Chemical: Drug
trimethoprim

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Prescribing Info (0) Drug Labels (3) Clinical Annotations (2)

PharmGKB contains no prescribing info for this . Contact us to report known genotype-based dosing guidelines, or if you are interested in developing guidelines.

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Annotated Labels

Annotation of FDA Label for sulfamethoxazole,trimethoprim and G6PD
Annotation of PMDA Label for sulfamethoxazole,trimethoprim and G6PD
Annotation of HCSC Label for sulfamethoxazole,trimethoprim and G6PD

last updated 01/15/2014

1. Annotation of FDA Label for sulfamethoxazole,trimethoprim and G6PD

On FDA Biomarker List

Actionable PGx

Summary

Sulfamethoxazole and trimethoprim is used to prevent and treat infections caused by certain bacteria. The label warns that hemolysis may occur in G6PD deficient individuals.

There's more of this label. Read more.

2. Annotation of PMDA Label for sulfamethoxazole,trimethoprim and G6PD

Actionable PGx

Summary

The PMDA package insert for sulfamethoxazole and trimethoprim (DAIPHEN) states that hemolysis may occur in patients with G6PD deficiency.

There's more of this label. Read more.

3. Annotation of HCSC Label for sulfamethoxazole,trimethoprim and G6PD

Actionable PGx

Summary

The product monograph for sulfamethoxazole and trimethoprim (SULFATRIM) states that hemolysis may occur in individuals taking the drug who are deficient in glucose-6-phosphate dehydrogenase (G6PD). However, it does not make any statements regarding testing for G6PD deficiency prior to treatment.

There's more of this label. Read more.

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.

Clinical Annotation for G6PD B (wildtype), G6PD Canton, Taiwan-Hakka, Gifu-like, Agrigento-like, sulfamethoxazole, sulfamethoxazole and trimethoprim, trimethoprim and Hemolysis (level 3 Toxicity/ADR)

Level of Evidence: Level 3
Type: Toxicity/ADR
Variant: B (wildtype), Canton, Taiwan-Hakka, Gifu-like, Agrigento-like
Genes: G6PD
Phenotypes: Hemolysis
OMB Race: Mixed Population

To see the rest of this clinical annotation please register or sign in.

Clinical Annotation for GSTM1 non-null, GSTM1 null, sulfamethoxazole, trimethoprim and Acquired Immunodeficiency Syndrome (level 3 Toxicity/ADR)

Level of Evidence: Level 3
Type: Toxicity/ADR
Variant: non-null, null
Genes: GSTM1
Phenotypes: Acquired Immunodeficiency Syndrome
OMB Race: Unknown

To see the rest of this clinical annotation please register or sign in.

