2'-Fluoro-2'-deoxyadenosine - CAS 64183-27-3
Category:
Nucleosides
Product Name:
2'-Fluoro-2'-deoxyadenosine
Catalog Number:
64183-27-3
Synonyms:
9-(2'-Deoxy-2'-fluoro-β-D-ribofuranosyl)-adenine
CAS Number:
64183-27-3
Molecular Weight:
269.23
Molecular Formula:
C10H12FN5O3
COA:
Inquire
MSDS:
Inquire
Structure\Application:
2'-Deoxy-Nucleosides
Chemical Structure
CAS 64183-27-3 2'-Fluoro-2'-deoxyadenosine

Related 2'-Deoxy-Nucleosides Products


Reference Reading


1.Cell-free biosynthesis of fluoroacetate and 4-fluorothreonine in Streptomyces cattleya.
Schaffrath C1, Cobb SL, O'Hagan D. Angew Chem Int Ed Engl. 2002 Oct 18;41(20):3913-5.
2.Susceptibility in vitro of clinically metronidazole-resistant Trichomonas vaginalis to nitazoxanide, toyocamycin, and 2-fluoro-2'-deoxyadenosine.
Wright JM1, Dunn LA, Kazimierczuk Z, Burgess AG, Krauer KG, Upcroft P, Upcroft JA. Parasitol Res. 2010 Sep;107(4):847-53. doi: 10.1007/s00436-010-1938-3. Epub 2010 Jun 9.
This study investigates the susceptibility of a clinically metronidazole (Mz)-resistant isolate of Trichomonas vaginalis to alternative anti-trichomonal compounds. The microaerobic minimal inhibitory concentration (MIC) of the 5-nitroimidazole (NI) drug, Mz, against a typical Mz-susceptible isolate of T. vaginalis is around 3.2 microM Mz while the clinically, highly Mz-resistant isolate has an MIC of 50-100 microM. This isolate was cross-resistant to other members of the 5-NI family of compounds including tinidazole and other experimental compounds and maintained resistance under anaerobic conditions. In addition, this isolate was cross-resistant to the 5-nitrothiazole compound nitazoxanide and the 5-nitrofuran derivative, furazolidone. Adenosine analogues toyocamycin and 2-fluoro-2'-deoxyadenosine with no nitro group were also less effective against the clinically Mz-resistant isolate than a Mz-susceptible one. Three other isolates which were determined to be Mz-resistant soon after isolation lost resistance in the long term.
3.Structure of a mutant human purine nucleoside phosphorylase with the prodrug, 2-fluoro-2'-deoxyadenosine and the cytotoxic drug, 2-fluoroadenine.
Afshar S1, Sawaya MR, Morrison SL. Protein Sci. 2009 May;18(5):1107-14. doi: 10.1002/pro.91.
A double mutant of human purine nucleoside phosphorylase (hDM) with the amino acid mutations Glu201Gln:Asn243Asp cleaves adenosine-based prodrugs to their corresponding cytotoxic drugs. When fused to an anti-tumor targeting component, hDM is targeted to tumor cells, where it effectively catalyzes phosphorolysis of the prodrug, 2-fluoro-2'-deoxyadenosine (F-dAdo) to the cytotoxic drug, 2-fluoroadenine (F-Ade). This cytotoxicity should be restricted only to the tumor microenvironment, because the endogenously expressed wild type enzyme cannot use adenosine-based prodrugs as substrates. To gain insight into the interaction of hDM with F-dAdo, we have determined the crystal structures of hDM with F-dAdo and F-Ade. The structures reveal that despite the two mutations, the overall fold of hDM is nearly identical to the wild type enzyme. Importantly, the residues Gln201 and Asp243 introduced by the mutation form hydrogen bond contacts with F-dAdo that result in its binding and catalysis.
4.Antitumor activity of 2-fluoro-2'-deoxyadenosine against tumors that express Escherichia coli purine nucleoside phosphorylase.
Parker WB1, Allan PW, Hassan AE, Secrist JA 3rd, Sorscher EJ, Waud WR. Cancer Gene Ther. 2003 Jan;10(1):23-9.
The selective expression of Escherichia coli purine nucleoside phosphorylase (PNP) in solid tumors has been successfully used to activate two purine nucleoside analogs [9-(2-deoxy-beta-D-ribofuranosyl)-6-methylpurine (MeP-dR) and 9-beta-D-arabinofuranosyl-2-fluoroadenine (F-araA)] resulting in lasting tumor regressions and cures. E. coli PNP also cleaves 2-fluoro-2'-deoxyadenosine (F-dAdo) to 2-F-adenine, which is the toxic purine analog liberated from F-araA that has high bystander activity and is active against nonproliferating tumor cells. As F-dAdo is 3000 times better than F-araA as a substrate for E. coli PNP, we have evaluated its antitumor activity against D54 gliomas that express E. coli PNP and have characterized its in vivo metabolism in order to better understand its mechanism of action with respect to the other two agents. Like MeP-dR and F-araA-5'-monophosphate (F-araAMP, a prodrug of F-araA), treatment of mice bearing D54 tumors that express E.