Thioguanine

167.19

167.19

157765

205-827-2

WIX31ZPX66

757348|752

2811

DTXSID6023652

C61970

NEEDLES FROM WATER|YELLOW, CRYSTALLINE POWDER

L - Antineoplastic and immunomodulating agents

29335990

111

-0.1

Yellow to green lyophilized powder

1.483 (estimate)

>360 °C

555.4±42.0 °C(Predicted)

232.4±26.5 °C

1.5605 (estimate)

Readily soluble in dilute aqueous alkali. Insoluble in water, alcohol, or chloroform.

Store at RT.

1.5E-17mmHg at 25°C

Peritoneal-rat LD50: 300 mg/kg; oral-mouse LD50: 160 mg/kg

Flammable; burning produces toxic nitrogen oxides and sulfur oxide fumes

ODORLESS OR PRACTICALLY ODORLESS

129.7 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]

This chemical may be sensitive to prolonged exposure to air. Insoluble in water.

Amines, Phosphines, and Pyridines

6-THIOGUANINE is incompatible with strong oxidizing agents. (NTP, 1992).

III

6.1

UN 2811 6.1/PG 3

3

25-23/24/25

28-36/37/39-45-28A

UP0740000

T,Xi

Warehouse ventilated, low temperature and dry

Irritant

Bulk: The compound was stable in solid form at room temperature in the absence of moisture. Solution: Alkaline solutions slowly undergo decomposition. Alkaline solutions should not be heated above 37 °C.

P301 + P310

H301

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Manufacturers, packers, and distributors of drug and drug products for human use are responsible for complying with the labeling, certification, and usage requirements as prescribed by the Federal Food, Drug, and Cosmetic Act, as amended (secs 201-902, 52 Stat. 1040 et seq., as amended; 21 U.S.C. 321-392).|The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl thioguanine, approved on the basis of safety and effectiveness by FDA under sections 505 and 507 of the Federal Food, Drug, and Cosmetic Act.

Flash point data for this chemical are not available; however, it is probably combustible. (NTP, 1992)

Fires involving this material can be controlled with a dry chemical, carbon dioxide or Halon extinguisher. A water spray may also be used. (NTP, 1992)

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

SMALL SPILLS AND LEAKAGE: If you spill this chemical, dampen the solid spill material with 5% ammonium hydroxide, then transfer the dampened material to a suitable container. Use absorbent paper dampened with 5% ammonium hydroxide to pick up any remaining material. Your contaminated clothing and the absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with 5% ammonium hydroxide followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should keep this material in a tightly closed container under an inert atmosphere, and store it under ambient temperatures. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)

highly toxic

Oral, mouse: LD50 = 160 mg/kg. Symptoms of overdose include nausea, vomiting, malaise, hypotension, and diaphoresis.

Azathioprine has been associated with several forms of hepatotoxicity, including mild, transient and asymptomatic rises in serum aminotransferase levels, an acute cholestatic injury developing during the first year of starting therapy, and a chronic hepatic injury marked by peliosis hepatis, veno-occlusive disease or nodular regenerative hyperplasia that typically arises 1 to 5 years after starting azathioprine.|As with other thiopurines, thioguanine has been associated with several forms of hepatotoxicity, including mild, transient and asymptomatic rises in serum aminotransferase levels, an acute hepatic injury developing during the first year of starting therapy, and a chronic hepatic injury marked by variable degrees of peliosis hepatis, veno-occlusive disease and/or nodular regenerative hyperplasia. Chronic injury typically arises 1 to 5 years after starting thioguanine and can present insidiously with signs and symptoms of portal hypertension.

