1997 article. Impact of Morning Versus Evening Schedule for Oral Methotrexate and 6-Mercaptopurine on Relapse Risk for Children with Acute Lymphoblastic Leukemia. Schmiegelow, Kjeld et al., Journal of Pediatric Hematology/Oncology, April 1997.
. On the NIH not 6-MP specific.
Circadian time-dependent response of childhood lymphoblastic leukemia to chemotherapy: a long-term follow-up study of survival. Rivard GE et. al., Chronobiol Int. ):201-4. .
6-MP and milk/foods. Many (but not all) parents are told by their oncologists to give 6-MP on an empty stomach, and never to give it at the same time as milk. The first link is to a MedLine abstract that discusses this topic, the second is to an article on the Pediatric Pharmacotherapy web site.
(Rivard GE, Lin KT, Leclerc JM, David M., Am J Pediatr Hematol Oncol. 1989 W 11(4): 402-6.)
. Click on the link to the Volume 1, number 5, 1995 article to download a pdf file.
More information on 6-MP, including references for the milk/food issues, on the .
(Neil K. Burton et al., Cancer Chemotherapy and Pharmacology Volume 18, Number 1, 90-91, 1986)
6-MP and allopurinol. 6-MP is a substrate for xanthine oxidase (XO) which converts it to 6-thiouric acid by oxidation. This appears to be an important route for inactivation of the drug. Allopurinol, a drug used to prevent the hyperuricemia and uricosuria that often follow marked cell kill consequent to leukemia therapy, inhibits this conversion. When 6-MP and allopurinol are used together, the dose of 6-MP is usually lowered. Notably, XO is found in high concentration in cow's milk, thus explaining why 6-MP should not be taken with milk.
6-MP/6-TG metabolites levels. The drug dose is determined by body surface area, but not all kids have the same levels of metabolites in their bloodstream after treatment. There is some evidence that this is an important factor.
History of 6-MP
Gertrude Elion synthesized and co-developed two of the first successful drugs for the treatment of leukemia (thioguanine and mercaptopurine). Read the fascinating article below:
More Information
, on the K.O.A.L.A. site. (Excellent resource.), on Invention and Technology
6-Thioguanine
say: 6-thigh-oh-GWAN-een
6-Thioguanine is closely related to 6-mercaptopurine, both in structure (see above) and in metabolism. Like 6-MP, 6-thioguanine is a purine antimetabolite. Thioguanine inhibits purine biosynthesis as does 6-MP, albeit at different steps: 6-TG is an analogue of huanine while 6-MP is an analogue of hypoxanthine. It is also incorporated into the DNA. (Please see the above discussion for 6-MP.)
Synonyms: 2-Aminopurine-6- L T TG; Wellcome U3B; X 27; 2-Amino 6MP; 2-Amino-6- 2-Amino-6- 2-Aminopurine-6(1H)- 6-Mercapto-2- 6-M 2-amino-1,7-dihydro-6H-purine-6- THG; 6-TG. It is a pale yellow crystalline powder with a melting point greater than 360 degrees centigrade. The CA RN for 6-thioguanine is 154-42-7.
In our protocol (CCG 1961), 6-TG and 6-MP are used at different times for maintenance. I do not know the reason for this, except to assume that past studies found it effective. Historically, these are some of the older chemotherapy drugs, having been used for about 35 years. Both these drugs are given orally on arm B of CCG 1961. In general, 6TG shows greater liver toxicity. (A lot more information on the advantages/disadvantages of these tw I'd advise a search of MedLine, the articles on the KOALA site, and Pui's book Childhood Leukemia if you are interested.)
Possible side effects:
low blood counts
mild nausea
Less common side effects:
mouth sores
abnormal liver function
stomach pain
loss of appetitethioguanine
Available Guidelines
last updated 09/18/2015
Start with reduced doses of thioguanine for patients with one nonfunctional TPMT allele, or drastically reduced doses for patients with malignancy and two n adjust dose based on degree of myelosuppression and disease-specific guidelines. Consider alternative nonthiopurine immunosuppressant therapy for patients with nonmalignant conditions and two nonfunctional alleles.
