Description:
The current state of the art
Like Antibodies, small nucleotide aptamers target specific biomarkers responsible for tumor progression. But they have no-immunogenicity, higher tissue penetration, higher specificity, and higher binding affinity than antibodies.
Problems with current state of art
Single CD44 aptamers and single EpCAM aptamers have been studied for treating ovarian tumorigenesis but their clinical application is limited due to their small size, susceptibility to nuclease attack, and short circulation half-life.
Advantages of our invention
Researchers at Augusta University invented a new means to increase the size of the aptamer by fusing two single CD44 and EpCAM aptamers with a double-stranded RNA linker. As a result, the aptamer size is increased to improve circulation half-life but is still small enough to allow better tissue penetration than antibodies. Moreover, the new bispecific aptamer retains their specificity to CD44 and EpCAM.
Compared to single CD44, EpCAM aptamer, or CD44 and EpCAM combination, bispecific aptamer effectively inhibited cell growth and induced apoptosis in a panel of ovarian cancer cell lines, and suppressed intraperitoneal ovarian cancer growth in the xenograft model. It did not exhibit toxicity to the host and didn’t trigger innate immunogenicity. Our study suggests that bispecific CD44-EpCAM aptamer may represent a promising therapeutic against advanced ovarian cancer.
AURI: #2017-015
IP status: Non-provisional filed; 15/899,473 Feb 20, 2018
Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5399600/