Next-Generation DNA Editing
Powered by Cas-Free, Innate Enzyme DNA Editing.
The Next Generation of DNA editing tech.
Our RIDE™ platform harnesses innate human enzymes, completely eliminating the need for bacterial Cas proteins. It delivers unprecedented precision with lifelong redosability.
Cas-Free & Innate
Activates native human base-repair enzymes, circumventing all immunogenicity issues associated with bacterial proteins.
Lifelong Redosability
A completely non-immunogenic profile allows for safe, repeated treatments throughout a patient's entire lifespan.
Limitless Versatility
Capable of resolving SNV (Single Nucleotide Variant), MNV (Multi-Nucleotide Variant), and complex deletion mutations.
How RIDE™ Works
Our RNA-based guide system intentionally creates a structural mismatch, acting as a beacon to recruit your body's own innate enzymes. This enables us to safely and flawlessly repair DNA sequences.
1. Design
We engineer a highly specific Guide RNA. At its tail, we design a specialized secondary structure—a "decoy"—that acts as a powerful beacon to lure and recruit innate human repair enzymes natively present in the cell.
2. Binding & Recruitment
Our Guard-RNA invades the double-stranded DNA at the target sequence. The resulting mismatch structure acts as a powerful metabolic beacon, successfully recruiting native, innate human DNA repair enzymes to the precise mutation site.
3. Seamless Restoration
The activated endogenous enzyme uses the RNA strand as a pristine template, smoothly correcting the biological error and rewriting the DNA.
Unprecedented Safety
Zero Off-Target Risks
Without CRISPR-Cas
Pioneering the Post-CRISPR era. By completely eliminating bacterial Cas nucleases, we bypass immunogenicity and cellular toxicity while executing flawless genetic correction without Double-Strand Breaks (DSB), removing the catastrophic risks of unpredicted translocations and unwanted indels.
Zero Off-Target
Utilizing highly specific Guide RNAs combined with our unique forced mismatch mechanism, RIDE™ drastically eliminates accidental off-target edits at the human genome level, setting an unprecedented standard for therapeutic safety.
PAM-Independent
Unlike CRISPR systems, RIDE™ is completely free from Protospacer Adjacent Motif (PAM) constraints. This grants us infinite expandability and unrestricted targeting capability across the entire human genome.
Proven Precision
Our technology's unparalleled sophistication has been empirically validated. We have formally demonstrated restorative success across complex mutations including SNPs, MNVs (Multi-Nucleotide Variants), and Insertions.
Expanding the Horizon of Cures.
CFTR Target
Cystic Fibrosis (CF). The G551D mutation impairs chloride channel function.
Validated mutation: G551D
SERPINA1 Target
Alpha-1 Antitrypsin Deficiency. The E366K mutation leads to compromised lung/liver function.
Validated mutation: E366K
GJB2 Target
Non-syndromic Hearing Loss (DFNB1). R143W affects the connexin 26 gap junction protein.
Validated mutation: R143W
RNH2B Target
Aicardi-Goutières Syndrome (AGS). The A177T mutation drives severe auto-inflammatory neurodegeneration.
Validated mutation: A177T
IDS Target
Hunter Syndrome (MPS II). R468Q is a severe mutation impeding mucopolysaccharide breakdown.
Validated mutation: R468Q
KRAS Target
Pancreatic/Colorectal Cancer. G12 and G13 are classic oncogenic driver mutations.
Validated mutations: G12, G13
PIK3CA Target
Breast and solid tumors. H1047R hyperactivates the PI3K signaling pathway.
Validated mutation: H1047R
GRIK2 Target
Neurodevelopmental Disorders (e.g., Autism spectrum/Intellectual disability). Target mutation A490V.
Validated mutation: A490V
ZNF292 Target
Intellectual Disability / Neurodevelopmental delay. Target mutation H1542R.
Validated mutation: H1542R
P53 Target
Universal Tumor Suppressor. R175H and R248Q are among the most common hot-spot mutations in human cancers.
Validated mutations: R175H, R248Q
The 'Gene Rewind' Era.
" Going beyond merely treating disease, we completely restore somatic mutations—accumulated through aging and stress, such asTP53andTP53 Mutation
Universal Tumor Suppressor. R175H and R248Q are among the most common hot-spot mutations in human cancers.
JAK2—back to their original healthy sequences. We are leading the realization of genetic age-reversal. "JAK2 Mutation
Associated with myeloproliferative neoplasms (blood cancers). The V617F mutation drives abnormal blood cell production.
GERNA Biotech R&D