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VM-AML-001Computational Validation Complete

CTSB-VEN-001

Cathepsin B-Activated Venetoclax Prodrug

Acute Myeloid Leukemia (AML)Small Molecule Prodrug
Reduced TLS risk vs oral venetoclax

Overview

Venetoclax-based regimens (azacitidine + venetoclax) deliver substantial responses in AML but are constrained by tumor lysis syndrome (TLS), an acute toxicity tied to rapid cytoreduction and high circulating drug exposure requiring dose ramp-up and intensive monitoring.

Unmet Medical Need

Efficacy is constrained by TLS risk and the need for slow oral ramp-up driven by high systemic Cmax. A therapy that decouples tumor kill from systemic Cmax would reduce TLS risk.

Therapeutic Hypothesis

IV, enzyme-activated small-molecule prodrug of venetoclax that is inert in circulation yet cleaved within lysosomes by Cathepsin B (CTSB)—enriched in AML blasts—releasing active venetoclax intracellularly. Uses cathepsin-cleavable dipeptide linkers (Val-Cit, Val-Ala) with PABC self-immolative spacer.

Computational Work Performed

  • AlphaFold 3 for protein/ligand complex prediction (CTSB binding)
  • DiffDock and AutoDock Vina 1.2 for dipeptide trigger docking
  • GROMACS MD and MM/PBSA for stability/binding-energy analysis
  • ADMET-AI for computational ADME/Tox screens
  • DeepImmuno for peptide-level immunogenicity risk scanning
  • Two lead constructs: PEG4-Val-Ala-PABC–VEN and PEG4-Val-Cit-PABC–VEN

Next Milestones (Success Criteria)

  • 1
    pH-differential CTSB cleavage kinetics (pH 5.0 > pH 7.4)
  • 2
    Human & mouse plasma stability (≥8h in human plasma)
  • 3
    Selectivity: AML vs non-malignant cells (selectivity index ≥10×)
  • 4
    IV PK showing low circulating free venetoclax Cmax
  • 5
    Strong intratumoral activation with BCL-2 target engagement

Competitive Landscape

Oral BCL-2 inhibitors beyond venetoclax (lisaftoclax, sonrotoclax) claim ramp-up convenience but don't address enzyme-triggered intracellular release. ABBV-167 is an oral phosphate prodrug for solubility—distinct from CTSB-activated approach.

Key Differentiation

  • Mechanism-differentiated: IV, lysosome-activated small molecule
  • Solves TLS at the source by constraining systemic free venetoclax
  • Concentrates activation in AML cells via CTSB-dependent release

Interested in This Asset?

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