5-Fluorouracil (5-FU) is an analogue of uracil and a potent antitumor agent. 5-Fluorouracil affects pyrimidine synthesis by inhibiting thymidylate synthetase thus depleting intracellular dTTP pools. 5-Fluorouracil induces apoptosis and can be used as a chemical sensitizer^[1][2]. 5-Fluorouracil also inhibits HIV^[3].

5-Fluorouracil (5-Fu) and NSC 123127 (Dox) show synergistic anticancer efficacy. The IC₅₀ value of 5-Fu/Dox-DNM toward human breast cancer (MDA-MB-231) cells is 0.25 μg/mL, presenting an 11.2-fold and 6.1-fold increase in cytotoxicity compared to Dox-DNM and 5-Fu-DNM, respectively^[1]. In 5-fluorouracil (5-FU) and CDDP treated NFBD1-inhibited NPC cells, the NFBD1 expression in NPC CNE1 cell lines is depleted using lentivirus-mediated short hairpin RNA, and the sensitivity of these cells is elevated. NFBD1 knockdown leads to an obvious induction of apoptosis in CDDP- or 5-FU-treated CNE1 cells^[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

5-Fluorouracil (23 mg/kg, 3 times/week) for 14 days, induces accelerated gastrointestinal transit associated with acute intestinal inflammation at day 3 after the start of treatment, which may have led to persistent changes in the ENS observed after days 7 and 14 of treatment contributing to delayed gastrointestinal transit and colonic dysmotility^[4].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

130.08

Solid

C₄H₃FN₂O₂

51-21-8

5-氟脲嘧啶；雙喃呋啶

Room temperature in continental US; may vary elsewhere.