SVG103 is an oral small-molecule PI3K/mTOR inhibitor in
development as a treatment for tuberous sclerosis
complex-associated epilepsy (TSC epilepsy).

The favorable blood-brain barrier permeability of SVG103 is expected to
allow sufficient inhibition of disease-driving physiological mechanisms in the brain
while maintaining relatively low systemic exposure, thereby providing a wide therapeutic safety margin.

Clinical trials of this program are currently ongoing in patients with
TSC and FCD II epilepsy in Australia and Korea.

SVG105 is a first-in-class antisense oligonucleotide (ASO)
drug candidate under development for the treatment of
Focal Cortical Dysplasia Type II (FCD II) epilepsy.

SVG105 directly targets the causative gene of FCD II to inhibit the signaling pathway,
aiming not only to suppress seizures but also to prevent accompanying comorbidities
such as developmental delay and intellectual disability, positioning it as a potential
disease-modifying therapy. In nonclinical studies, SVG105 demonstrated selective
inhibition of the signaling pathway in the brain mutant cells while minimizing
systemic exposure, suggesting a favorable safety profile.

Currently, SVG105 is undergoing IND-enabling studies to support clinical trial authorization.

SVG301 is a first-in-class antisense oligonucleotide (ASO)
drug candidate being developed as a treatment for BRAF-mutant
low-grade glioma (LGG).

SVG301 is administered intrathecally to bypass the blood-brain barrier (BBB) while directly
targeting the BRAF gene, and is expected to provide an effective and safe therapeutic option for
patients with LGG harboring various BRAF mutations.
In nonclinical studies, administration of the ASO was shown to induce differentiation of
BRAF‑mutant neural stem cells into non‑malignant normal cells,
thereby demonstrating its therapeutic potential.

Currently, SVG301 is undergoing research to select and finalize the clinical development candidate.