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Doxifluridine

$75

  • Brand : BIOFRON

  • Catalogue Number : AV-B81291

  • Specification : 98%

  • CAS number : 3094-09-5

  • Formula : C9H11FN2O5

  • Molecular Weight : 246.19

  • PUBCHEM ID : 18343

  • Volume : 5mg

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Catalogue Number

AV-B81291

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

246.19

Appearance

Botanical Source

Structure Type

Category

Standards;Natural Pytochemical;API

SMILES

CC1C(C(C(O1)N2C=C(C(=O)NC2=O)F)O)O

Synonyms

5-Fluorodesoxyuridine/RO-21-9738/doxifluridine/5'DFURD/Uridine, 5'-deoxy-5-fluoro-/Flutron/Furtulon/1-(5-Deoxy-β-D-ribofuranosyl)-5-fluorouracil/5'-DFUR/doxyfluridine/1-(b-D-5'-Deoxyribofuranosyl)-5-fluorouracil/5-Fluoro-5'-deoxyuridine/5'-Deoxy-5-fluorouridine/5'-dFUrd/5'-DEOXYFLUOROURIDINE/(+)-5-Fluoro-5'-deoxyuridine/Doxifluidine/DOXIFLUIRDINE

IUPAC Name

1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-methyloxolan-2-yl]-5-fluoropyrimidine-2,4-dione

Applications

Doxifluridine(Ro 21-9738; 5'-DFUR) is a thymidine phosphorylase activator for PC9-DPE2 cells with IC50 of 0.62 μM. IC50 value: 0.62 μM(PC9-DPE2 cell).Target: Nucleoside antimetabolite/analogDoxifluridine is a fluoropyrimidine derivative and oral prodrug of the antineoplastic agent 5-fluorouracil (5-FU) with antitumor activity. Doxifluridine, designed to circumvent the rapid degradation of 5-FU by dihydropyrimidine dehydrogenase in the gut wall, is converted into 5-FU in the presence of pyrimidine nucleoside phosphorylase. 5-FU interferes with DNA synthesis and subsequent cell division by reducing normal thymidine production and interferes with RNA transcription by competing with uridine triphosphate for incorporation into the RNA strand.in vitro: 5'-DFUR's metabolic product(N3-Me-5'-dFUR) was found to be non-toxic in all the cell growth experiments performed. The absence of cytotoxicity could be explained by the observation that the metabolite was not recognized as a substrate by thymidine phosphorilase, the enzyme responsible for 5-fluorouracil (5-FU) release from doxifluridine, as ascertained by high-performance liquid chromatography/ultraviolet (HPLC-UV) analysis of the incubation mixture[1].in vivo: Administration of 200 mg of Furtulon to 23 beagle dogs, the plasma concentrations of doxifluridine, 5-FU, and 5-FUrd were measured simultaneously, using LC-MS/MS. The parent-metabolite compartment model with first-order absorption and Michaelis-Menten kinetics described the pharmacokinetics of doxifluridine, 5-FU, and 5-FUrd. Michaelis-Menten kinetics sufficiently explained the generation and elimination processes of 5-FU and 5-FUrd[2].Clinical trial: A phase II study of doxifluridine and docetaxel combination chemotherapy for advanced or recurrent gastric cancer was reported in 2009[3].

Density

1.6±0.1 g/cm3

Solubility

activatable probes; cancer theranostics; optical imaging; organic nanoparticles

Flash Point

Boiling Point

Melting Point

188-192 °C(lit.)

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2933590000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:3094-09-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

31206855

Abstract

Cancer theranostics holds potential promise for precision medicine; however, most existing theranostic nanoagents are simply developed by doping both therapeutic agents and imaging agent into one particle entity, and thus have an “always-on” pharmaceutical effect and imaging signals regardless of their in vivo location. Herein, the development of an organic afterglow protheranostic nanoassembly (APtN) that specifically activates both the pharmaceutical effect and diagnostic signals in response to a tumor-associated chemical mediator (hydrogen peroxide, H2 O2 ) is reported. APtN comprises an amphiphilic macromolecule and a near-infrared (NIR) dye acting as the H2 O2 -responsive afterglow prodrug and the afterglow initiator, respectively. Such a molecular architecture allows APtN to passively target tumors in living mice, specifically release the anticancer drug in the tumor, and spontaneously generate the uncaged afterglow substrate. Upon NIR light preirradiation, the afterglow initiator generates singlet oxygen to react and subsequently transform the uncaged afterglow substrate into an active self-luminescent form. Thus, the intensity of generated afterglow luminescence is correlated with the drug release status, permitting real-time in vivo monitoring of prodrug activation. This study proposes a background-free design strategy toward activatable cancer theranostics.

