Antisense Drug Technology: Principles, Strategies, and by Stanley T. Crooke

By Stanley T. Crooke

Greatly revised and up to date, Antisense Drug know-how: ideas, innovations, and purposes, moment variation displays the logarithmic growth made long ago 4 years of oligonucleotide-based remedies, and, specifically, antisense therapeutics and study. reading classes discovered from the medical trials of first new release medications, the publication evaluates the expertise as an entire and gives new instructions and avenues of analysis and improvement. Divided into 5 components, the ebook starts off with an intensive advent to the mechanism of antisense drug motion together with the RNase H mechanism, small RNA silencing pathways, and the aptitude therapeutics of splice switching oligonucleotides. prime researchers reveal the fundamentals of oligonucleotide therapeutics partly through delineating medicinal chemistry, pharmacokinetics, and supply routes equivalent to liposomal formulations for nucleic acid delivery.  half 3 info hybridization dependent medications and considers the dramatic advances represented by way of 2’ methoxyethyl chimeric antisense inhibitors and duplex RNA medicines. different chemical periods of gear and mechanisms of motion are defined partially 4 with extra discussions on bettering the second one new release antisense medicines. the ultimate half delves deeply into healing functions. Contributing authors study the possibility of antisense medications for the relief of cardiovascular ailments, metabolic ailments, inflammatory illnesses, melanoma, neurological issues, and immune modulation. offering a hugely targeted, lucid dialogue of the notable advances within the box, Antisense Drug know-how: rules, techniques, and purposes, moment variation offers the platform for researchers to proceed to aggressively pursue the nice chance represented through this interesting expertise.

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Extra resources for Antisense Drug Technology: Principles, Strategies, and Applications, Second Edition

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Thus, it is clear that attempting to evaluate the effects of the efficiency of a particular splicing event on the activity of antisense drugs is likely to be challenging. Indeed, that has proven to be the case. To begin to address the effects of splice-site strength on the activities of antisense inhibitors, some years ago we [88] constructed a luciferase receptor gene with ␤-globin or adenovirus introns. Mutating the weaker splice signals in the ␤-globin construct progressively toward the stronger adenovirus signals progressively increased the extent of splicing.

Nearest-neighbor rules support the prediction of the free energy of binding for DNA–DNA and RNA–RNA hybrids with relatively high precision [42,43]. A common misconception is that DNA–RNA duplexes are more stable than DNA–DNA duplexes. In fact, the relative stability of these duplexes varies as a function of the sequence. RNA–RNA duplexes are typically the most stable [9]. As with other drug–receptor interactions, activity requires a minimum level of affinity. For many targets and types of oligonucleotides, the minimum length of an oligonucleotide may be 12–14 nucleotides.

That sequence is input and algorithms design antisense inhibitors to 40–80 different sites within the RNA excluding known problematic motifs and sequences that may lead to internal structures in the antisense agents. These are then screened at active concentrations in cells. Multiple active antisense inhibitors are then studied in detailed dose–response curves in vitro. For targets of substantial interest, at this stage we often screen antisense inhibitors to as many as several hundred additional sites.

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