DCA (Dichloroacetate Sodium)

PDK inhibitor reactivating mito OXPHOS/ROS for apoptosis; downregulates HIF-1α; pilot human data as chemo/radiation adjunct with neuropathy caution.

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Human-reviewed · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed

🏥⭐⭐⭐ Moderate — Supported by human pilot studies and strong mechanistic data; RCTs are limited.Dichloroacetate SodiumDichloroacetic acid sodium salt

Forms: DCA powder/capsules (oral, 500–2000 mg)

Educational only, not medical advice. OncoForge makes no claim that DCA (Dichloroacetate Sodium) treats, prevents, or cures any condition, beyond what the linked studies show. Evidence levels vary; effects may not translate to people, and some compounds can cause harm. Always coordinate with your oncology team.

Simple Summary

By blocking PDK, DCA forces tumors to burn fuel in mitochondria again—raising ROS and tipping cells into apoptosis. Human pilot data exist; it can help sensitize to chemo/radiation. Requires clinician oversight due to neuropathy risk.

Evidence at a glance

Tier 3 · early humanGlioblastomaVarious solid tumors (pilots)

Human pilots strong; mechanistic/preclinical robust; RCTs needed.

How it may work

DCA inhibits pyruvate dehydrogenase kinase (PDK), reactivating pyruvate dehydrogenase to shift cancer cell metabolism from glycolysis to oxidative phosphorylation, countering the Warburg effect. This elevates mitochondrial ROS, triggering caspase-3-mediated apoptosis. DCA downregulates Bcl-2, enhances p53 activity, and inhibits HIF-1α, reducing angiogenesis. It sensitizes tumors to chemotherapy and radiation.

Targets & pathways

Curated mechanistic targets reported for this agent — how it may act on cells, not proof of a clinical effect.

Pyruvate Dehydrogenase Kinase (PDK)↓
Oxidative Phosphorylation↑Shifts from glycolysis
Mitochondrial ROS↑
Apoptosis↑Caspase-3 mediated; Bcl-2 ↓; p53 ↑
HIF-1α↓Reduces angiogenesis

PDKMitoApoptosisHIF-1α

Often studied / combined with

Combinations reported in the literature, not a protocol or a recommendation.

Platinum chemo: Resistance reversal.
Radiation: ROS sensitization.
Metformin: Metabolic co-targeting.

Overlapping mechanisms

Mito ↑ / ROS ↑: Avoid with other strong mito/ROS agents without rationale.

Safety & interactions

Severity and how well-established each signal is are shown separately. Verify everything with your oncologist or pharmacist — absence here does not mean safe.

Risk categories

Neuropathy RiskHepatotoxicity Risk MildGi Upset MildPregnancy Avoid

Potential interactions

Metformin / BiguanidesMonitorModerateTheoreticalAdditive lactate risk (rare).
CNS depressantsMonitorMinorTheoreticalSedation possible.
Platinum chemo / RadiationConsiderBeneficialTheoreticalSensitization; enhanced efficacy.

Timing

With meals: Reduces GI upset.
Divided doses: Steady levels; pulsed schedules common.

References

Research

No published studies for DCA (Dichloroacetate Sodium) yet

New studies appear here once they’ve been reviewed. Browse all studies.

Dose: as studied, not a recommendation

These are doses as studied or reported, never a recommendation. The right amount of DCA (Dichloroacetate Sodium) depends on you, your other medicines, and your situation; decide it with your oncology team and pharmacist, not from a web page.

Ranges seen in adjunct / practice use: 500–2000 mg (po) Divided into 2–3 doses daily. Pilot studies use 6.25–12.5 mg/kg (~375–750 mg for 60 kg); up to 25 mg/kg (~1500 mg) with monitoring., Rx/compounded often required. Pulsed (e.g., 5 days on/2 off) to mitigate neuropathy. Co-factors (thiamine, ALA) may help. Strict clinician oversight..

Trials studying DCA (Dichloroacetate Sodium)

No actively-recruiting trials matched right now. Recruiting is not the same as proven. Search ClinicalTrials.gov →

Inclusion here is not an endorsement. OncoForge makes no claim beyond what the linked studies show. Discuss anything on this page with your oncology team before acting on it.

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