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

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	Gene ?	Variant? (147)	Alternate Names ?	Chemicals ?	Alleles ? (+ chr strand)	Function ?	Amino Acid? Translation
CA	G6PD	B (wildtype)		sulfamethoxazole sulfamethoxazole and trimethoprim trimethoprim	N/A	N/A	N/A
CA VA	G6PD	Canton, Taiwan-Hakka, Gifu-like, Agrigento-like		sulfamethoxazole sulfamethoxazole and trimethoprim trimethoprim	N/A	N/A	N/A
CA	GSTM1	non-null		sulfamethoxazole trimethoprim	N/A	N/A	N/A
CA VA	GSTM1	null		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*4		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*5		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*5A		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*5B		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*6		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*6A		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*6B		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*7		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*7A		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*7B		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*13		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*14A		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	*14B		sulfamethoxazole trimethoprim	N/A	N/A	N/A
VA	NAT2	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	sulfamethoxazole trimethoprim	C > T	SNP	Y94Y
VA	NAT2	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	sulfamethoxazole trimethoprim	G > A	SNP	R268K
VA	NAT2	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	sulfamethoxazole trimethoprim	C > T	SNP	L161L
VA	NAT2	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	sulfamethoxazole trimethoprim	G > A	SNP	R197Q
VA	NAT2	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	sulfamethoxazole trimethoprim	G > A	SNP	G286E
VA	NAT2	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	sulfamethoxazole trimethoprim	T > C	SNP	I114T
VA	SLC47A1	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	metformin trimethoprim	G > A	SNP
VA	SLC22A2	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	metformin trimethoprim	A > C	SNP	S270A
VA	NAT2	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	sulfamethoxazole trimethoprim	A > T	SNP	M205L
VA	CYB5R3	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	sulfamethoxazole trimethoprim	C > G	SNP
VA	CYB5A	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	sulfamethoxazole trimethoprim	A > C	SNP	S5A
VA	CYB5R3	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	sulfamethoxazole trimethoprim	C > T	SNP	R297H
VA	CYB5A	rs7663179	NC_000004.11:g.25092357T>C, NC_000004.12:g.25090735T>C	sulfamethoxazole trimethoprim	T > C	SNP
VA	CYB5A	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	sulfamethoxazole trimethoprim	C > T	SNP
VA	CYB5R3	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	sulfamethoxazole trimethoprim	A > G	SNP
VA	CYB5R3	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	sulfamethoxazole trimethoprim	G > A	SNP

Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 147

[ see larger image ] [ see 3D structure ]

provided by PubChem

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

ATC: Trimethoprim and derivatives (J01EA)
UMLS: Trimethoprim (C0041041)
RxNorm: Trimethoprim (10829)
NDFRT: TRIMETHOPRIM (N0000146103)

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

Average Molecular Weight

290.3177

Source: Drug Bank

Monoisotopic Molecular Weight

290.137890462

Source: Drug Bank

SMILES

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

Source: PubChem

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: PubChem

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 ?

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Evidence	Gene
DL	ABCB1
VA	CYB5A
VA	CYB5R3
DL	CYP2C8
DL	CYP2C9
DL CA VA	G6PD
CA VA	GSTM1
VA	NAT2
DL	SLC22A1
DL VA	SLC22A2
VA	SLC47A1

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 ?

view legend

Evidence	Disease
CA VA	Acquired Immunodeficiency Syndrome
VA	Anemia
VA	Anemia, Hemolytic
DL	Bronchitis, Chronic
DL	Diarrhea
DL	Dysentery, Bacillary
CA VA	Hemolysis
VA	HIV
VA	Hypersensitivity
VA	Infection
VA	Malaria
DL	Otitis Media
VA	Pneumonia
DL	Pneumonia, Pneumocystis
DL	Seizures
VA	Sepsis
VA	severe cutaneous adverse reactions
DL	Urinary Tract Infections

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

May Treat

trimethoprim may treat AIDS-Related Opportunistic Infections
trimethoprim may treat Bronchitis
trimethoprim may treat Enterobacteriaceae Infections
trimethoprim may treat Escherichia coli Infections
trimethoprim may treat Eye Infections, Bacterial
trimethoprim may treat Pneumonia, Pneumocystis
trimethoprim may treat Proteus infection NOS
trimethoprim may treat Respiratory Tract Infections
trimethoprim may treat Staphylococcal Infections
trimethoprim may treat Toxoplasmosis
trimethoprim may treat Urinary Tract Infections

Contraindicated With

trimethoprim contraindicated with Anemia, Megaloblastic
trimethoprim contraindicated with Drug Hypersensitivity
trimethoprim contraindicated with Folic Acid Deficiency

