Jin Rong OW

• 2026: A*STAR IEO Decentralized Gap Grant – ASO medicine for inflammatory diseases
• 2026: A*STAR IEO Decentralized Gap Grant – Preclinical data package for efficacy and safety in human and mouse ALS models
• 2026: Nucleic Acid Therapeutics Initiative (NATi) CFP A02 – Splice-switching oligonucleotide restoration of functional Ornithine Transcarbamylase (OTC) protein expression for OTC deficiency
• 2024: National Medical Research Council Open Fund – Young Individual Research Grant (NMRC OF-YIRG) – Splice-switching oligonucleotides as a therapeutic modality for hepatic genetic disease
• 2021: A*STAR Career Development Fund – Establishing an integrative RNA therapeutics discovery and development platform for ultra-rare genetic disorders

RESEARCH

Our group’s research interests focus on the development of RNA therapeutics, particularly antisense oligonucleotides (ASO) to address unmet medical needs in metabolic diseases, neurodegenerative diseases and fibrotic diseases. A major theme in the research of the lab is also the application of personalized RNA medicine for genetic rare diseases caused by splicing defects and deep intronic variants. With an established in vitro-to-preclinical RNA therapeutics pipeline that integrates ASO design, chemistry optimization and preclinical evaluation, the team has developed novel ASO candidates for diseases such as Citrin deficiency, OTC deficiency, sporadic amyotrophic lateral sclerosis (ALS), and idiopathic pulmonary fibrosis (IPF).

Current efforts include evaluating the pharmacodynamics of preclinical ASO candidates, investigating precision RNA therapy for common pathogenic variants in East Asian populations, and generating humanized animal models to better understand disease biology and therapeutic efficacy. Collectively, the group’s research aims to bridge fundamental RNA biology with translational therapeutics, enabling the development of next-generation nucleic acid medicines for patients with limited treatment options.

• BLOC1S1 depletion via splice-switching oligonucleotides improves mitochondrial respiration and rescues ALS phenotypes.
  Hor JH*, Ow JR*, Ng W, Ramasamy B, Tabaglio T, Lim KNH, Bin Muzakar MI, Lim VJW, Gurrampati RR, Rajarethinam R, Ngo ST, Ramadass V, Ling SC, Lakshmanan M, Wee KB, Ng SY. (2026).
  Mol Ther.

• Chemical Modification Patterns Conferring High Efficiency (WO/2026/084650)
  The present invention relates to a method of identifying a chemical modification pattern which confers an increased splice-modulation efficiency to a single-stranded RNA oligonucleotide with a predetermined nucleobase sequence, as compared to a single-stranded RNA oligonucleotide with the same predetermined nucleobase sequence having every nucleotide chemically modified with a 2' ribose modification, the method comprising: (a) applying a plurality of chemical modification patterns (Patterns A to G) to a plurality of single-stranded RNA oligonucleotides respectively, wherein each of the plurality of single-stranded RNA oligonucleotides has one of Patterns A to G applied to it, (i) wherein each of the plurality of chemical modification patterns comprises: (A) at least one nucleotide chemically modified with the 2' ribose modification; and (B) one to eight nucleotides chemically modified with a constrained nucleotide (CN); and (ii) wherein the plurality of chemical modification patterns comprises Patterns A to G of CN-modified nucleotides; and (b) measuring the splice- modulation efficiencies of the chemically-modified single-stranded RNA oligonucleotides and comparing these with the splice-modulation efficiency of the single-stranded RNA oligonucleotide having every nucleotide chemically modified with the 2' ribose modification to determine the chemical modification pattern which confers the increased splice-modulation efficiency.
  
  
• Linkage Groups, Oligonucleotide Conjugates, and Methods Thereof. (WO/2026/015080)
  This disclosure concerns linkage groups and uses thereof for conjugating ligands to nucleic acids. Also provided are oligonucleotide-ligand conjugates containing the linkage group, and uses thereof for targeted nucleic acid delivery and as a medicament.
  
  
• Splice-switching Oligonucleotide (SSO) Targeting SLC25A13-PE5 as Therapeutics Candidate for Citrin Deficiency (WO2024005715)
  The present invention relates to splice-switching oligonucleotides (SSOs) capable of altering the slicing of a pre-mRNA encoding a variant of the SLC25A13 gene, as well as the use of the same SSOs for treating citrin deficiency. In an embodiment, a SSO that binds to a site within a target region present on a pre-mRNA transcript of the SLC25A13 gene, wherein the binding of the SSO induces the exclusion of SLC25A13-PE5 from a mature mRNA transcript of the SLC25A13 gene. In another embodiment, the target region having at least 95% sequence identity to SEQ ID NO: 28.
  
  
• Splice-switching Oligonucleotide (SSO) Targeting OTC-PE5 as Therapeutics Candidate for Ornithine Transcarbamylase (OTC) Deficiency Disorders (WO2025151083)
  The present invention relates generally to the field of RNA splicing. In particular, the invention relates to splice-switching oligonucleotides (SSOs) capable of altering the splicing of a pre-mRNA encoding a variant of the ornithine transcarbamylase (OTC) gene. The invention also relates to the use of SSOs as therapeutic candidates for treating a urea cycle disorder, particularly OTC deficiency. In an aspect of the invention, there is provided a SSO that specifically binds to a site within a target region present on a pre-mRNA transcript of a variant of the OTC gene, the target region comprising the sequence of SEQ ID NO: 31, wherein the pre-mRNA transcript comprises a c.540+265G>A mutation and binding of the SSO induces the exclusion of pseudoexon OCT-PE5 from a mature mRNA transcript of the variant of the OTC gene.