Pancreatic ductal adenocarcinoma (PDAC)
Mito Laboratories is focused on pancreatic ductal adenocarcinoma — one of the most lethal solid tumors and an area of profound unmet medical need.
Unmet need
Pancreatic ductal adenocarcinoma remains among the deadliest major cancers. Despite advances in surgical technique and chemotherapy regimens, long-term survival remains low, and durable responses in advanced disease are uncommon.
The majority of patients present with locally advanced or metastatic disease. Even in resectable cases, recurrence rates are high. Incremental improvements have not yet translated into transformative survival gains.
Metabolic vulnerability in PDAC
PDAC is characterised by profound metabolic adaptation. Tumors frequently exhibit:
- High glycolytic flux and elevated lactate production
- Upregulated lactate dehydrogenase (LDHA)
- Increased pyruvate dehydrogenase kinase (PDK1) activity
- Hypoxic, nutrient-constrained microenvironments
- Dependence on anti-apoptotic Bcl-2 family signaling
These adaptations enable tumor survival under metabolic stress, contribute to therapy resistance, and support immune evasion. Because mitochondria integrate metabolic flux and apoptotic signaling, they represent a strategic point of vulnerability.
Our focus within PDAC
Mito Laboratories is developing a biomarker-defined approach targeting glycolytic pancreatic tumors with elevated LDHA and PDK1 expression.
Our central hypothesis is that simultaneous inhibition of LDH and PDK1 forces mitochondrial oxidative stress in this metabolic subtype, increasing reliance on anti-apoptotic Bcl-2 family proteins. Concurrent pan–anti-apoptotic inhibition is designed to exploit this stress-induced dependency and induce subtype-selective tumor cell death.
Biomarker-defined selection
Focus on LDHA-high / PDK1-high tumors to identify metabolically vulnerable patient subsets.
Synthetic metabolic lethality
Simultaneous LDH + PDK1 inhibition to induce mitochondrial stress and ROS accumulation.
Apoptotic exploitation
Pan–Bcl-2 family inhibition under metabolic stress to trigger non-linear apoptotic activation.
Why pancreatic cancer first
PDAC combines extreme unmet need with clear biological rationale. Its glycolytic phenotype, hypoxic microenvironment, and apoptotic resistance mechanisms make it a compelling setting for a mitochondria-integrated therapeutic strategy.
Our development approach is hypothesis-driven, biomarker-anchored, and milestone-gated — designed to generate decision-quality preclinical evidence in a cancer where new strategies are urgently needed.