Targeting metabolic vulnerabilities in pancreatic cancer.
Mito Laboratories is developing a biomarker-defined therapeutic strategy for glycolytic, LDHA-high / PDK1-high pancreatic tumors. By simultaneously inhibiting lactate dehydrogenase (LDH), pyruvate dehydrogenase kinase 1 (PDK1), and anti-apoptotic Bcl-2 family proteins, we aim to induce catastrophic mitochondrial stress and tumor-selective apoptosis.
Mechanism-driven precision
Our platform is anchored in a defined metabolic phenotype. Dual metabolic inhibition forces oxidative flux and mitochondrial stress in glycolytic pancreatic tumors, creating an exploitable apoptotic vulnerability. Concurrent pan–anti-apoptotic Bcl-2 inhibition is designed to trigger non-linear, subtype-selective tumor cell death.
Metabolic Selection
Identification of pancreatic tumors with elevated LDHA and PDK1 expression, defining a glycolytic, stress-sensitive subtype.
Synthetic Lethality
Simultaneous inhibition of LDH and PDK1 induces mitochondrial ROS and metabolic collapse, sensitising tumors to apoptosis.
Dose-Sparing Strategy
Metabolic stress reduces the exposure required for pan–Bcl-2 family inhibition, with the goal of expanding the therapeutic window in defined tumor subtypes.
Seed-stage milestones
Validate
Stratify PDAC models by LDHA / PDK1 expression and demonstrate subtype-selective triple-combination synergy in vitro.
Protect
File provisional intellectual property covering biomarker-defined simultaneous inhibition and dose-sparing apoptotic activation.
Advance
Generate in vivo proof-of-concept data and initiate staged proprietary inhibitor discovery programs.
Investor & Partner Enquiries
Mito Laboratories is seeking seed-stage capital and scientific collaborators to advance preclinical validation in pancreatic cancer.