By Stanley T. Crooke
Greatly revised and up to date, Antisense Drug know-how: rules, concepts, and functions, moment version displays the logarithmic growth made long ago 4 years of oligonucleotide-based cures, and, particularly, antisense therapeutics and learn. analyzing classes realized from the scientific trials of first iteration medicinal drugs, the publication evaluates the know-how as an entire and gives new instructions and avenues of study and improvement. Divided into 5 components, the booklet starts with a radical advent to the mechanism of antisense drug motion together with the RNase H mechanism, small RNA silencing pathways, and the capability therapeutics of splice switching oligonucleotides. best researchers exhibit the fundamentals of oligonucleotide therapeutics partially by way of delineating medicinal chemistry, pharmacokinetics, and supply routes comparable to liposomal formulations for nucleic acid delivery. half 3 information hybridization dependent medications and considers the dramatic advances represented by means of 2’ methoxyethyl chimeric antisense inhibitors and duplex RNA medicinal drugs. different chemical periods of substances and mechanisms of motion are defined partially 4 with additional discussions on bettering the second one new release antisense medicinal drugs. the ultimate half delves deeply into healing functions. Contributing authors learn the potential for antisense medicinal drugs for the relief of cardiovascular illnesses, metabolic ailments, inflammatory illnesses, melanoma, neurological problems, and immune modulation. offering a hugely particular, lucid dialogue of the awesome advances within the box, Antisense Drug know-how: ideas, concepts, and functions, moment version presents the platform for researchers to proceed to aggressively pursue the nice chance represented by way of this fascinating know-how.
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Extra resources for Antisense Drug Technology: Principles, Strategies, and Applications, Second Edition
However, antisense inhibitors designed to bind to sites in coding sequences have also been shown to be active. Here again, meaningful progress has been reported and significant questions remain to be answered. 1 Is It Feasible to Arrest Translation with Antisense Drugs? Yes. Translation arrest can be induced by a variety of chemical classes of antisense drugs in vitro and in vivo. Well-documented examples include inhibition of intercellular adhesion molecule 1 (ICAM-1) , Hepatitis C virus (HCV) [93–95], and c-Myc .
This protein was reported to enhance RNA hybridization by up to a thousandfold. Its activity was dependent on the ratio of protein to RNA, the length of the RNA, and ionic strength. It did not require adenosine triphosophate (ATP) hydrolysis. It also enhanced hybridization of DNA. The promiscuity of this protein suggests that it can participate in facilitating the hybridization of antisense drugs of various chemistries to target RNAs. Its localization to the polysomes, m-RNPs, and in the nucleus makes it an excellent candidate to facilitate the hybridization of antisense drugs in all cellular compartments.
Presence of exonic enhancers or silencers f. Chemical class or the antisense drug 3. Is it possible to design antisense drugs that affect exonic enhancer or silencer function? 4. Is efficacy influenced by cell or tissue context? 5. How robust a mechanism is alteration of splicing? 1 Can Antisense Drugs Be Used to Alter Splicing in Vitro and in Vivo? Today, there is no question that appropriately designed antisense drugs can alter splicing. The evidence for this is, of course, broader and more compelling in vitro, but there are now also multiple well-documented examples of antisense drugs altering splicing in vivo.