INDUCTION OF 6-THIOGUANINE RESISTANCE WAS STUDIED IN HUMAN CELLS TREATED WITH THE DIRECT-ACTING CARCINOGEN N-ACETOXY-2-ACETYLAMINOFLUORENE. AT 2.5-7.5 MUMOL INDUCTION OF RESISTANT CLONES WAS LINEAR & FOLLOWED 1-HIT KINETICS, WHILE AT 10 MUMOL THE YIELD OF RESISTANT CLONES WAS HIGHER & APPEARED TO RESULT FROM COMBINATION OF 1-HIT & 2-HIT KINETICS.|6-MERCAPTOPURINE & 6-THIOGUANINE SYNERGISTICALLY INHIBITED MILK XANTHINE OXIDASE.|PRETREATMENT OF L1210 LEUKEMIA CELLS WITH METHOTREXATE ENHANCED CYTOTOXICITY OF 6-THIOGUANINE. METHOTREXATE PRETREATMENT & ENHANCEMENT OF 6-THIOGUANINE CYTOTOXICITY FOLLOWING METHOTREXATE EXPOSURE IS NOT ASSOC WITH 6-THIOGUANINE INCORPORATION INTO DNA, BUT RATHER WITH INCORPORATION OF 6-THIOGUANINE INTO RNA. THIS DRUG SEQUENCE MAY BE BENEFICIAL IN CLINICAL TREATMENT OF LEUKEMIA.

LD50 Rat ip 350 mg/kg|LD40 Mouse ip 50 mg/kg

For remission induction and remission consolidation treatment of acute nonlymphocytic leukemias.|FDA Label|Drug: Thioguanine

Azathioprine is a purine analogue and prodrug of mercaptopurine that is used as an immunosuppressive agent in organ transplantation to prevent rejection and in autoimmune diseases as a corticosteroid sparing agent. Azathioprine is associated with minor, usually transient and asymptomatic elevations in serum aminotransferase levels during therapy and with rare instances of acute, cholestatic liver injury and, with long term use, noncirrhotic portal hypertension as a result of nodular regenerative hyperplasia or sinusoidal obstruction syndrome.|Thioguanine (also referred to as 6-thioguanine and as tioguanine) is a purine analogue that is used in the therapy of acute and chronic myelogenous leukemias. Thioguanine therapy is associated with minor, usually transient and asymptomatic elevations in serum aminotransferase levels and has also been linked to rare instances of cholestatic acute liver injury and to chronic liver injury, resulting in portal hypertension due to nodular regenerative hyperplasia.

Antineoplastic Agents

Antimetabolites, Antineoplastic|CLINICALLY, THIOGUANINE HAS BEEN USED IN THE TREATMENT OF ACUTE LEUKEMIA AND, IN COMBINATION WITH CYTARABINE, IS ONE OF THE MOST EFFECTIVE AGENTS FOR INDUCTION OF REMISSIONS IN ACUTE GRANULOCYTIC LEUKEMIA; IT HAS NOT BEEN USEFUL IN THE TREATMENT OF PATIENTS WITH SOLID TUMORS. THIS CMPD HAS BEEN USED AS AN IMMUNOSUPPRESSIVE AGENT, PARTICULARLY IN PATIENTS WITH NEPHROSIS AND WITH COLLAGEN-VASCULAR DISORDERS. TOXIC MANIFESTATIONS INCLUDE BONE MARROW DEPRESSION AND GI EFFECTS, ALTHOUGH THE LATTER MAY BE LESS PRONOUNCED THAN WITH MERCAPTOPURINE.|SHORT TERM TREATMENT WITH DOXORUBICIN, CYTARABINE, & 6-THIOGUANINE WAS GIVEN TO 90 PATIENTS WITH ACUTE MYELOGENOUS LEUKEMIA. FIFTY PATIENTS RECEIVED HIGH DOSES (REGIMEN 1) & 41 RECEIVED VERY HIGH DOSES (REGIMEN 2). REMISSION RATE WAS SIGNIFICANTLY HIGHER WITH REGIMEN 1 THAN WITH REGIMEN 2. DURATION OF REMISSION WAS, HOWEVER, SIGNIFICANTLY LONGER WITH REGIMEN 2.|IN ADVANCED COLORECTAL ADENOCARCINOMA, TWO DIFFERENT SCHEDULES OF COMBINATION METHYL-CCNU, 6-THIOGUANINE, & 5-FLUOROURACIL EXHIBITED SIMILAR EFFICACIES, WITH A COMBINED COMPLETE & PARTIAL REMISSION RATE OF 17% & A MEDIAN SURVIVAL OF 53+ WK. SIGNIFICANT SYMPTOMATIC BENEFIT WAS SEEN IN 52% OF PATIENTS. TOXICITY WAS PREDOMINATELY HEMOPOIETIC & GI.|For more Therapeutic Uses (Complete) data for THIOGUANINE (14 total), please visit the HSDB record page.

