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5-Fluoro-2'-deoxycytidine Sale

(Synonyms: 5-氟脱氧胞苷) 目录号 : GC61662

2'-Deoxy-5-fluorocytidine (5-fluoro-2(')-deoxycytidine, FCdR), a pyrimidine analog, is a DNA methyltransferase (DMNT) inhibitor currently in clinical trials for solid tumors.

5-Fluoro-2'-deoxycytidine Chemical Structure

Cas No.:10356-76-0

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产品描述

2'-Deoxy-5-fluorocytidine (5-fluoro-2(')-deoxycytidine, FCdR), a pyrimidine analog, is a DNA methyltransferase (DMNT) inhibitor currently in clinical trials for solid tumors.

[1] Zhao Q, et al. Springerplus. 2012 Dec;1(1):65.

Chemical Properties

Cas No. 10356-76-0 SDF
别名 5-氟脱氧胞苷
Canonical SMILES OC[C@@H]1[C@@H](O)C[C@@H](O1)N2C(N=C(N)C(F)=C2)=O
分子式 C9H12FN3O4 分子量 245.21
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Research Update

5-Fluoro-2'-deoxycytidine as a Probe for the Study of B/Z-DNA Transition by 19F NMR Spectroscopy

ACS Omega 2019 Nov 15;4(22):19716-19722.PMID:31788603DOI:10.1021/acsomega.9b02461.

5-Fluoro-2'-deoxycytidine was synthesized by treating 5-fluoro-2'-deoxyuridine with 2,4,6-trimethylphenol in the presence of 1-methylpyrrolidine and trifluoroacetic anhydride, followed by aminolysis. Among N-acetyl, pivaloyl, and benzoyl, N-acetyl was found to be suitable for the protection of the exocyclic amine of 5-Fluoro-2'-deoxycytidine because of the stability of the N 4-protected nucleoside under acidic conditions and its ease of removal after solid-phase synthesis. This modified nucleoside was incorporated into d(CG)6 sequences through the phosphoramidite chemistry-based solid-phase synthesis. Circular dichroism experiments suggest that replacement of 2'-deoxycytidine with 5-Fluoro-2'-deoxycytidine does not lead to detectable conformational changes, either in the B- or Z-form. 19F NMR spectroscopy of d(CG)6 containing 5-Fluoro-2'-deoxycytidine revealed that B/Z-DNA transition induced by sodium chloride is likely initiated at terminal ends, leading to unwinding at the middle of duplexes, and eventual switch of handedness when sodium chloride concentration reaches a threshold value.

PBRM1 Deficiency Sensitizes Renal Cancer Cells to DNMT Inhibitor 5-Fluoro-2'-deoxycytidine

Front Oncol 2022 Jun 3;12:870229.PMID:35719970DOI:10.3389/fonc.2022.870229.

PBRM1 is a tumor suppressor frequently mutated in clear cell renal cell carcinoma. However, no effective targeted therapies exist for ccRCC with PBRM1 loss. To identify novel therapeutic approaches to targeting PBRM1-deficient renal cancers, we employed a synthetic lethality compound screening in isogenic PBRM1+/+ and PBRM1-/- 786-O renal tumor cells and found that a DNMT inhibitor 5-Fluoro-2'-deoxycytidine (Fdcyd) selectively inhibit PBRM1-deficient tumor growth. RCC cells lacking PBRM1 show enhanced DNA damage response, which leads to sensitivity to DNA toxic drugs. Fdcyd treatment not only induces DNA damage, but also re-activated a pro-apoptotic factor XAF1 and further promotes the genotoxic stress-induced PBRM1-deficient cell death. This study shows a novel synthetic lethality interaction between PBRM1 loss and Fdcyd treatment and indicates that DNMT inhibitor represents a novel strategy for treating ccRCC with PBRM1 loss-of-function mutations.

Intravenous 5-Fluoro-2'-deoxycytidine administered with tetrahydrouridine increases the proportion of p16-expressing circulating tumor cells in patients with advanced solid tumors

Cancer Chemother Pharmacol 2020 May;85(5):979-993.PMID:32314030DOI:10.1007/s00280-020-04073-5.

Purpose: Following promising responses to the DNA methyltransferase (DNMT) inhibitor 5-Fluoro-2'-deoxycytidine (FdCyd) combined with tetrahydrouridine (THU) in phase 1 testing, we initiated a non-randomized phase 2 study to assess response to this combination in patients with advanced solid tumor types for which tumor suppressor gene methylation is potentially prognostic. To obtain pharmacodynamic evidence for DNMT inhibition by FdCyd, we developed a novel method for detecting expression of tumor suppressor protein p16/INK4A in circulating tumor cells (CTCs). Methods: Patients in histology-specific strata (breast, head and neck [H&N], or non-small cell lung cancers [NSCLC] or urothelial transitional cell carcinoma) were administered FdCyd (100 mg/m2) and THU (350 mg/m2) intravenously 5 days/week for 2 weeks, in 28-day cycles, and progression-free survival (PFS) rate and objective response rate (ORR) were evaluated. Blood specimens were collected for CTC analysis. Results: Ninety-three eligible patients were enrolled (29 breast, 21 H&N, 25 NSCLC, and 18 urothelial). There were three partial responses. All strata were terminated early due to insufficient responses (H&N, NSCLC) or slow accrual (breast, urothelial). However, the preliminary 4-month PFS rate (42%) in the urothelial stratum exceeded the predefined goal-though the ORR (5.6%) did not. An increase in the proportion of p16-expressing cytokeratin-positive CTCs was detected in 69% of patients evaluable for clinical and CTC response, but was not significantly associated with clinical response. Conclusion: Further study of FdCyd + THU is potentially warranted in urothelial carcinoma but not NSCLC or breast or H&N cancer. Increase in the proportion of p16-expressing cytokeratin-positive CTCs is a pharmacodynamic marker of FdCyd target engagement.