Publications related to trimethoprim: 34

view legend

	CYP2B6 genotype-based efavirenz dose recommendations during rifampicin-based antituberculosis cotreatment for a sub-Saharan Africa population. Pharmacogenomics. 2016. Mukonzo Jackson K, et al.
	Pharmacogenomics of antimicrobial agents. Pharmacogenomics. 2014. Aung Ar Kar, et al.
VA	Trimethoprim-Metformin Interaction and its Genetic Modulation by OCT2 and MATE1. British journal of clinical pharmacology. 2013. Grün Barbara, et al.
VA	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.
	Influence of NAT2 polymorphisms on sulfamethoxazole pharmacokinetics in renal transplant recipients. Antimicrobial agents and chemotherapy. 2012. Kagaya Hideaki, et al.
	Genome-wide association study of serious blistering skin rash caused by drugs. The pharmacogenomics journal. 2011. Shen Y, et al.
CA VA	Prevalence of G6PD deficiency in a large cohort of HIV-infected patients. The Journal of infection. 2010. Serpa Jose A, et al.
	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.
CA VA	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.
	TNF, LTA, HSPA1L and HLA-DR gene polymorphisms in HIV-positive patients with hypersensitivity to cotrimoxazole. Pharmacogenomics. 2009. Alfirevic Ana, et al.
	Trimethoprim and the CYP2C83 allele have opposite effects on the pharmacokinetics of pioglitazone. Drug metabolism and disposition: the biological fate of chemicals.* 2008. Tornio Aleksi, et al.
	Glucose-6-phosphate dehydrogenase deficiency. Lancet. 2008. Cappellini M D, et al.
CA VA	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.
CA	Pneumocystis carinii pneumonia in Hong Kong: a 10 year retrospective study. Journal of medical microbiology. 2006. Hui M, et al.
	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.
VA	Slow acetylator phenotype and genotype in HIV-positive patients with sulphamethoxazole hypersensitivity. British journal of clinical pharmacology. 2003. Alfirevic Ana, et al.
	Variant of SCN5A sodium channel implicated in risk of cardiac arrhythmia. Science (New York, N.Y.). 2002. Splawski Igor, et al.
VA	Acetylator phenotype and genotype in HIV-infected patients with and without sulfonamide hypersensitivity. Journal of clinical pharmacology. 2002. O'Neil William M, et al.
CA VA	Prospective evaluation of detoxification pathways as markers of cutaneous adverse reactions to sulphonamides in AIDS. Pharmacogenetics. 2000. Wolkenstein P, et al.
VA	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.
VA	N-acetyltransferase 2 polymorphism in patients infected with human immunodeficiency virus. Clinical pharmacology and therapeutics. 1996. Kaufmann G R, et al.
	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.
	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.
	Acetylation phenotype and cutaneous hypersensitivity to trimethoprim-sulphamethoxazole in HIV-infected patients. AIDS (London, England). 1994. Carr A, et al.
	Glucose-6-phosphate dehydrogenase deficiency. WHO Working Group. Bulletin of the World Health Organization. 1989.
CA VA	Use of trimethoprim-sulfamethoxazole in a glucose-6-phosphate dehydrogenase-deficient population. Reviews of infectious diseases. 1987. Markowitz N, et al.
CA	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.
CA VA	Drug-induced haemolysis in glucose-6-phosphate dehydrogenase deficiency. British medical journal. 1976. Chan T K, et al.
CA	Letter: Glucose-6-phosphate dehydrogenase deficiency and co-trimoxazole. Lancet. 1975. Chan M C, et al.
CA VA	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.
CA VA	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.
CA	Acute haemolysis associated with typhoid fever and G.-6-P.D. deficiency. Lancet. 1973. Meyer H A.
CA	Acute haemolysis complicating co-trimoxazole therapy for typhoid fever in a patient with G.-6-P.D. deficiency. Lancet. 1972. Owusu S K.
CA	The importance of glucose-6-phosphate dehydrogenase screening in a urologic practice. The Journal of urology. 1972. Allen S D, et al.

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

Clinical Trials

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Sources for PharmGKB drug information: DrugBank, PubChem.

Chemical: Drug trimethoprim

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May Treat

Contraindicated With

Publications related to trimethoprim: 34

LinkOuts

Chemical: Drug
trimethoprim