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Supplier: Thermo Scientific
Description: Thymine 99%
Catalog Number: (APOSBIMN2031-1G)
Supplier: Apollo Scientific
Description: 1-(2-Deoxy-2-fluoro-beta-D-arabinofuranosyl)thymine (2’-FANA-T) ≥95%
UOM: 1 * 1 g


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Supplier: Thermo Scientific
Description: Thymine 97%
Catalog Number: (PHR1345-250MG)
Supplier: Merck
Description: Organic Standard, Thymine(Zidovudine Related Compound C)
UOM: 1 * 250 mg


Catalog Number: (BOSSBS-8288R)
Supplier: Bioss
Description: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.
UOM: 1 * 100 µl


Catalog Number: (BOSSBS-2950R-CY7)
Supplier: Bioss
Description: Converts cytosine to uracil or 5-methylcytosine to thymine by deaminating carbon number 4.
UOM: 1 * 100 µl


Catalog Number: (BOSSBS-8288R-A350)
Supplier: Bioss
Description: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.
UOM: 1 * 100 µl


Catalog Number: (BOSSBS-8288R-CY3)
Supplier: Bioss
Description: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.
UOM: 1 * 100 µl


Catalog Number: (BOSSBS-8288R-CY5)
Supplier: Bioss
Description: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.
UOM: 1 * 100 µl


Catalog Number: (BOSSBS-2950R-A750)
Supplier: Bioss
Description: Converts cytosine to uracil or 5-methylcytosine to thymine by deaminating carbon number 4.
UOM: 1 * 100 µl


Catalog Number: (BOSSBS-8288R-A680)
Supplier: Bioss
Description: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterised by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.
UOM: 1 * 100 µl


Catalog Number: (BOSSBS-8288R-FITC)
Supplier: Bioss
Description: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.
UOM: 1 * 100 µl


Supplier: Thermo Scientific
Description: Thymidine (2'-deoxythymidine) 99+%
Catalog Number: (BOSSBS-2950R-CY5)
Supplier: Bioss
Description: Converts cytosine to uracil or 5-methylcytosine to thymine by deaminating carbon number 4.
UOM: 1 * 100 µl


Catalog Number: (BOSSBS-2950R-A488)
Supplier: Bioss
Description: Converts cytosine to uracil or 5-methylcytosine to thymine by deaminating carbon number 4.
UOM: 1 * 100 µl


Catalog Number: (BOSSBS-8288R-CY5.5)
Supplier: Bioss
Description: Dihydropyrimidine dehydrogenase (DPYD) catalyzes the first rate-limiting step of the NADPH-dependent catabolism of uracil and thymine to dihydrouracil and dihydrothymine; thus, a deficiency of DPYD leads to an accumulation of uracil and thymine. Abnormal concentrations of these metabolites in bodily fluids may be the cause of neurological disease and a contraindication for treatment of cancer patients with certain pyrimidine analogs. DPYD also catalyzes the anticancer agent 5-fluorouracil (5-FU) pathway and is involved in the efficacy and toxicity of 5-FU. Variations in DPYD concentration may arise from alterations at the transcriptional level of the dihydropyrimidine dehydrogenase gene. Specifically, hypermethylation of the DPYD promoter downregulates dihydropyrimidine dehydrogenase expression. Deficient DPYD alleles may constitute a risk factor for severe toxicity following treatment with 5-FU.Involvement in disease:Defects in DPYD are the cause of dihydropyrimidine dehydrogenase deficiency (DPYD deficiency) ; also known as hereditary thymine-uraciluria or familial pyrimidinemia. DPYD deficiency is a disease characterized by persistent urinary excretion of excessive amounts of uracil, thymine and 5-hydroxymethyluracil. Patients suffering from this disease show a severe reaction to the anticancer drug 5-fluorouracil. This reaction includes stomatitis, Leukopenia, thrombocytopenia, hair loss, diarrhea, fever, marked weight loss, cerebellar ataxia, and neurologic symptoms, progressing to semicoma.
UOM: 1 * 100 µl


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