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Scientists Devise New Way to DramaticallyRaise RNA Treatment Potency(/genomics/2029-functional-genomics/6403-scientists-devise-new-way-to-dramatically-raise-rna-treatment-potency/)

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FUNCTIONAL GENOMICS (/GENOMICS/2029-FUNCTIONAL-GENOMICS/) August 07, 2013View Comments (/genomics/2029-functional-genomics/6403-scientists-devise-new-way-to-dramatically-raise-rna-treatment-potency/#comments_block)

Matthew Disney, Ph.D., is an associate professor in the Department of Chemistry on the Florida campus ofthe Scripps Research Institute. Photo: Courtesy of The Scripps Research Institute

Jupiter, FL (Scicasts) – Scientists from the Jupiter campus of The Scripps Research Institute (TSRI) have showna novel way to dramatically raise the potency of drug candidates targeting RNA, resulting in a 2,500-foldimprovement in potency and significantly increasing their potential as therapeutic agents.

The new study, published recently online ahead of print by the journal Angewandte Chemie, confirms for the firsttime that a small molecule actually binds to a disease-causing RNA target—a breakthrough that should helpscientists identify precise RNA targets within living cells, profile their interactions, and predict drug candidates' sideeffects.

"We're trying to make tools that can target any RNA motif," said Matthew Disney, a TSRI associate professor whoauthored the research with a research associate in his lab, Lirui Guan. "This study completely validates our design—it validates that our compound targets the desired RNA sequence in a complex cellular environment thatcontains many hundreds of thousands of RNAs."

While targeting DNA has been used as a therapeutic strategy against cancer, few similar approaches have beenattempted for disease-associated RNAs.

In the new study, the scientists created a small molecule that binds to the genetic defect in RNA that causesmyotonic dystrophy type 1 and improves associated defects in cell culture.

Myotonic dystrophy type 1 involves a type of RNA defect known as a "triplet repeat," a series of three nucleotidesrepeated more times than normal in an individual's genetic code. In this case, the repetition of the cytosine-uracil-guanine (CUG) in the RNA sequence leads to disease by binding to a particular protein, MBNL1, rendering itinactive and resulting in a number of protein-splicing abnormalities.

To achieve the increase in the drug candidate's potency, Disney and his colleagues attached a reactive molecule(a derivative of chlorambucil, a chemotherapy drug that has been used to treatment a form of leukaemia) to thesmall molecule they had identified. As a result, the new compound not only binds to the target, it becomes apermanent part of the target—as if it were super glued to it, Disney said. Once attached, it switches off the CUGdefect and prevents the cell from turning it back on.

Disney was surprised at the approximately 2,500-fold improvement in potency with the new approach.

"I was shocked by the increase," he said. "This takes the potency into the realm where one would like to see if thecompound were to have real therapeutic potential."

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As a result, the new compound, known as 2H-4-CA, is the most potent compound known to date that improvesDM1-associated splicing defects. Importantly, 2H-4-CA does not affect the alternative splicing of a transcript notregulated by MBNL1, demonstrating selectivity for the CUG repeat and suggesting that it might have minimal sideeffects.

"We can now use this approach to attach reactive molecules to other RNA targeted small molecules," Disney said.

The reactive molecule model also provides a potentially general method to identify cellular targets of RNA-directedsmall molecules. Such probes could also identify unintended targets, information that could be used to design andidentify compounds with improved selectivity in an approach similar to activity-based profiling, Disney said.

Publication: Covalent Small-Molecule–RNA Complex Formation Enables Cellular Profiling of Small-Molecule–RNA Interactions. Dr. Lirui Guan, Prof. Dr. Matthew D. Disney. Angewandte Chemie InternationalEdition (2013): http://onlinelibrary.wiley.com/doi/10.1002/anie.201301639/full(http://onlinelibrary.wiley.com/doi/10.1002/anie.201301639/full)

Comments( Open Comments

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