? 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

KEYWORDS

activatable probes; cancer theranostics; optical imaging; organic nanoparticles

Title

An Organic Afterglow Protheranostic Nanoassembly.

Author

He S, Xie C, Jiang Y, Pu K.

Publish date

2019 Aug;

PMID

30972456

Abstract

PURPOSE:
Several retrospective studies have shown that the antitumor efficacy of capecitabine-containing chemotherapy decreases when co-administered with a proton pump inhibitor (PPI). Although a reduction in capecitabine absorption by PPIs was proposed as the underlying mechanism, the effects of PPIs on capecitabine pharmacokinetics remain unclear. We prospectively examined the effects of rabeprazole on the pharmacokinetics of capecitabine and its metabolites.

METHODS:
We enrolled patients administered adjuvant capecitabine plus oxaliplatin (CapeOX) for postoperative colorectal cancer (CRC) patients and metastatic CRC patients receiving CapeOX with/without bevacizumab. Patients receiving a PPI before registration were allocated to the rabeprazole group, and the PPI was changed to rabeprazole (20 mg/day) at least 1 week before the initiation of capecitabine treatment. On day 1, oral capecitabine (1000 mg/m2) was administered 1 h after rabeprazole intake. Oxaliplatin (and bevacizumab) administration on day 1 was shifted to day 2 for pharmacokinetic analysis of the first capecitabine dose. Plasma concentrations of capecitabine, 5′-deoxy-5-fluorocytidine, 5′-deoxy-5-fluorouridine, and 5-fluorouracil were analyzed by high-performance liquid chromatography. Effects of rabeprazole on inhibition of cell proliferation by each capecitabine metabolite were examined with colon cancer cells (COLO205 and HCT116).

RESULTS:
Five and 9 patients enrolled between September 2017 and July 2018 were allocated to rabeprazole and control groups, respectively. No significant effects of rabeprazole on area under the plasma concentration-time curve divided by capecitabine dose for capecitabine and its three metabolites were observed. Rabeprazole did not affect the proliferation inhibition of colon cancer cells by the respective capecitabine metabolites.

CONCLUSION:
Rabeprazole does not affect capecitabine pharmacokinetics.

KEYWORDS

Capecitabine; Capecitabine metabolites; Colorectal cancer; Pharmacokinetics; Proton pump inhibitor; Rabeprazole

Title

Rabeprazole intake does not affect systemic exposure to capecitabine and its metabolites, 5'-deoxy-5-fluorocytidine, 5'-deoxy-5-fluorouridine, and 5-fluorouracil.

Author

Sekido M, Fujita KI, Kubota Y, Ishida H, Takahashi T, Ohkuma

Publish date

2019 Jun;

PMID

29540833

Abstract

Tumor suppressor genes play critical roles orchestrating anti-cancer programs that are both context dependent and mechanistically diverse. Beyond canonical tumor suppressive programs that control cell division, cell death, and genome stability, unexpected tumor suppressor gene activities that regulate metabolism, immune surveillance, the epigenetic landscape, and others have recently emerged. This diversity underscores the important roles these genes play in maintaining cellular homeostasis to suppress cancer initiation and progression, but also highlights a tremendous challenge in discerning precise context-specific programs of tumor suppression controlled by a given tumor suppressor. Fortunately, the rapid sophistication of genetically engineered mouse models of cancer has begun to shed light on these context-dependent tumor suppressor activities. By using techniques that not only toggle “off” tumor suppressor genes in nascent tumors, but also facilitate the timely restoration of gene function “back-on again” in disease specific contexts, precise mechanisms of tumor suppression can be revealed in an unbiased manner. This review discusses the development and implementation of genetic systems designed to toggle tumor suppressor genes off and back-on again and their potential to uncover the tumor suppressor’s tale.

Title

Off and back-on again: a tumor suppressor's tale.

Author

Acosta J, Wang W, Feldser DM.

Publish date

2018 Jun