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2004-03-7

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2004-03-7 Usage

Chemical Properties

Light Yellow Powder

Uses

6-Methylpurine (MeP) is a toxic adenine analog used as a bisubstrate inhibitor of enzymes that bind adenosyl moieties and which may become phosphorylated to levels that inhibit RNA and protein synthesis.

Definition

ChEBI: Purine bearing a methyl substituent at position 6.

Synthesis Reference(s)

Journal of the American Chemical Society, 95, p. 6407, 1973 DOI: 10.1021/ja00800a042

Check Digit Verification of cas no

The CAS Registry Mumber 2004-03-7 includes 7 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 4 digits, 2,0,0 and 4 respectively; the second part has 2 digits, 0 and 3 respectively.
Calculate Digit Verification of CAS Registry Number 2004-03:
(6*2)+(5*0)+(4*0)+(3*4)+(2*0)+(1*3)=27
27 % 10 = 7
So 2004-03-7 is a valid CAS Registry Number.
InChI:InChI=1/C6H6N4/c1-4-5-6(9-2-7-4)10-3-8-5/h2-3H,1H3,(H,7,8,9,10)

2004-03-7Relevant articles and documents

-

Lettre et al.

, p. 224 (1963)

-

Improved synthesis of β-D-6-methylpurine riboside and antitumor effects of the β-D- and α-D-anomers

Marasco Jr., Canio J.,Pera, Paula J.,Spiess, Arthur J.,Bernacki, Ralph,Sufrin, Janice R.

, p. 1015 - 1020 (2007/10/03)

6-Methylpurine-β-D-riboside (β-D-MPR) has been synthesized by coupling 6-methylpurine and 1-O-acety1-2,3,5-tri-O-benzoyl-D-ribose using conditions that produce the β-D-anomer exclusively. The in vitro antitumor effects of β-D-MPR and 6-methyl-purine-α-D-riboside (α-D-MPR) in five human tumor cell lines showed that β-D-MPR was highly active (IC50 values ranging from 6 to 34 nM). a-D-MPR, although less active than β-D-MPR, also exhibited significant antitumor effects (IC50 values ranging from 1.47 to 4.83 μM).

Gene therapy of cancer: activation of nucleoside prodrugs with e. colipurine nucleoside phosphorylase

Secrist III, John A.

, p. 745 - 757 (2007/10/03)

During the last few years, many gene therapy strategies have been developed for various disease targets. The development of anticancer gene therapy strategies to selectively generate cytotoxic nucleoside or nucleotide analogs is an attractive goal. One such approach involves the delivery of herpes simplex virus thymidine kinase followed by the acyclic nucleoside analog ganciclovir. We have developed another gene therapy methodology for the treatment of cancer that has several significant attributes. Specifically, our approach involves the delivery of E. coli purine nucleoside phosphorylase, followed by treatment with a relatively non-toxic nucleoside prodrug that is cleaved by the enzyme to a toxic compound. .This presentation describes the concept, details our search for suitable prodrugs, and summarizes the current biological data. Copyright

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