Annotation
Advance online publication January 2013.The , have been published in Clinical Pharmacology and Therapeutics.
Literature published between June 2010-November 2012 was reviewed and there is no new evidence that would change the original guidelines. Therefore, the dosing recommendations in the original publication remain clinically current. These guidelines are applicable to:pediatric patients adult patientsDownload and read: March 2011Advance online publication January 2011.Guidelines regarding the use of pharmacogenomic tests in dosing for azathioprine, thioguanine and mercaptopurine were published in Clinical Pharmacology and Therapeutics by the Clinical Pharmacogenetics Implementation Consortium ().
Excerpt from the 2011 thiopurine dosing guidelines:"Thiopurines are most commonly used to treat nonmalignant conditions but are also critical anticancer agents. The approach to dosing adjustments based on TPMT status may differ depending on the clinical indication and the propensity to initiate therapy at higher vs. lower starting doses. We and others advocate testing for TPMT status prior to initiating thiopurine therapy, so that starting dosages can be adjusted accordingly."Download and read:
Table 1: Recommended dosing of thioguanine by TPMT phenotypeAdapted from Tables 1 and 2 of the 2011 guideline manuscript. Phenotype (Genotype)
Examples of diplotypes
Implications for pharmacologic measures after thioguanine
Dosing recommendations for thioguanine
Classification of recommendations
Homozygous wild-type or normal, high activity (two functional *1 alleles)
Lower concentrations of TGN metabolites, but note that TGN after thioguanine are 5-10x higher than TGN after mercaptopurine or azathioprine
Start with normal starting dose. Adjust doses of thioguanine and of other myelosuppressive therapy without any special emphasis on thioguanine . Allow 2 weeks to reach steady state after each dose adjustment.
Heterozygote or intermediate activity (one functional allele - *1, plus one nonfunctional allele - *2, *3A, *3B, *3C, or *4)
*1/*2, *1/*3A, *1/*3B, *1/*3C, *1/*4
Moderate to high concentrations of TGN but note that TGN after thioguanine are 5-10x higher than TGN after mercaptopurine or azathioprine
Start with reduced doses (reduce by 30-50%) and adjust doses of thioguanine based on degree of myelosuppression and disease-specific guidelines. Allow 2-4 weeks to reach steady state after each dose adjustment. In setting of myelosuppression, and depending on other therapy, emphasis should be on reducing thioguanine over other agents.
Homozygous variant, mutant, low, or deficient activity (two nonfunctional alleles - *2, *3A, *3B, *3C, or *4)
*3A/*3A, *2/*3A, *3C/*3A, *3C/*4, *3C/*2, *3A/*4
Extremely high concentrations of TGN fatal toxicity possible without dose decrease
Start with drastically reduced doses (reduce daily dose by 10-fold and dose thrice weekly instead of daily) and adjust doses of thioguanine based on degree of myelosuppression and disease-specific guidelines. Allow 4-6 weeks to reach steady state after each dose adjustment. In setting of myelosuppression, emphasis should be on reducing thioguanine over other agents. For nonmalignant conditions, consider alternative nonthiopurine immunosuppressant therapy.
last updated 08/10/2011
Select an alternative drug rather than thioguanine for intermediate and poor TPMT metabolizers.
Annotation
The Royal Dutch Pharmacists Association - Pharmacogenetics Working Group has evaluated therapeutic dose recommendations for thioguanine based on TPMT genotype [Article:].
They recommend selecting an alternative drug for patients carrying inactive alleles. Phenotype (Genotype)
Therapeutic Dose Recommendation
Level of Evidence
Clinical Relevance
IM (one inactive allele: *2, *3, *4-*18)
Select alternative drug.
Insufficient data to allow calculation of dose adjustment.
Published controlled studies of moderate quality* relating to phenotyped and/or genotyped patients or healthy volunteers, and having relevant pharmacokinetic or clinical endpoints.