Preclinical studies of 5-Fluoro-2'-deoxycytidine and tetrahydrouridine in pediatric brain tumors

J Neurooncol 2016 Jan;126(2):225-34.PMID:26518542DOI:10.1007/s11060-015-1965-0.

Chemotherapies active in preclinical studies frequently fail in the clinic due to lack of efficacy, which limits progress for rare cancers since only small numbers of patients are available for clinical trials. Thus, a preclinical drug development pipeline was developed to prioritize potentially active regimens for pediatric brain tumors spanning from in vitro drug screening, through intracranial and intra-tumoral pharmacokinetics to in vivo efficacy studies. Here, as an example of the pipeline, data are presented for the combination of 5-Fluoro-2'-deoxycytidine and tetrahydrouridine in three pediatric brain tumor models. The in vitro activity of nine novel therapies was tested against tumor spheres derived from faithful mouse models of Group 3 medulloblastoma, ependymoma, and choroid plexus carcinoma. Agents with the greatest in vitro potency were then subjected to a comprehensive series of in vivo pharmacokinetic (PK) and pharmacodynamic (PD) studies culminating in preclinical efficacy trials in mice harboring brain tumors. The nucleoside analog 5-Fluoro-2'-deoxycytidine (FdCyd) markedly reduced the proliferation in vitro of all three brain tumor cell types at nanomolar concentrations. Detailed intracranial PK studies confirmed that systemically administered FdCyd exceeded concentrations in brain tumors necessary to inhibit tumor cell proliferation, but no tumor displayed a significant in vivo therapeutic response. Despite promising in vitro activity and in vivo PK properties, FdCyd is unlikely to be an effective treatment of pediatric brain tumors, and therefore was deprioritized for the clinic. Our comprehensive and integrated preclinical drug development pipeline should reduce the attrition of drugs in clinical trials.

Metabolic channeling of 5-Fluoro-2'-deoxycytidine utilizing inhibitors of its deamination in cell culture

Mol Pharmacol 1985 May;27(5):584-94.PMID:2581125doi

The metabolism of 5-Fluoro-2'-deoxycytidine (FdC) with and without tetrahydrouridine (H4U) or 2'-deoxytetrahydrouridine (dH4U) was examined in log phase HEp-2 cells using HPLC and TLC methods which quantified: the incorporation of FdC-related antimetabolites into RNA and DNA and pool size levels of FdC-related antimetabolites. [3H]-FdC administered to log phase HEp-2 cells at a concentration of 0.01 microM for 24 hr resulted in the incorporation of 5.22 X 10(-8) mol of FdC/mol of DNA phosphate, a 0.021% substitution of FdC for dC. Coadministration of 1.0 mM H4U or dH4U resulted in 2- and 25-fold increases in the incorporation of FdC, respectively. No detectable incorporation of 5-fluoro-2'-deoxyuridine (FdU) into HEp-2 DNA resulted (detection limit, approximately 5 fmol). In contrast, treatment of HEp-2 cells with 0.1 microM FdU resulted in the incorporation of 1.83 X 10(-9) mol of FdU (74.7 fmol detected)/mol of DNA phosphate. A linear incorporation of FdC into the DNA of HEp-2 cells was found with increasing concentrations of FdC and 1.0 mM dH4U . 0.1 microM FdC resulted in the incorporation of 2.39 X 10(-6) mol of FUMP/mol of cytoplasmic RNA phosphate and 2.23 X 10(-5) mol of FUMP/mol of nuclear RNA phosphate. Similarly, HEp-2 cells treated with 0.1 microM FdU resulted in the incorporation of 1.10 X 10(-5) mol of FUMP/mol of nuclear RNA phosphate and 9.44 X 10(-7) mol of FUMP/mol of cytoplasmic RNA phosphate. In contrast, no detectable FUMP incorporation into either nuclear or cytoplasmic RNAs of HEp-2 cells resulted when H4U or dH4U was coadministered with 0.1 microM FdC. Pool size analyses of log phase HEp-2 cells following a 30-min exposure to FdU or FdC with and without H4U or dH4U were also performed; 0.1 microM FdC treatment resulted in the formation of 169 fmol of FUMP/1.0 X 10(6) viable HEp-2 cells. Treatment with 0.1 microM FdU produced 253 fmol of FUMP/1.0 X 10(6) viable HEp-2 cells. In contrast, no detectable FUMP pools were formed when H4U or dH4U was coadministered with 0.1 microM FdC (detection limit, approximately 5 fmol). Pool levels of FdUMP, the inhibitor of thymidylate synthetase, were also assayed; 36.9 fmol of FdUMP/1.0 X 10(6) viable HEp-2 cells were detected upon administration of 0.1 microM FdC.(ABSTRACT TRUNCATED AT 400 WORDS)