Risk-benefit should be considered when the following medical problems exist: Bone marrow depression; chickenpox, existing or recent (including recent exposure; herpes zoster (risk of severe generalized disease); gout, history of; urate renal stones, history of (risk of hyperuricemia); hepatic function impairment (reduced biotransformation; lower dosage is recommended); infection; renal function impairment (reduced elimination; lower dosage is recommended); or sensitivity to thioguanine. Caution should be used also in patients who have had cytotoxic drug therapy and radiation therapy within 4 to 6 weeks.|Because normal defense mechanisms may be suppressed by thioguanine therapy, concurrent use with alive virus vaccine may potentiate the replication of the vaccine virus, may increase the side/adverse effects of the vaccine virus, and/or may decrease the patient's antibody response to the vaccine; immunization of these patients should be undertaken only with extreme caution after careful review of the patient's hematologic status and only with the knowledge and consent of the physician managing the thioguanine therapy. The interval between discontinuation of medication that cause immunosuppression and restoration of the patient's ability to respond to the vaccine depends on the intensity and type of immunosuppression-causing medication used, the underlying disease, and other factors; estimates vary from 3 months to 1 year. Patients with leukemia in remission should not receive live virus vaccine until at least 3 months after their last chemotherapy. Immunization with oral poliovirus vaccine should also be postponed in persons in close contact with the patient, especially family members.|Because normal defense mechanisms may be suppressed by thioguanine therapy, the patient's antibody response to the vaccine may be decreased. The interval between discontinuation of medications that cause immunosuppression and restoration of the patient's ability to respond to the vaccine depends on the intensity and type of immunosuppression-causing medication used, the underlying disease, and other factors; estimates vary from 3 months to 1 year.|TOXIC MANIFESTATIONS INCL BONE MARROW DEPRESSION & GI EFFECTS ... .|For more Drug Warnings (Complete) data for THIOGUANINE (9 total), please visit the HSDB record page.

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).

Antimetabolites that are useful in cancer chemotherapy. (See all compounds classified as Antimetabolites, Antineoplastic.)

Absorption of an oral dose is incomplete and variable, averaging approximately 30% of the administered dose (range: 14% to 46%)|Incompletely and variably (about 30%) absorbed from the gastrointestinal tract.|THIOGUANINE IS INCOMPLETELY ABSORBED WHEN GIVEN ORALLY, AVERAGING ABOUT 30% OF AN ADMIN DOSE. ... THE ELIMINATION HALF-LIFE OF THE PARENT DRUG IS 1.5 HR, BUT PEAK PLASMA LEVELS OF METABOLITES ARE REACHED IN 6-8 HR. BETWEEN 24% & 46% IS EXCRETED IN THE URINE AS METABOLITES WITHIN 24 HR. ... THIS DRUG IS CLEARED RAPIDLY FROM PLASMA AFTER IV ADMINISTRATION; MORE THAN 80% EXCRETED WITHIN 24 HR. ALTHOUGH THIOGUANINE.../SRP: HAS LIMITED ACCESS ACROSS/ THE BLOOD-BRAIN BARRIER IN ANIMALS AFTER LARGE DOSES, VERY LITTLE ENTERS THE CEREBROSPINAL FLUID OF HUMANS AFTER THE USUAL CLINICAL DOSES ARE EMPLOYED.|THE METABOLISM AND PHARMACOKINETICS OF 6-THIOGUANINE WERE STUDIED IN DOGS AFTER IV ADMIN OF 5 MG/KG (35)S-THIOGUANINE (TG). THIOGUANINE WAS RAPIDLY & EXTENSIVELY DEGRADED. METABOLITES WERE NOT FOUND IN THE CEREBROSPINAL FLUID IN SIGNIFICANT CONCENTRATIONS.

