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5-Fluorouracil

CAS No. : 51-21-8

MCE 國(guó)際站：5-Fluorouracil

產(chǎn)品活性：5-Fluorouracil (5-FU) 是一種尿嘧啶的類似物 (nucleoside antimetabolite/analog)，是一種有效的抗腫瘤藥。5-Fluorouracil 通過(guò)抑制胸苷酸合成酶影響嘧啶的合成，從而耗盡細(xì)胞內(nèi)dTTP 池。5-Fluorouracil 誘導(dǎo)細(xì)胞凋亡 (apoptosis)，可用作化學(xué)敏化劑。5-Fluorouracil 還可抑制 HIV 病毒。5-Fluorouracil (5-FU) 可破壞外泌體特異性的 rRNA。

研究領(lǐng)域：Cell Cycle/DNA Damage  |  Anti-infection  |  Apoptosis  |  Metabolic Enzyme/Protease

作用靶點(diǎn)：Nucleoside Antimetabolite/Analog  |  HIV  |  Apoptosis  |  Endogenous Metabolite

In Vitro: 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. 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.

In Vivo: 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.

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