DADA 250 mg/ml – solution 20 ml
research-grade
liquid solution
supplied in a 20 ml glass bottle. DADA (diisopropylamine dichloroacetate) is a small-molecule metabolic modulator studied in experimental models of mitochondrial bioenergetics, pyruvate dehydrogenase (PDH) / PDK regulation, liver metabolism and tumor cell metabolism.
Research Use Only:
All products are intended exclusively for laboratory and scientific research. Not for human or veterinary use.
Purity
High-purity research grade
Content
250 mg DADA (diisopropylamine dichloroacetate) per ml; 20 ml per bottle
Solvent
Aqueous solution (water-based)
Packaging
20 ml glass bottle with secure closure
Storage
Store at 2–8 °C, protected from light; keep tightly closed.
Molecular formula
C8H17Cl2NO2 (diisopropylamine dichloroacetate)
Molecular weight
≈ 230.1 g·mol⁻¹
IUPAC name
Diisopropylamine dichloroacetate (2,2-dichloroacetic acid; N-propan-2-ylpropan-2-amine salt)
Research Overview
DADA (diisopropylamine dichloroacetate) is a small-molecule salt of dichloroacetic acid and diisopropylamine used as a tool compound in metabolic research. In experimental systems, it is employed to investigate regulation of the pyruvate dehydrogenase complex via pyruvate dehydrogenase kinase (PDK) inhibition, mitochondrial oxidative phosphorylation, lactate handling and bioenergetic adaptations in liver, muscle and tumor models.
Primary Research Areas
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PDH / PDK signaling and mitochondrial bioenergetics:
Used to probe how inhibition of pyruvate dehydrogenase kinases influences flux through the pyruvate dehydrogenase complex, mitochondrial ATP production and the balance between glycolytic and oxidative metabolism.
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Liver metabolism and metabolic-disorder models:
Applied in preclinical liver research to study changes in hepatic energy metabolism, lipid handling and mitochondrial function in models of metabolic stress and chronic liver dysfunction.
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Tumor metabolism and cancer cell bioenergetics:
Employed in in vitro and in vivo oncology research to examine how modulation of mitochondrial oxidation, lactate production and PDH/PDK signaling affects tumor cell survival and metabolic phenotypes.
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Systemic stress and multi-organ energy failure models:
Investigated in experimental models of severe systemic stress and infection to evaluate whether restoring mitochondrial enzyme activity and ATP generation can influence organ-level energy homeostasis.
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Exercise and workload-related metabolic research:
Used in laboratory studies exploring shifts between glycolytic and oxidative metabolism, lactate dynamics and mitochondrial efficiency under varying workload or exercise-like conditions in experimental models.
