 2006. Hui M, 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
The effect of trimethoprim on CYP2C8 mediated rosiglitazone metabolism in human liver microsomes and healthy subjects. British journal of clinical pharmacology. 2005. Hruska M W, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Slow acetylator phenotype and genotype in HIV-positive patients with sulphamethoxazole hypersensitivity. British journal of clinical pharmacology. 2003. Alfirevic Ana, 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
Variant of SCN5A sodium channel implicated in risk of cardiac arrhythmia. Science (New York, N.Y.). 2002. Splawski Igor, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Acetylator phenotype and genotype in HIV-infected patients with and without sulfonamide hypersensitivity. Journal of clinical pharmacology. 2002. O'Neil William M, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Prospective evaluation of detoxification pathways as markers of cutaneous adverse reactions to sulphonamides in AIDS. Pharmacogenetics. 2000. Wolkenstein P, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
The arylamine N-acetyltransferase (NAT2) polymorphism and the risk of adverse reactions to co-trimoxazole in children. European journal of clinical pharmacology. 1998. Zielińska E, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
N-acetyltransferase 2 polymorphism in patients infected with human immunodeficiency virus. Clinical pharmacology and therapeutics. 1996. Kaufmann G R, 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
Options in the management of pneumonia caused by Pneumocystis carinii in patients with acquired immune deficiency syndrome and intolerance to trimethoprim/sulfamethoxazole. Southern medical journal. 1996. Korraa H, 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
Apparent hemolysis in an AIDS patient receiving trimethoprim/sulfamethoxazole: case report and literature review. The Journal of pharmacy technology : jPT : official publication of the Association of Pharmacy Technicians. 1996. Reinke C M, 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
Acetylation phenotype and cutaneous hypersensitivity to trimethoprim-sulphamethoxazole in HIV-infected patients. AIDS (London, England). 1994. Carr A, 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
Glucose-6-phosphate dehydrogenase deficiency. WHO Working Group. Bulletin of the World Health Organization. 1989. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Use of trimethoprim-sulfamethoxazole in a glucose-6-phosphate dehydrogenase-deficient population. Reviews of infectious diseases. 1987. Markowitz N, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Co-trimoxazole in the treatment of typhoid fever in children with glucose-6-phosphate dehydrogenase deficiency. The Southeast Asian journal of tropical medicine and public health. 1978. Lexomboon U, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Drug-induced haemolysis in glucose-6-phosphate dehydrogenase deficiency. British medical journal. 1976. Chan T K, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Letter: Glucose-6-phosphate dehydrogenase deficiency and co-trimoxazole. Lancet. 1975. Chan M C, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Haemolytic effect of trimethoprim-sulphamethoxazole in G-6-PD deficiency. Transactions of the Royal Society of Tropical Medicine and Hygiene. 1974. Chan T K, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
A comparative evaluation of sulfalene-trimethoprim and sulphormethoxine-pyrimethamine against falciparum malaria in Thailand. The American journal of tropical medicine and hygiene. 1973. Chin W, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Acute haemolysis associated with typhoid fever and G.-6-P.D. deficiency. Lancet. 1973. Meyer H A. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Acute haemolysis complicating co-trimoxazole therapy for typhoid fever in a patient with G.-6-P.D. deficiency. Lancet. 1972. Owusu S K. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
The importance of glucose-6-phosphate dehydrogenase screening in a urologic practice. The Journal of urology. 1972. Allen S D, et al. PubMed

LinkOuts

Web Resource:
Wikipedia
National Drug Code Directory:
61570-057-01
DrugBank:
DB00440
ChEBI:
9731
KEGG Compound:
C01965
KEGG Drug:
D00145
PubChem Compound:
5578
PubChem Substance:
156267
46507125
Drugs Product Database (DPD):
2243116
BindingDB:
18069
ChemSpider:
5376
Therapeutic Targets Database:
DAP000927

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