Clinical effect (S): long-standing discomfort (& 168 hr), permanent symptom or invalidating injury e.g. failure of prophylaxis of ve decreased effect of clopidogrel on inhibition of
ADE resulting from increased bioavail INR & 6.0; neutropenia 0.5-1.0x109/l; leucopenia 1.0-2.0x109/l; thrombocytopenia 25-50x109/l; severe diarrhea.
PM (two inactive alleles: *2, *3, *4-*18)
Select alternative drug.
Insufficient data to allow calculation of dose adjustment.
Published case reports, well documented, and having relevant pharmacokinetic or clinical endpoints. Well documented case series.
Clinical effect (S): unanticipated myelosuppression. *See
for definition of "moderate" quality.S: statistically significant difference.
Annotated Labels
last updated 10/25/2013
Actionable PGx
The drug label recommends substantial dosage reductions for individuals with an inherited deficiency of the enzyme thiopurine methyltransferase (TPMT) to avoid the development of life-threatening bone marrow suppression in these patients. Prescribers should be aware that some laboratories offer testing for TPMT deficiency.
Annotation
The pharmacogenomic releationship between thioguanine and TPMT is well described. See the TPMT VIP and Thiopurines Pathway for more details. Recent work by the Clinical Pharmacogenomics Implementation Consortium (CPIC) has published guidelines for dosing of thioguanine in individuals with TPMT variants.Excerpt from the Thioguanine (Tabloid) drug label: There are individuals with an inherited deficiency of the enzyme thiopurine methyltransferase (TPMT) who may be unusually sensitive to the myelosuppressive effects of thioguanine and prone to developing rapid bone marrow suppression following the initiation of treatment. Substantial dosage reductions may be required to avoid the development of life-threatening bone marrow suppression in these patients. Prescribers should be aware that some laboratories offer testing for TPMT deficiency. Since bone marrow suppression may be associated with factors other than TPMT deficiency, TPMT testing may not identify all patients at risk for severe toxicity. Therefore, close monitoring of clinical and hematologic parameters is important. Bone marrow suppression could be exacerbated by coadministration with drugs that inhibit TPMT, such as olsalazine, mesalazine, or sulphasalazine.For the complete drug label text with sections containing pharmacogenetic information highlighted, see the .*Disclaimer: The contents of this page have not been endorsed by the FDA and are the sole responsibility of PharmGKB.
Genes and/or phenotypes found in this label
Precautions section
source: PHONT
Indications & usage section, Warnings section, Adverse reactions section, Precautions section
source: PHONT
Indications & usage section, Warnings section, Adverse reactions section, Precautions section
source: PHONT
Warnings section, Adverse reactions section, Precautions section
source: PHONT
Dosage & administration section, Warnings section, Precautions section, metabolism/PK
source: FDA Label
last updated 06/08/2015
Actionable PGx
The product monograph for thioguanine (LANVIS) notes that individuals with deficiency of the thiopurine methyltransferase (TPMT) enzyme may be at increased risk of developing myelosuppression when receiving the drug, and that testing for TPMT deficiency is available.
Annotation
Thioguanine (LANVIS) is indicated for treatment of acute leukemia, as well as chronic granulocytic leukemia. Excerpt from the thioguanine (LANVIS) product monograph: There are individuals with an inherited deficiency of the enzyme thiopurine methyltransferase (TPMT) who may be unusually sensitive to the myelosuppressive effect of thioguanine and prone to developing rapid bone marrow depression following the initiation of treatment with LANVIS®. This problem could be exacerbated by coadministration with drugs that inhibit TPMT, such as olsalazine, mesalazine or sulphasalazine. Some laboratories offer testing for TPMT deficiency, although these tests have not been shown to identify all patients at risk of severe toxicity. Therefore, close monitoring of blood counts is still necessary.For the complete product monograph text with sections containing pharmacogenetic information highlighted, see the .*Disclaimer: The contents of this page have not been endorsed by HCSC and are the sole responsibility of PharmGKB.
Clinical Variants that meet the highest level of criteria, manually curated by PharmGKB, are shown below.
To see more Clinical Variants with lower levels of criteria, click the button at the bottom of the page.