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.|... WHEN THIOGUANINE IS ADMIN TO MAN, THE S-METHYLATION PRODUCT, 2-AMINO-6-METHYLTHIOPURINE, RATHER THAN FREE THIOGUANINE APPEARS IN URINE; INORGANIC SULFATE IS ALSO A MAJOR URINARY METABOLITE. LESSER AMT OF 6-THIOURIC ACID ARE FORMED, SUGGESTING THAT DEAMINATION CATALYZED BY THE ENZYME GUANASE DOES NOT HAVE A MAJOR ROLE IN THE METABOLIC INACTIVATION OF THIOGUANINE.|THE PHARMACOKINETICS OF RADIOLABELED 6-THIOGUANINE (TG) WERE COMPARED WITH THAT OF BETA-2'-DEOXYTHIOGUANOSINE (BETA-TGDR) AFTER IV ADMIN. URINARY EXCRETION OF THE RADIOLABEL WAS 75% OF THE DOSE 24 HR AFTER ADMIN. BOTH THIOPURINES WERE RAPIDLY & EXTENSIVELY DEGRADED & EXCRETED AS 6-THIOXANTHINE, INORGANIC SULFATE, S-METHYL-6-THIOXANTHINE, & 6-THIOURIC ACID IN ADDITION TO OTHER PRODUCTS. SMALL AMOUNTS OF UNCHANGED DRUG WERE ALSO EXCRETED. STUDIES SUGGEST THAT BETA-TGDR IS A LATENT FORM OF TG. SINCE RESISTANCE TO ANTILEUKEMIC AGENT 6-THIOGUANINE INEVITABLY DEVELOPS IN ANIMAL TUMORS, THIS NEW AGENT BETA-TGDR IS OF POTENTIAL CLINICAL USE.

When the compound was given in singles doses of 65 to 300 mg/m^2, the median plasma half-disappearance time was 80 minutes (range 25-240 minutes)

