WARNING: This product is for research use only, not for human or veterinary use.

MedKoo CAT#: 100850

CAS#: 154-42-7

Description: Tioguanine (INN, BAN), or thioguanine (AAN, USAN), commonly referred to as 6-thioguanine (6-TG) is a medication used to treat a number of types of leukemia. It has been used less frequently in recent years because of safety concerns. However, it is becoming more widely used for treating ulcerative colitis and some autoimmune diseases.

Chemical Structure

CAS# 154-42-7

Theoretical Analysis

MedKoo Cat#: 100850
Name: Thioguanine
CAS#: 154-42-7
Chemical Formula: C5H5N5S
Exact Mass: 167.02657
Molecular Weight: 167.19
Elemental Analysis: C, 35.92; H, 3.01; N, 41.89; S, 19.18

Price and Availability

Size Price Availability Quantity
1.0g USD 250.0 2 Weeks
2.0g USD 350.0 2 Weeks
5.0g USD 550.0 2 Weeks
10.0g USD 850.0 2 Weeks
20.0g USD 1450.0 2 Weeks
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Synonym: Tabloid; Tabloid brand thioguanine; Tioguanine. Foreign brand names: Lanvis; Tioguanin. Abbreviations: 6TG; TG. Code names: BW 5071; Wellcome U3B; WR1141; X 27. Chemical structure names: * 2Amino 6MP; * 2Amino17dihydro6Hpurine6thione; * 2Amino6mercaptopurine; * 2Amino6purinethiol; * 2Aminopurin6thiol; * 2Aminopurine6(1H)thione; * 2Aminopurine6thiol; * 6 Mercaptoguanine; * 6 Thioguanine; * 6HPurine6thione 2amino17dihydro (9CI); * 6Mercapto2aminopurine; * 6mercaptoguanine; * 6thioguanine.

IUPAC/Chemical Name: 2-amino-1H-purine-6(7H)-thione


InChi Code: InChI=1S/C5H5N5S/c6-5-9-3-2(4(11)10-5)7-1-8-3/h1H,(H4,6,7,8,9,10,11)


Appearance: Solid powder

Purity: >98% (or refer to the Certificate of Analysis)

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical. This product is stable enough for a few weeks during ordinary shipping and time spent in Customs.

Storage Condition: Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).

Solubility: Soluble in DMSO, not in water

Shelf Life: >2 years if stored properly

Drug Formulation: This drug may be formulated in DMSO

Stock Solution Storage: 0 - 4 C for short term (days to weeks), or -20 C for long term (months).

HS Tariff Code: 2934.99.9001

Preparing Stock Solutions

The following data is based on the product molecular weight 167.19 Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.

Recalculate based on batch purity %
Concentration / Solvent Volume / Mass 1 mg 5 mg 10 mg
1 mM 1.15 mL 5.76 mL 11.51 mL
5 mM 0.23 mL 1.15 mL 2.3 mL
10 mM 0.12 mL 0.58 mL 1.15 mL
50 mM 0.02 mL 0.12 mL 0.23 mL

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  1: Ren X, Xu YZ, Karran P. Photo-oxidation of 6-Thioguanine by UVA: The Formation of Addition Products with Low Molecular Weight Thiol Compounds. Photochem Photobiol. 2010 Jun 21. [Epub ahead of print] PubMed PMID: 20573042.

2: Ren X, Li F, Jeffs G, Zhang X, Xu YZ, Karran P. Guanine sulphinate is a major stable product of photochemical oxidation of DNA 6-thioguanine by UVA irradiation. Nucleic Acids Res. 2010 Apr;38(6):1832-40. Epub 2009 Dec 21. PubMed PMID: 20026585; PubMed Central PMCID: PMC2847230.

3: Brem R, Li F, Karran P. Reactive oxygen species generated by thiopurine/UVA cause irreparable transcription-blocking DNA lesions. Nucleic Acids Res. 2009 Apr;37(6):1951-61. Epub 2009 Feb 10. PubMed PMID: 19208641; PubMed Central PMCID: PMC2665240.

4: Hawwa AF, Millership JS, Collier PS, Vandenbroeck K, McCarthy A, Dempsey S, Cairns C, Collins J, Rodgers C, McElnay JC. Pharmacogenomic studies of the anticancer and immunosuppressive thiopurines mercaptopurine and azathioprine. Br J Clin Pharmacol. 2008 Oct;66(4):517-28. Epub 2008 Jun 28. PubMed PMID: 18662289; PubMed Central PMCID: PMC2561120.

5: Vethe NT, Bremer S, Bergan S. IMP dehydrogenase basal activity in MOLT-4 human leukaemia cells is altered by mycophenolic acid and 6-thioguanosine. Scand J Clin Lab Invest. 2008;68(4):277-85. PubMed PMID: 18609073.