Level of Evidence
Toxicity/ADR
Mixed Population
Race Notes
Various races as well as in vitro studies
To see the rest of this clinical annotation please
Level of Evidence
To see the rest of this clinical annotation please
Level of Evidence
Toxicity/ADR
Phenotypes
Mixed Population
Race Notes
Various races as well as in vitro studies
To see the rest of this clinical annotation please
Level of Evidence
Toxicity/ADR
Mixed Population
Race Notes
Various races as well as in vitro studies
To see the rest of this clinical annotation please
Show lower-evidence Clinical Annotations
Hide lower-evidence Clinical Annotations
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.
The following icons indicate that data of a certain type is available:
Dosing Guideline information is available
Drug Label information is available
High-level Clinical Annotation is available
Variant Annotation is available
VIP information is available
Pathway is available
Alternate Names
). If the reference allele is not known, then all alleles are listed with (/). All alleles are given on the positive chromosomal strand, not necessarily the plus strand of the gene. This information is automatically pulled from dbSNP.">?
(+ chr strand)
Amino Acid?
Translation
T>C, T>C, 29457A>G, 719A>G, TPMT*3C, Tyr240Cys
C>A, 8934170G>T, G>T
A>G, 206+1868T>C, 60+1868T>C, A>G
C>T, C>T, 21147G>A, 460G>A, Ala154Thr, TPMT*3B
16420G>C, C>G, C>G, 238G>C, Ala80Pro, TPMT*2, TPMT:238G>C
C>T, C>T, 29363G>A, 626-1G>A, TPMT*4
12542C>A, 779-1748C>A, 779-1751C>A, 8044208C>A, 8104208C>A
A>G, 13698T>C, 148-169T>C, 295-169T>C, 304-169T>C, 373-169T>C, 403-169T>C, A>G
C>T, 17776G>A, 198-642G>A, C>T
C>T, 8787092G>A, G>A
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 144
provided by
2-Amino 6MP
2-Amino-6-mercaptopurine
2-Amino-6-merkaptopurin
2-Amino-6-purinethiol
2-Aminopurin-6-thiol
2-Aminopurine-6(1H)-thione
2-Aminopurine-6-thiol
6-Mercapto-2-aminopurine
6-Mercaptoguanine
6-Thioguanine
Tioguanine
Wellcome U3B
PharmGKB Accession Id
Description
An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia.
Source: Drug Bank
Indication
For remission induction and remission consolidation treatment of acute nonlymphocytic leukemias.
Source: Drug Bank
Other Vocabularies
(C0039902)
Information pulled from DrugBank has not been reviewed by PharmGKB.
Pharmacology, Interactions, and Contraindications
Mechanism of Action
Thioguanine competes with hypoxanthine and guanine for the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRTase) and is itself converted to 6-thioguanilyic acid (TGMP), which reaches high intracellular concentrations at therapeutic doses. TGMP interferes with the synthesis of guanine nucleotides by its inhibition of purine biosynthesis by pseudofeedback inhibition of glutamine-5-phosphoribosylpyrophosphate amidotransferase, the first enzyme unique to the de novo pathway of purine ribonucleotide synthesis. TGMP also inhibits the conversion of inosinic acid (IMP) to xanthylic acid (XMP) by competition for the enzyme IMP dehydrogenase. Thioguanine nucleotides are incorporated into both the DNA and the RNA by phosphodiester linkages, and some studies have shown that incorporation of such false bases contributes to the cytotoxicity of thioguanine. Its tumor inhibitory properties may be due to one or more of its effects on feedback inhibition of de n inhibition of purine nucleot or incorporation into the DNA and RNA. The overall result of its action is a sequential blockade of the utilization and synthesis of the purine nucleotides.