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 novo purine synthesis; inhibition of purine nucleotide interconversions; 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.|THIOGUANINE, THE 6-THIO ANALOGUE OF GUANINE, IS A PRODRUG THAT IS CONVERTED TO 6-THIOGUANINE-RIBOSE-PHOSPHATE, AN ACTIVE METABOLITE. ... 6-THIOGUANINE-RIBOSE-PHOSPHATE IS A FEEDBACK INHIBITOR OF THE INITIAL (AMIDOTRANSFERASE) STEP IN PURINE BIOSYNTHESIS. THIS METABOLITE ALSO BLOCKS CONVERSIONS OF INOSINIC ACID TO GUANYLIC ACID & OF GUANYLIC ACID TO GDP. THIOGUANINE ALSO IS CONVERTED TO THE DEOXYNUCLEOTIDE TRIPHOSPHATE, WHICH CAN BE INCORPORATED INTO TUMOR CELL DNA. ALTHOUGH SOME INVESTIGATORS BELIEVE THAT THIS IS THE MAJOR MECHANISM OF CYTOTOXICITY, THE RELATIVE IMPORTANCE OF THE VARIOUS SITES OF ACTION HAS NOT BEEN DETERMINED. ... THIOGUANINE IS CELL-CYCLE SPECIFIC FOR THE S PHASE.|APPARENTLY, THE METABOLISM OF 6-THIOGUANINE TO 6-THIOGUANOSINE IN SARCOMA 180 & 180/TG CELLS IS MEDIATED BY PURINE NUCLEOSIDE PHOSPHORYLASE & NEWLY SYNTHESIZED 6-THIOGUANOSINE IS READILY EFFLUXED INTO THE CELLULAR ENVIRONMENT. THE FORMATION OF 6-THIOGUANINE, BY PURINE NUCLEOSIDE PHOSPHORYLASE, MAY BE IMPORTANT TO THE EXPRESSION OF CELLULAR SENSITIVITY TO 6-THIOGUANINE, IN THAT IT DECR THE AVAIL OF 6-THIOGUANINE FOR DIRECT CONVERSION BY HYPOXANTHINE-GUANINE PHOSPHORIBOSYLTRANSFERASE TO THE NUCLEOTIDE LEVEL, A PHENOMENON CRITICAL TO THE EXPRESSION OF THE ANTINEOPLASTIC ACTIVITY OF THE 6-THIOPURINES.|PHENYL SUBSTITUTION AT C-8 OF 2-AMINO-6-MERCAPTOPURINE ABOLISHED THE IMMUNOSUPPRESSIVE ACTIVITY. THEREFORE, A NONSUBSTITUTED 8 POSITION OF 2-AMINO-6-MERCAPTOPURINE IS ESSENTIAL FOR IMMUNOSUPPRESSIVE ACTION.|SPONTANEOUSLY CYCLING LYMPHOCYTES (IN CELL DIVISION IN CULTURES WITHOUT ADDITION OF PHYTOHEMAGGLUTININ, PHA) GO THROUGH VARIOUS PHASES OF 1ST DIVISION WITH THE SAME KINETICS AS PHA-STIMULATED CELLS. IN SAMPLES FROM 10 REFERENTS, THE FREQUENCY OF SPONTANEOUSLY CYCLING LYMPHOCYTES VARIED FROM 8.9X10-5 TO 9.5X10-3 AS INDICATED WITH AUTORADIOGRAPHY ON CELLS IN (S + G2) PHASE DETERMINED BY FLOW SORTING. IN PHA-STIMULATED SAMPLES FROM THE SAME PERSONS THE FREQUENCY OF 6-THIOGUANINE (TG)-RESISTANT VARIANTS WAS BETWEEN 4X10-7 & 2.6X10-6, WHICH INDICATES THAT MOST OF THE SPONTANEOUSLY CYCLING CELLS WERE TG-SENSITIVE.|For more Mechanism of Action (Complete) data for THIOGUANINE (7 total), please visit the HSDB record page.

SYMPTOMS: Symptoms of exposure to this compound may include jaundice, vomiting, diarrhea (watery to bloody), collapse, burning in the throat, abdominal pain, oliguria, fall of blood pressure, anuria, cardiovascular collapse, delirium, convulsions, muscular weakness, respiratory failure, hematuria, proteinuria and hemoglobin casts. Other symptoms include bone marrow depression, hypoplasia, hepatotoxicity, crystalluria, pellagra, portal hypotension with esophageal varices and severe hematemesis. Gastrointestinal effects may occur. Exposure may cause anemia, leukopenia, thrombocytopenia, pancytopenia, hyperuricemia, nausea, anorexia, stomatitis, occasionally abnormal liver enzyme and other liver function studies, hepatomegaly, veno-occlusive liver disease, intestinal necrosis and perforation, malaise, hypertension, diaphoresis and azotemia. Symptoms of exposure to this type of compound may include local irritant effects, allergic reactions such as skin rashes, pruritus and erythema, fever, headache, weakness, anaphylaxis, vesicant or irritant action on the skin and mucous membranes, thrombophlebitis (site of injection), bleeding, immunosuppression, mouth ulcers, esophagitis, diarrhea, alopecia, delayed wound healing, suppression of ovarian and testicular function resulting in amenorrhea and the inhibition of spermatogenesis, gynecomastia, acute renal failure due to uric acid nephropathy, hyperphosphatemia and other electrolyte balance, and pigmentation of the skin and rashes. ACUTE/CHRONIC HAZARDS: This compound is harmful if ingested, inhaled or absorbed through the skin. It may cause irritation. When heated to decomposition it emits toxic fumes of carbon monoxide, carbon dioxide, nitrogen oxides and sulfur oxides. (NTP, 1992)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