6: Krishnamurthy P, Schwab M, Takenaka K, Nachagari D, Morgan J, Leslie M, Du W, Boyd K, Cheok M, Nakauchi H, Marzolini C, Kim RB, Poonkuzhali B, Schuetz E, Evans W, Relling M, Schuetz JD. Transporter-mediated protection against thiopurine-induced hematopoietic toxicity. Cancer Res. 2008 Jul 1;68(13):4983-9. PubMed PMID: 18593894.

7: Yuan B, Wang Y. Mutagenic and cytotoxic properties of 6-thioguanine, S6-methylthioguanine, and guanine-S6-sulfonic acid. J Biol Chem. 2008 Aug 29;283(35):23665-70. Epub 2008 Jun 30. PubMed PMID: 18591241.

8: Zeng X, Kinsella TJ. Mammalian target of rapamycin and S6 kinase 1 positively regulate 6-thioguanine-induced autophagy. Cancer Res. 2008 Apr 1;68(7):2384-90. PubMed PMID: 18381446.

9: Saczewski F, Maruszak M, Bednarski PJ. Synthesis and cytotoxic activity of imidazo[1,2-a]-1,3,5-triazine analogues of 6-mercaptopurine. Arch Pharm (Weinheim). 2008 Feb;341(2):121-5. PubMed PMID: 18186543.

10: Kalra S, Jena G, Tikoo K, Mukhopadhyay AK. Preferential inhibition of xanthine oxidase by 2-amino-6-hydroxy-8-mercaptopurine and 2-amino-6-purine thiol. BMC Biochem. 2007 May 18;8:8. PubMed PMID: 17511860; PubMed Central PMCID: PMC1885804.