Source: Drug Bank
Pharmacology
Thioguanine is an antineoplastic anti-metabolite used in the treatment of several forms of leukemia including acute nonlymphocytic leukemia. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA. They prevent these substances becoming incorporated in to DNA during the "S" phase (of the cell cycle), stopping normal development and division. Thioguanine was first synthesized and entered into clinical trial more than 30 years ago. It is a 6-thiopurine analogue of the naturally occurring purine bases hypoxanthine and guanine. Intracellular activation results in incorporation into DNA as a false purine base. An additional cytotoxic effect is related to its incorporation into RNA. Thioguanine is cross-resistant with mercaptopurine. Cytotoxicity is cell cycle phase-specific (S-phase).
Source: Drug Bank
Absorption, Distribution, Metabolism, Elimination & Toxicity
Biotransformation
Hepatic. First converted to 6-thioguanilyic acid (TGMP). TGMP is further converted to the di- and tri-phosphates, thioguanosine diphosphate (TGDP) and thioguanosine triphosphate (TGTP) by the same enzymes that metabolize guanine nucleotides.
Source: Drug Bank
Absorption
Absorption of an oral dose is incomplete and variable, averaging approximately 30% of the administered dose (range: 14% to 46%)
Source: Drug Bank
80 minutes (range 25-240 minutes)
Source: Drug Bank
Oral, mouse: LD 50 = 160 mg/kg. Symptoms of overdose include nausea, vomiting, malaise, hypotension, and diaphoresis.
Source: Drug Bank
Chemical Properties
Chemical Formula
Source: Drug Bank
Isomeric SMILES
c1[nH]c2c(=S)[nH]c(nc2n1)N
Source: OpenEye
Canonical SMILES
NC1=NC(=S)C2=C(N1)N=CN2
Source: Drug Bank
Average Molecular Weight
Source: Drug Bank
Monoisotopic Molecular Weight
Source: Drug Bank
PharmGKB Curated Pathways
Pathways created internally by PharmGKB based primarily on literature evidence.
External Pathways
Links to non-PharmGKB pathways.
PharmGKB contains no links to external pathways for this drug. To report a pathway,
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
The following icons indicate that data of a certain type is available:
Dosing Guideline information is available
Drug Label information is available
High-level Clinical Annotation is available
Variant Annotation is available
VIP information is available
Pathway is available
EvidenceGene
Drug Targets
Description
(source: Drug Bank)
(source: Drug Bank)
(source: Drug Bank)
Drug Interactions
Description
The 5-ASA derivative increases the toxicity of thiopurine
(source: Drug Bank)
The 5-ASA derivative increases the toxicity of thiopurine
(source: Drug Bank)
The 5-ASA derivative increases the toxicity of thiopurine
(source: Drug Bank)
The 5-ASA derivative increases the toxicity of thiopurine
(source: Drug Bank)
Busulfan increases the hepatoxicity of Thioguanine during long-term concomitant therapy.
(source: Drug Bank)
Complete cross resistance may occur.
(source: Drug Bank)
The 5-ASA derivative increases the toxicity of thiopurine
(source: Drug Bank)
The 5-ASA derivative increases the toxicity of thiopurine
(source: Drug Bank)
The immunosuppressant, Thioguanine, may increase the adverse effects of Natalizumab. Increased risk of Progressive Multifocal Leukoencephalopathy (PML) and other infections. Concurrent therapy should be avoided.
(source: Drug Bank)
The 5-ASA derivative increases the toxicity of thiopurine
(source: Drug Bank)
The 5-ASA derivative increases the toxicity of thiopurine
(source: Drug Bank)
The 5-ASA derivative increases the toxicity of thiopurine
(source: Drug Bank)
The 5-ASA derivative increases the toxicity of thiopurine
(source: Drug Bank)
Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events.
(source: Drug Bank)
Curated Information
The following icons indicate that data of a certain type is available:
Dosing Guideline information is available
Drug Label information is available
High-level Clinical Annotation is available
Variant Annotation is available
VIP information is available
Pathway is available
EvidenceDisease
Relationships from
Contraindicated With
contraindicated with
contraindicated with
Publications related to thioguanine: 165
Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 2015. Pui Ching-Hon, et al.
Blood. 2015. Moriyama Takaya, et al.
British journal of clinical pharmacology. 2015. Ogungbenro Kayode, et al.