TREATMENT OF POISONING WITH...THESE AGENTS CONSISTS OF DISCONTINUING DRUG, GIVING BLOOD TRANSFUSIONS, & TREATING BONE MARROW DEPRESSION. /ANTICANCER AGENTS/

Bone marrow depression (black, tarry stools; blood in urine or stools; cough or hoarseness; fever or chills; lower back or side pain; painful or difficult urination; pinpoint red spots on skin; unusual bleeding or bruising).|Gastrointestinal ulceration (black, tarry stools); hepatotoxicity, hepatic fibrosis, or toxic hepatitis (Yellow eyes or skin); stomatitis, dose-related (sores in mont and on lips).|Hyperuricemia or uric acid nephropathy (joint pain, lower back or side pain, swelling of feet or lower legs); unsteadiness when walking. Note: Hyperuricemia or uric acid nephropathy occurs most commonly during initial treatment of patients with leukemia or lymphoma, as a result of rapid cell breakdown, which leads to elevated serum uric acid concentrations.|Immunosuppression, leukopenia, or infection (usually asymptomatic; less frequently, fever or chills, cough or hoarseness, lower back or side pain, painful or difficult urination); thrombocytopenia (usually asymptomatic; less frequently, unusual bleeding or bruising; black, tarry stool; blood in urine or stools). Note: Bone marrow depression usually occurs over 2 to 4 weeks, although a rapid fall in leukocyte count may occur within 1 to 2 weeks.|For more Human Toxicity Excerpts (Complete) data for THIOGUANINE (9 total), please visit the HSDB record page.

2 Amino 6 Purinethiol

Refined grades

A HIGH-PERFORMANCE LIQUID CHROMATOGRAPHIC-FLOW FLUOROMETRIC ASSAY FOR MEASURING RATES OF INTRACELLULAR FORMATION BY HUMAN LEUKEMIC BLASTS OF 6-THIOGUANINE NUCLEOTIDE METABOLITES OF 6-MERCAPTOPURINE & 6-THIOGUANINE IS DESCRIBED. THE ASSAY MAY BE APPLIED TO DETECT RESISTANT DISEASE AT AN EARLY STAGE IN THERAPY, & THEREBY PROVIDES THE OPPORTUNITY FOR ALTERNATIVE TREATMENTS TO BE INSTITUTED.|THE DETERMINATION OF 6-THIOGUANINE IN HUMAN PLASMA & URINE BY USING ISOCRATIC REVERSED-PHASE HIGH PRESSURE LIQ CHROMATOGRAPHY IS DESCRIBED. SENSITIVITY OF ASSAY IS 0.2 UG/ML WITH A PRECISION OF 3.7%.|A FLUORIMETRIC METHOD FOR MEASURING THERAPEUTIC CONCENTRATIONS OF 6-THIOGUANINE IN HUMAN PLASMA IS DESCRIBED. LIMIT OF SENSITIVITY IS 5 NG/ML.|CONCN IN DIL BLOOD SERUM & URINE WAS MEASURED BY FLUORESCENCE OF THE 6-THIOGUANINE S-OXIDE DERIV (EXCITATION 330 NM & EMISSION 415 NM). DETECTION LIMIT WAS 2 UG/ML.|For more Clinical Laboratory Methods (Complete) data for THIOGUANINE (6 total), please visit the HSDB record page.

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