Disulfiram + Cu †Rx
DSF + Cu inhibits ALDH/proteasome/CSCs via Cu-DDC; elevates ROS/apoptosis; NF-κB ↓; early human data as chemo/radiation adjunct with alcohol/neuro/hepatic cautions.
Forms: DSF tablets (oral, 250–500 mg) + Cu gluconate capsules (oral, 2–4 mg)
Simple Summary
Repurposed alcoholism drug + copper that blocks protein disposal and hits ALDH-high cancer stem cells. It can heighten chemo/radiation effects. Human signals exist (mixed across cancers), so use is investigational and requires close MD oversight.
Evidence at a glance
Early-phase human trials strong in select contexts; mechanistic/preclinical robust; larger RCTs mixed/ongoing.
How it may work
Disulfiram (DSF), when combined with copper (Cu), forms the Cu-DDC (copper-diethyldithiocarbamate) complex, which potently inhibits proteasome activity, disrupting protein degradation and inducing endoplasmic reticulum stress in cancer cells. It suppresses NF-κB signaling, reducing inflammation-driven tumor growth and metastasis. DSF/Cu targets cancer stem cells (CSCs) by inhibiting aldehyde dehydrogenase (ALDH), increasing reactive oxygen species (ROS), and activating caspase-mediated apoptosis. It also enhances chemotherapy and radiation sensitivity by impairing DNA repair pathways.
Targets & pathways
Curated mechanistic targets reported for this agent — how it may act on cells, not proof of a clinical effect.
Often studied / combined with
Combinations reported in the literature, not a protocol or a recommendation.
- Platinum chemo: Resistance reversal via DNA repair inhibition.
- Radiation: Radiosensitization via ROS/DNA damage.
- Curcumin: ROS/apoptosis boost.
- Resveratrol: NF-κB co-inhibition.
- EGCG: CSC co-targeting.
- Quercetin: Proteasome/ROS synergy.
Overlapping mechanisms
- ROS ↑ / Apoptosis ↑ / CSC ↓: Avoid stacking with other strong proteasome/ROS/CSC agents without rationale; monitor cumulative toxicity.
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.
- AlcoholAvoidSevereTheoreticalDisulfiram-ethanol reaction (hypotension, nausea).
- CYP2E1 inducers/inhibitorsMonitorModerateTheoreticalAlters DSF metabolism.
- Platinum chemo / RadiationConsiderBeneficialTheoreticalSensitization; enhanced efficacy via DNA repair inhibition.
- Curcumin / Resveratrol / EGCG / QuercetinConsiderBeneficialTheoreticalSynergistic ROS/apoptosis/NF-κB/CSC targeting.
Timing
- With food: Reduces GI upset for DSF.
- Divided doses: DSF BID for steady levels; Cu once daily.
- Pulsed (optional): E.g., 3 days on/4 off to mitigate cumulative toxicity.
References
Research
No published studies for Disulfiram + Cu †Rx yet
New studies appear here once they’ve been reviewed. Browse all studies.
Dose: as studied, not a recommendation
Ranges seen in adjunct / practice use: 250–500 mg (po) DSF: Divided into 1–2 doses daily. Typical oncology repurposing: 250–500 mg/day (e.g., 250 mg BID). Cu: 2–4 mg elemental copper/day (e.g., 15–30 mg copper gluconate). Human equivalent doses from animal studies (e.g., mouse 100 mg/kg DSF + 4 mg/kg Cu) translate to ~8 mg/kg DSF (~560 mg for 70 kg) but clinical pilots use lower (125–500 mg DSF + 2 mg Cu)., Rx required for DSF; Cu as supplement. Start low, titrate. Pulsed schedules (e.g., 3 days on/4 off) explored to reduce toxicity. Strict clinician oversight; monitor serum copper, LFTs, neuropathy..
Trials studying Disulfiram + Cu †Rx
No actively-recruiting trials matched right now. Recruiting is not the same as proven. Search ClinicalTrials.gov →