Additional Information

T hioguanine is a synthetic guanosine analogue antimetabolite. Phosphorylated by hypoxanthine-guanine phosphoribosyltransferase, thioguanine incorporates into DNA and RNA, resulting in inhibition of DNA and RNA syntheses and cell death. This agent also inhibits glutamine-5-phosphoribosylpyrophosphate amidotransferase, thereby inhibiting purine synthesis. Check for active clinical trials or closed clinical trials using this agent. (NCI Thesaurus).Its principal use is in acute leukaemias and chronic myeloid leukaemia. It has been investigated for use in treatment of psoriasis.
Mechanism of Action
After incorporation into DNA, the thiocarbonyl of thioguanine has a tendency to be methylated. This produces a base similar to 6-O-methylguanine. During a second round of replication, the mismatch repair system will recognize the mismatch between the methylated base and cytosine. The attempt to repair such a mismatch is abortive since no nucleotides can be properly matched with the methylated base. This leads to persistent 100-200 base single strand breaks. Such a genotoxic stress will trigger cell cycle arrest and cell death. In this regard, thioguanine and mercaptopurine, although categorized as antimetabolites, exert their functions more like a genotoxic methylating agents, such as temozolomide, which methylates DNA and generate 6-O-methylguanine and cytosine mismatch. The ability of thioguanine and mercaptopurine to trigger genotoxic stress is also exemplified by their treatment-related acute myeloid leukemia (AML), which is uncommon for antimetabolites, but common for alkylating agents and topoisomerase inhibitors. (source:
TABLOID brand Thioguanine was synthesized and developed by Hitchings, Elion, and associates at the Wellcome Research Laboratories. It is one of a large series of purine analogues which interfere with nucleic acid biosynthesis, and has been found active against selected human neoplastic diseases. Thioguanine, known chemically as 2-amino-1,7-dihydro-6H-purine-6-thione, is an analogue of the nucleic acid constituent guanine, and is closely related structurally and functionally to PURINETHOL® (mercaptopurine). TABLOID brand Thioguanine is available in tablets for oral administration. Each scored tablet contains 40 mg thioguanine and the inactive ingredients gum acacia, lactose, magnesium stearate, potato starch, and stearic acid.
Clinical studies have shown that the absorption of an oral dose of thioguanine in humans is incomplete and variable, averaging approximately 30% of the administered dose (range: 14% to 46%). Following oral administration of 35S-6-thioguanine, total plasma radioactivity reached a maximum at 8 hours and declined slowly thereafter. Parent drug represented only a very small fraction of the total plasma radioactivity at any time, being virtually undetectable throughout the period of measurements. The oral administration of radiolabeled thioguanine revealed only trace quantities of parent drug in the urine. However, a methylated metabolite, 2-amino-6-methylthiopurine (MTG), appeared very early, rose to a maximum 6 to 8 hours after drug administration, and was still being excreted after 12 to 22 hours. Radiolabeled sulfate appeared somewhat later than MTG but was the principal metabolite after 8 hours. Thiouric acid and some unidentified products were found in the urine in small amounts. Intravenous administration of 35S-6-thioguanine disclosed a median plasma half-disappearance time of 80 minutes (range: 25 to 240 minutes) when the compound was given in single doses of 65 to 300 mg/m2. Although initial plasma levels of thioguanine did correlate with the dose level, there was no correlation between the plasma half-disappearance time and the dose. Thioguanine is incorporated into the DNA and the RNA of human bone marrow cells. Studies with intravenous 35S-6-thioguanine have shown that the amount of thioguanine incorporated into nucleic acids is more than 100 times higher after 5 daily doses than after a single dose. With the 5-dose schedule, from one-half to virtually all of the guanine in the residual DNA was replaced by thioguanine. Tissue distribution studies of 35S-6-thioguanine in mice showed only traces of radioactivity in brain after oral administration. No measurements have been made of thioguanine concentrations in human cerebrospinal fluid (CSF), but observations on tissue distribution in animals, together with the lack of CNS penetration by the closely related compound, mercaptopurine, suggest that thioguanine does not reach therapeutic concentrations in the CSF. Monitoring of plasma levels of thioguanine during therapy is of questionable value. There is technical difficulty in determining plasma concentrations, which are seldom greater than 1 to 2 mcg/mL after a therapeutic oral dose. More significantly, thioguanine enters rapidly into the anabolic and catabolic pathways for purines, and the active intracellular metabolites have appreciably longer half-lives than the parent drug. The biochemical effects of a single dose of thioguanine are evident long after the parent drug has disappeared from plasma. Because of this rapid metabolism of thioguanine to active intracellular derivatives, hemodialysis would not be expected to appreciably reduce toxicity of the drug. Thioguanine competes with hypoxanthine and guanine for the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRTase) and is itself converted to 6-thioguanylic acid (TGMP). This nucleotide reaches high intracellular concentrations at therapeutic doses. TGMP interferes at several points with the synthesis of guanine nucleotides. It inhibits de novo purine biosynthesis by pseudo-feedback inhibition of glutamine-5-phosphoribosylpyrophosphate amidotransferase-the first enzyme unique to the de novo pathway for purine ribonucleotide synthesis. TGMP also inhibits the conversion of inosinic acid (IMP) to xanthylic acid (XMP) by competition for the enzyme IMP dehydrogenase. At one time TGMP was felt to be a significant inhibitor of ATP:GMP phosphotransferase (guanylate kinase), but recent results have shown this not to be so. Thioguanylic acid is further converted to the di- and tri-phosphates, thioguanosine diphosphate (TGDP) and thioguanosine triphosphate (TGTP) (as well as their 2' -deoxyribosyl analogues) by the same enzymes which metabolize guanine nucleotides. Thioguanine nucleotides are incorporated into both the RNA and the DNA by phosphodiester linkages and it has been argued that incorporation of such fraudulent bases contributes to the cytotoxicity of thioguanine. Thus, thioguanine has multiple metabolic effects and at present it is not possible to designate one major site of action. Its tumor inhibitory properties may be due to one or more of its effects on (a) feedback inhibition of de novo purine synthesis; (b) inhibition of purine nucleotide interconversions; or (c) incorporation into the DNA and the RNA. The net consequence of its actions is a sequential blockade of the synthesis and utilization of the purine nucleotides. The catabolism of thioguanine and its metabolites is complex and shows significant differences between humans and the mouse. In both humans and mice, after oral administration of 35S-6-thioguanine, urine contains virtually no detectable intact thioguanine. While deamination and subsequent oxidation to thiouric acid occurs only to a small extent in humans, it is the main pathway in mice. The product of deamination by guanase, 6-thioxanthine is inactive, having negligible antitumor activity. This pathway of thioguanine inactivation is not dependent on the action of xanthine oxidase, and an inhibitor of that enzyme (such as allopurinol) will not block the detoxification of thioguanine even though the inactive 6-thioxanthine is normally further oxidized by xanthine oxidase to thiouric acid before it is eliminated. In humans, methylation of thioguanine is much more extensive than in the mouse. The product of methylation, 2-amino-6-methylthiopurine, is also substantially less active and less toxic than thioguanine and its formation is likewise unaffected by the presence of allopurinol. Appreciable amounts of inorganic sulfate are also found in both murine and human urine, presumably arising from further metabolism of the methylated derivatives. In some animal tumors, resistance to the effect of thioguanine correlates with the loss of HGPRTase activity and the resulting inability to convert thioguanine to thioguanylic acid. However, other resistance mechanisms, such as increased catabolism of TGMP by a nonspecific phosphatase, may be operative. Although not invariable, it is usual to find cross-resistance between thioguanine and its close analogue, PURINETHOL (mercaptopurine).