As implied in the article by Paul Smaglik, "Making Sense of Antisense" (The Scientist, 12[17]:1, Aug. 31, 1998), the clinical usefulness of antisense compounds will be determined, in large part, by our ability to identify drugs that bind their intended targets much more readily than they bind to bystander RNAs and other cellular components. Selective drugs will be those that recognize highly accessible, "optimal"-target sites. In assessing the likelihood that we will ever be able to develop gene-specific antisense drugs, it will be important to know the size and distribution of optimal target sites. As [I have] discussed previously (A.D. Branch, "Antisense Drug Discovery: Can Cell-Free Screens Speed the Process?" Antisense and Nucleic Acid Drug Development, 8:249-54, June 1998), if optimal sites occur once every 400 bases and are 10 nucleotides long, the prospects for developing highly selective drugs are bright. Alternatively, if optimal sites occur once every 100 nucleotides ...
Making Sense of Antisense
As implied in the article by Paul Smaglik, "Making Sense of Antisense" (The Scientist, 12[17]:1, Aug. 31, 1998), the clinical usefulness of antisense compounds will be determined, in large part, by our ability to identify drugs that bind their intended targets much more readily than they bind to bystander RNAs and other cellular components. Selective drugs will be those that recognize highly accessible, "optimal"-target sites. In assessing the likelihood that we will ever be able to develop gen
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