Cancer chemotherapy and pharmacology. 2015. Levinsen Mette, et al.
Pharmacogenetics and genomics. 2015. Kim Hyun-Young, et al.
British journal of haematology. 2014. Lennard Lynne, et al.
The American surgeon. 2014. El-Sedfy Abraham, et al.
British journal of clinical pharmacology. 2014. Konidari Anastasia, et al.
British journal of clinical pharmacology. 2014. Lennard Lynne.
Pharmacogenetics and genomics. 2014. Roberts Rebecca L, et al.
Pharmacogenomics. 2014. Matimba Alice, et al.
Nature genetics. 2013. Perez-Andreu Virginia, et al.
British journal of clinical pharmacology. 2013. Lennard Lynne, et al.
Pharmacogenetics and genomics. 2013. Appell Malin L, et al.
Clinical pharmacology and therapeutics. 2013. Relling M V, et al.
Human molecular genetics. 2012. Stocco Gabriele, et al.
Pharmacogenomics. 2012. Dorababu Patchva, et al.
PloS one. 2012. Kim Hyery, et al.
Pediatric blood & cancer. 2011. Peregud-Pogorzelski Jaros?aw, et al.
Alimentary pharmacology & therapeutics. 2011. González-Lama Y, et al.
Experimental and clinical transplantation : official journal of the Middle East Society for Organ Transplantation. 2011. Aghdaie Mahdokht Hossein, et al.
Nature reviews. Nephrology. 2011. Budhiraja Pooja, et al.
Inflammatory bowel diseases. 2011. Landy J, et al.
Pharmacogenomics. 2011. Newman William G, et al.
British journal of clinical pharmacology. 2011. Adam de Beaumais Tiphaine, et al.
Clinical pharmacology and therapeutics. 2011. Relling M V, et al.
Clinical pharmacology and therapeutics. 2011. Swen J J, et al.
Nature genetics. 2011. Yang Jun J, et al.
Drug metabolism and disposition: the biological fate of chemicals. 2010. Li Fang, et al.
PloS one. 2011. Hosni-Ahmed Amira, et al.
Pharmacogenetics and genomics. 2010. Appell Malin Lindqvist, et al.
Pharmacogenomics. 2010. Becker Mara L, et al.
Pharmacogenomics. 2010. Beaulieu Mathieu, et al.
The pharmacogenomics journal. 2010. Fridley B L, et al.
Cancer chemotherapy and pharmacology. 2010. Hedeland Rikke L, et al.
Leukemia research. 2010. Kapoor Gauri, et al.
British journal of pharmacology. 2010. de Graaf P, et al.
World journal of gastroenterology : WJG. 2010. Dong Xian-Wen, et al.
Pharmacogenetics and genomics. 2010. Wang Liewei, et al.
Pharmacogenomics. 2010. Errasti-Murugarren Ekaitz, et al.
Biochemical pharmacology. 2010. Feng Qiping, et al.
Pharmacogenomics. 2010. Smith Melissa A, et al.
Journal of clinical pharmacy and therapeutics. 2010. Gazouli M, et al.
Pharmacogenomics. 2010. Higgs Jenny E, et al.
Journal of clinical gastroenterology. 2010. Kim Jae Hak, et al.
Pharmacogenomics. 2009. Serpe Loredana, et al.
Blood. 2009. Stanulla Martin, et al.
British journal of clinical pharmacology. 2009. Kham Shirley Kow Yin, et al.
Clinical therapeutics. 2009. Vannaprasaht Suda, et al.
Journal of gastroenterology and hepatology. 2009. Takatsu Noritaka, et al.
Expert opinion on drug metabolism & toxicology. 2009. Grossman Iris.
Leukemia. 2009. Karas-Kuzelicki N, et al.
European journal of clinical pharmacology. 2009. Xin Hua-Wen, et al.
Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2009. Schmiegelow K, et al.
Pediatric blood & cancer. 2009. Samochatova Elena V, et al.
Inflammatory bowel diseases. 2008. Rahhal Riad M, et al.
Therapeutic drug monitoring. 2008. Silva Marcilene Rezende, et al.
