i-Motif Technology Platform
i-Motifs are rationally engineered C-rich oligonucleotide structures that exploit protonated cytosine-cytosine base pairing to form stable four-stranded tetraplexes suitable for therapeutic application. When optimized with phosphorothioate backbones and modified sugars, i-motif-based antisense oligonucleotides (ASOs) function as selective molecular sponges that sequester pathogenic nucleotide targets and prevent adoption of disease-promoting secondary structures.
This mechanism underpins a novel class of antisense (ASO) therapeutics capable of disrupting pathogenic nucleic acid interactions. In the context of microbial infections, i-motif ASOs target critical G-rich sequences required for viral genome replication, bacterial virulence factor expression, and pathogen-mediated immune evasion. The dual mechanism of sequence-specific recognition and structure-based disruption provides enhanced specificity and reduced off-target activity compared to conventional antisense approaches by preventing target sequences from adopting harmful secondary structures. Validated in vitro proof-of-concept across diverse microbial targets supports development as a precision therapeutic platform for infectious disease, particularly incontexts of drug resistance or unmet clinical needs.
Myocardial Infarction (MI)
Myocardial Infarction, commonly known as a heart attack, occurs when the blood flow to a part of the heart muscle is significantly reduced or blocked, leading to damage or death of the affected tissue. Typically caused by the rupture of a plaque in a coronary artery, MI presents with symptoms such as chest pain, shortness of breath, nausea, and sweating. Prompt medical intervention is critical to restore blood flow and minimize heart damage. Treatment may involve medications such as aspirin, thrombolytics, and beta-blockers, as well as procedures like percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) to restore blood flow to the affected area. Post-MI management focuses on lifestyle changes, including a heart-healthy diet, regular exercise, smoking cessation, and medication adherence, to reduce the risk of recurrent events. Long-term prognosis varies depending on the extent of heart damage and the effectiveness of treatment and lifestyle modifications. Our drug molecule has the potential to cure the symptoms of the disorder using antisense oligonucleotide therapy, which is showing remarkable results in pre-clinical trials.