Therapeutic Areas

Our primary focus lies in identifying and advancing first-in-class therapeutics with the potential to address unmet medical needs. Our therapeutic area encompasses therapies for oncology, Alzheimer's disease, and other CNS diseases including Parkinson's disease.

Oncology Digmbio is developing a novel, brain-penetrating PARP1-selective inhibitor, DM5167, which is one of the safest inhibitors in the class and demonstrates improved antitumor activity compared with advanced agents in clinical development. DM5167 demonstrated equivalent or superior anti-tumor efficacy compared to Olaparib and Saruparib in in vivo xenograft models at a dose range from 10 to 50 mg/kg, leading to tumor regression in BRCAm cancer cell line-derived mouse xenograft models. It has a high brain-to-plasma drug exposure with a B/P ratio of Kp.uu value of 1.18. Safety profiles demonstrate DM5167 showing low general toxicity and only a few transient changes in hematological parameters in the 4-week GLP toxicity study. Phase 1 clinical study showed more than 40 times higher drug exposure levels in humans compared to animals. Also, they showed human efficacy, with 3 partial responses and 2 stable disease for the PARPi naïve patients at the cohort doses of 25mg to 100mg without any DLT and hematological toxicities. The exposure levels are highly comparable to or higher than those of Saruparib at similar dose ranges. PK exposures are dose-dependently increased across all dose ranges. RP2D will be determined, and further Part 2 cohort expansion studies with two arms of PARPi naïve 20 patients and brain-meta 20 patients. Furthermore, Digmbio is planning to conduct Phase 2a studies for ultra-rare cancer in the USA, along with ODD and FTD applications. Based on current clinical data findings, DM5167 is expected to offer therapeutic benefits with minimal hematological toxicity and a favorable safety profile.

Neurogenesis and Neuroprotection Our neurodegenerative disease assets, DM3159 and DM3190, take a novel approach by targeting the taste receptor T1R3 to promote neuroprotection and neurogenesis as a disease-modifying therapy for AD and PD, distinguishing them from traditional therapies focused on beta-amyloid or Tau protein. T1R3 is a component of sweet taste receptors and belongs to the G protein-coupled receptor family. Preclinical data for DM3159 and DM3190 demonstrate differentiated efficacy and toxicity, and strong BBB penetration. In transgenic AD models (5xFAD, 3xTg-AD), DM3159 demonstrated potent efficacy across multiple neurodegenerative pathways. After oral administration, DM3159 significantly upregulated neurogenesis markers, including doublecortin (DCX; +40%) and Ki-67 (+53%), in the subgranular zone (SGZ) of the hippocampal dentate gyrus and the subventricular zone (SVZ) of the lateral ventricle. Simultaneously, DM3159 attenuated neuroinflammatory signaling by reducing Iba-1 expression in the CA1 (-26%) and CA3 (-33%) regions of the hippocampus, and reduced β-amyloid deposition (CA1 -18%, CA3 -23%). These molecular effects were accompanied by marked behavioral recovery, with 20 weeks of oral administration completely restoring spatial memory and learning abilities in the Morris Water Maze to levels comparable to those of age-matched wild-type animals. In a mouse model of α-synuclein/PFF-induced Parkinson's disease (PD), DM3159 demonstrated behavioral efficacy comparable to that of co-administration with L-DOPA and rasagiline, along with DM3190, another candidate. Digmbio is currently advancing DM3159 and DM3190 through IND-enabling studies and is actively seeking strategic collaborations for clinical development.