Alimentary pharmacology & therapeutics. 2008. Ansari A, et al.
Pharmacogenetics and genomics. 2008. Ujiie Shuta, et al.
Biochemical pharmacology. 2008. Garat A, et al.
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2008. Gardiner Sharon J, et al.
American journal of hematology. 2008. Yenson Paul R, et al.
Clinical chemistry and laboratory medicine : CCLM / FESCC. 2008. Tamm Riin, et al.
Internal medicine (Tokyo, Japan). 2008. Ban Hiromitsu, et al.
Medical oncology (Northwood, London, England). 2008. Taja-Chayeb Lucia, et al.
American journal of hematology. 2007. Tumer Tugba Boyunegmez, et al.
Pharmacogenetics and genomics. 2007. Lindqvist Malin, et al.
Alimentary pharmacology & therapeutics. 2007. Winter J W, et al.
Cancer research. 2007. Hartford Christine, et al.
C international journal of clinical chemistry. 2007. Zhang Li-Rong, et al.
Liver international : official journal of the International Association for the Study of the Liver. 2007. Tamori Akihiro, et al.
Therapeutic drug monitoring. 2007. Dilger Karin, et al.
Journal of clinical pharmacy and therapeutics. 2006. Song D-K, et al.
Therapeutic drug monitoring. 2006. Dokmanovic Lidija, et al.
Clinical pharmacology and therapeutics. 2006. Lennard Lynne, et al.
Gut. 2006. Hindorf U, et al.
Lancet. 2006. Vora Ajay, et al.
Human mutation. 2006. Schaeffeler Elke, et al.
The British journal of dermatology. 2006. Moloney F J, et al.
Alimentary pharmacology & therapeutics. 2006. De Ridder L, et al.
Biochemical and biophysical research communications. 2006. Fotoohi Alan Kambiz, et al.
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2006. Zelinkova Zuzana, et al.
Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver. 2005. Stocco G, et al.
Pharmacological reports : PR. 2006. Chrzanowska Maria, et al.
Pharmacology. 2006. Milek M, et al.
Biological & pharmaceutical bulletin. 2005. Okada Yuko, et al.
Pharmacogenetics and genomics. 2005. Salavaggione Oreste E, et al.
Internal medicine journal. 2005. Gearry R B, et al.
Journal of biotechnology. 2005. Ganter Brigitte, et al.
Therapeutic drug monitoring. 2005. Kurzawski Mateusz, et al.
Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society. 2005. Breen David P, et al.
Gastroentérologie clinique et biologique. 2005. Daniel Fady, et al.
Journal of the neurological sciences. 2005. Heckmann Jeannine M, et al.
JAMA : the journal of the American Medical Association. 2005. Stanulla Martin, et al.
Biochemical pharmacology. 2005. Hamdan-Khalil Rima, et al.
Clinical and experimental rheumatology. 2005. Jun J B, et al.
Therapeutic drug monitoring. 2004. Hindorf Ulf, et al.
American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons. 2004. Formea Christine M, et al.
Scandinavian journal of gastroenterology. 2004. Hindorf U, et al.
Transplant international : official journal of the European Society for Organ Transplantation. 2004. Fabre Margarete A, et al.
Pharmacogenetics. 2004. Schaeffeler Elke, et al.
Human mutation. 2004. Duan Jianxin, et al.
Clinical pharmacology and therapeutics. 2004. Nygaard Ulrikka, et al.
European journal of clinical pharmacology. 2004. Ganiere-Monteil Catherine, et al.
Pharmacogenetics. 2004. Lindqvist Malin, et al.
Therapeutic drug monitoring. 2004. Evans William E.
Clinical chemistry. 2004. Haglund Sofie, et al.
European journal of gastroenterology & hepatology. 2003. Cheung Seau-Tak, et al.
Biochemical and biophysical research communications. 2003. Hamdan-Khalil Rima, et al.
Oncogene. 2003. Krynetski Eugene, et al.
Therapeutic drug monitoring. 2003. Indjova Dessislava, et al.
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