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Ribonucleoside- diphosphate reductase subunit M2 Ribonucleoside- diphosphate reductase subunit M2 B Equilibrative nucleoside transporter 1 Sodium/nucleoside cotransporter 2 Nuclear pore complex 5'-nucleotidase Deoxycytidine kinase Adenylate kinase 9 Nucleoside diphosphate kinase A Fludarabine triphosphate Fludarabine triphosphate 9-β-D-arabinosyl-2- fluoroadenine 9-β-D-arabinosyl-2- fluoroadenine an oxidized thioredoxin dADP H2O ADP reduced thioredoxin Fludarabine fludarabine phosphate fludarabine diphosphate Na+ Na+ ATP ADP ATP ADP Zinc (II) ion DNA synthesis DNA polymerase subunit alpha B DNA polymerase alpha catalytic subunit DNA primase small subunit DNA primase large subunit DNA ligase 1 Fe2+ Magnesium Cytosol Fludarabine is converted to its monophosphate, diphosphate and, finally, its triphosphate forms in the nucleoside salvage pathway. T or B Cell Blood vessel T or B Cell Apoptosis The apoptosis of the T and B cells results in the death of the cancerous white blood cells but also in the immunosuppression of the patient by the death of the B and T cells and, also, by the arrest of antibodies production. Due to the inhibition of the DNA synthesis, the inhibition of the DNA polymerase, and the inhibition of the ribonucleoside reductase, the T and B cells will go through apoptosis. Fludarabine triphosphate (F-ara-ATP) accumulates and is incorporated in the DNA due to its structure. Through competitive inhibition, this drug also inhibits the DNA polymerase, the DNA primase and the DNA ligase. Nucleus The accumulation of the triphosphate metabolite is due to the fact that the structure of the purine analog makes it a poor substrate for the adenosine deaminase. This molecule is, in consequence, resistant to deamination. The incorporation in the DNA results in DNA breaks and the inhibition of DNA synthesis and repair. During the replication of the DNA, this will cause the apoptosis of the T or B cells through the p53 pathway. The accumulation of fludarabine triphosphate inhibits the ribonuclotide reductase. This leads to an imbalance in dNTPs availability. The imbalanced dNTP pool leads to DNA strand breaks and to the inhibition of the DNA synthesis. Through depletion of the dNTP pool, fludarabine self-potentiates the incorporation of fludarabine triphosphate into DNA. This results in less DNA synthesis and repair. Erythrocyte
Nucleus RRM2 RRM2B SLC29A1 SLC28A2 NUP98 NT5E DCK AK9 NME1 Fludarabine triphosphate Fludarabine triphosphate 9-β-D- arabinosyl-2- fluoroadenine 9-β-D- arabinosyl-2- fluoroadenine an oxidized thioredoxin dADP Water Adenosine diphosphate reduced thioredoxin Fludarabine fludarabine phosphate fludarabine diphosphate Sodium Sodium Adenosine triphosphate Adenosine diphosphate Adenosine triphosphate Adenosine diphosphate DNA synthesis POLA2 POLA1 PRIM1 PRIM2 LIG1
RRM2 RRM2B SLC29A1 SLC28A2 NUP98 NT5E DCK AK9 NME1 Flu tri Flu tri F-ara-A F-ara-A AOT dADP H2O ADP RT Famp flu pho flu dip Na+ Na+ ATP ADP ATP ADP Zinc DNA syn POLA2 POLA1 PRIM1 PRIM2 LIG1 Fe2+ Mg2+ Cytosol Fludarabine is converted to its monophosphate, diphosphate and, finally, its triphosphate forms in the nucleoside salvage pathway. T or B Cell Blood vessel T or B Cell Apoptosis The apoptosis of the T and B cells results in the death of the cancerous white blood cells but also in the immunosuppression of the patient by the death of the B and T cells and, also, by the arrest of antibodies production. Due to the inhibition of the DNA synthesis, the inhibition of the DNA polymerase, and the inhibition of the ribonucleoside reductase, the T and B cells will go through apoptosis. Fludarabine triphosphate (F-ara-ATP) accumulates and is incorporated in the DNA due to its structure. Through competitive inhibition, this drug also inhibits the DNA polymerase, the DNA primase and the DNA ligase. Nucleus The accumulation of the triphosphate metabolite is due to the fact that the structure of the purine analog makes it a poor substrate for the adenosine deaminase. This molecule is, in consequence, resistant to deamination. The incorporation in the DNA results in DNA breaks and the inhibition of DNA synthesis and repair. During the replication of the DNA, this will cause the apoptosis of the T or B cells through the p53 pathway. The accumulation of fludarabine triphosphate inhibits the ribonuclotide reductase. This leads to an imbalance in dNTPs availability. The imbalanced dNTP pool leads to DNA strand breaks and to the inhibition of the DNA synthesis. Through depletion of the dNTP pool, fludarabine self-potentiates the incorporation of fludarabine triphosphate into DNA. This results in less DNA synthesis and repair. Erythrocyte
Nucleus RRM2 RRM2B SLC29A1 SLC28A2 NUP98 NT5E DCK AK9 NME1 Flu tri Flu tri F-ara-A F-ara-A AOT dADP H2O ADP RT Famp flu pho flu dip Na+ Na+ ATP ADP ATP ADP DNA syn POLA2 POLA1 PRIM1 PRIM2 LIG1