CLDN18.2 × CD3 × 4-1BB
trispecific TCE
Gastric / GEJ adenocarcinoma. Tumor-restricted T-cell engagement with 4-1BB costimulation to address CD3-bispecific exhaustion. Provisional filed Q2 '26.
Patent-defensible multi-specifics across oncology, neurology and senolytics — each on the same eight-to-sixteen-week path from sequence to in-vitro PoC; in-vivo schedule partner-lab dependent.
Gastric / GEJ adenocarcinoma. Tumor-restricted T-cell engagement with 4-1BB costimulation to address CD3-bispecific exhaustion. Provisional filed Q2 '26.
Blood-brain-barrier penetration shuttle for CNS-restricted biologics. Bispecific VHH design optimized for transcytosis kinetics over receptor sequestration.
Carbohydrate-binding active space — the flagship moat. Senescence-cell targeting via GD3 ganglioside (Iltis et al., Nat Aging 2024). Second arm provides survival-pathway gating; specific co-target under wet-lab evaluation.
The same design–build–test–learn path runs under every program. Wet-lab results feed back into the Module Library, so each cycle starts from a stronger corpus. In-vivo schedule is partner-lab dependent.
The pipeline today — all figures below are in-silico predictions and design targets; wet-lab validation is scheduled, not yet complete, and is labelled as such. P2 is the most advanced (in-vitro); P1 leads on clinical-relevance scope; P3 is the flagship on quantum-corrected glycan binding.
CVaR-VQE active-space correction over the glycan binding pose. Lead candidate CAND-P3-LEAD-08 ranked at a predicted 42 pM Kd; SPR and ADCC validation are scheduled, not yet run. Quantum-corrected glycan binding is the moat — no surveyed competitor ships this.
CLDN18.2 tumor restriction × attenuated CD3 × 4-1BB conditional agonism. The third arm is a costimulation gate that only triggers in the tumor microenvironment — designed to address the exhaustion phenotype of classical CD3 bispecifics. Lead candidate CAND-P1-LEAD-04 assembled from MOD-0492 + MOD-0617 + MOD-0744.
TfR1 (low-affinity, transcytosis-optimized) × IGF-1R (capacity-additive). Deliberately weak TfR1 binding avoids receptor sequestration; IGF-1R adds a parallel BBB-crossing route. Target brain exposure >3% — roughly 30× industry standard of 0.1% — to be confirmed in the Q3 '26 in-vivo study. Cargo-agnostic scaffold.