Database Query Results : Disulfiram, ,

DSF, Disulfiram: Click to Expand ⟱
Features:
Disulfiram is a synthetic small-molecule drug best known for its use in the treatment of chronic alcohol use disorder. It is a thiuram disulfide compound with the chemical formula C₁₀H₂₀N₂S₄ and acts primarily as an aldehyde dehydrogenase (ALDH) inhibitor. 
Main Actions:
-Potent copper-dependent pro-oxidant
-Targets ALDH⁺ cancer stem cells
-Strong clinical repurposing interest

Key pathways
-Cu-mediated redox cycling
-Proteasome inhibition
-Mitochondrial ROS

Chemo relevance
-Often synergistic
-Highly mechanism-dependent
Rank Pathway / Axis Cancer Cells Normal Cells Label Primary Interpretation Notes
1 Metal chelation / Disulfiram–Cu complex formation ↑ DSF–Cu complex formation ↔ limited formation Driver Copper-dependent cytotoxic chemistry Elevated copper in cancer cells enables formation of cytotoxic DSF–Cu complexes; this is the initiating event for most anticancer effects
2 Proteasome / p97–NPL4 axis ↓ proteasome function; ↑ proteotoxic stress ↔ minimal disruption Driver Protein homeostasis collapse DSF–Cu disrupts protein degradation pathways, leading to accumulation of misfolded proteins and stress signaling
3 Reactive oxygen species (ROS) ↑ ROS (metal-dependent) ↔ buffered Secondary Oxidative stress amplification ROS rise follows DSF–Cu redox cycling and proteotoxic stress; not the primary trigger
4 Mitochondrial integrity / intrinsic apoptosis ↓ ΔΨm; ↑ caspase activation ↔ preserved Secondary Execution of cell death Mitochondrial dysfunction and apoptosis occur downstream of proteostasis and redox stress
5 ALDH activity (ALDH1A1 / stemness) ↓ ALDH activity ↓ ALDH (clinically tolerated) Secondary Cancer stem-like cell targeting ALDH inhibition preferentially impacts cancer stem-like populations; normal cells tolerate inhibition at therapeutic exposure
6 NF-κB signaling ↓ NF-κB activation ↓ inflammatory NF-κB tone Secondary Suppression of survival transcription NF-κB inhibition reflects upstream proteotoxic and redox stress rather than direct targeting
7 Cell cycle progression ↓ proliferation / ↑ arrest ↔ largely spared Phenotypic Cytostatic growth control Growth inhibition reflects impaired protein turnover and metabolic stress
8 Apoptosis / non-apoptotic death ↑ apoptosis or proteotoxic death ↔ protected Phenotypic Threshold-dependent cell death Cell death modality depends on copper availability and stress magnitude


Scientific Papers found: Click to Expand⟱
4913- DSF,    Anticancer effects of disulfiram: a systematic review of in vitro, animal, and human studies
- Review, Var, NA
Apoptosis↑, tumCV↑, eff↑, toxicity↓, antiNeop↑, ChemoSen↑, RadioS↑, OS↑, ROS↑, SOD↓, MMP1↓, eff↑, Half-Life↓,
4914- DSF,  immuno,    Disulfiram and cancer immunotherapy: Advanced nano-delivery systems and potential therapeutic strategies
- Review, Var, NA
AntiTum↑, eff↑, ALDH↓, Dose↝, RadioS↑, angioG↓, TumMeta↓, BioAv↝, ROS↑, DNAdam↑, P-gp↓, CSCs↓, EMT↓, Imm↑, SOD↓, MAPK↓, NF-kB↓, ChemoSen↑, eff↑, toxicity↝, BioAv↑, *Inflam↓, Sepsis↓,
4915- DSF,  Cu,    Disulfiram: A novel repurposed drug for cancer therapy
- Review, Var, NA
ROS↑, TumCD↑, NF-kB↓, CSCs↓, ChemoSen↑, RadioS↑, eff↑, selectivity↑, Proteasome?,
4916- DSF,  Cu,    The immunomodulatory function and antitumor effect of disulfiram: paving the way for novel cancer therapeutics
- Review, Var, NA
TumCP↓, TumCMig↓, TumCI↓, eff↑, Imm↑, ROS↑, NF-kB↓, chemoP↑, JNK↑, FOXO↑, Myc↑, TumCCA↑, Apoptosis↑, RadioS↑, PD-L1↑, eff↑, CSCs↓, Dose↝, Half-Life↑,
4917- DSF,  Chemo,  Cu,    Effect of Disulfiram and Copper Plus Chemotherapy vs Chemotherapy Alone on Survival in Patients With Recurrent Glioblastoma
- Trial, GBM, NA
OS∅, toxicity↑,
5006- DSF,  Cu,    Disulfiram targeting lymphoid malignant cell lines via ROS-JNK activation as well as Nrf2 and NF-kB pathway inhibition
- vitro+vivo, lymphoma, NA
TumCD↑, TumCP↑, Apoptosis↑, NRF2↓, ROS↑, p‑JNK↑, p65↓, eff↓, NF-kB↓,
5007- DSF,  Cu,    Nrf2/HO-1 Alleviates Disulfiram/Copper-Induced Ferroptosis in Oral Squamous Cell Carcinoma
- vitro+vivo, Oral, NA
AntiTum↑, TumCP↓, Ferroptosis↑, Iron↑, lipid-P↑, NRF2↓, HO-1↓,
5008- DSF,  Cu,    Overcoming the compensatory elevation of NRF2 renders hepatocellular carcinoma cells more vulnerable to disulfiram/copper-induced ferroptosis
- in-vitro, HCC, NA
selectivity↑, TumCD↑, TumCMig↓, TumCI↓, angioG↓, mtDam↑, Iron↑, lipid-P↑, Ferroptosis↑, NF-kB↑, p‑p62↑, Keap1↓, eff↑, eff↓, ChemoSen↑,
5009- DSF,  Cu,    Activation of Oxidative Stress and Down-Regulation of Nuclear Factor Erythroid 2-Related Factor May Be Responsible for Disulfiram/Copper Complex Induced Apoptosis in Lymphoid Malignancy Cell Lines
- vitro+vivo, lymphoma, NA
AntiTum↑, ROS↑, JNK↑, NRF2↓, eff↓, TumCD↑,
5010- DSF,  Cu,  Rad,    Disulfiram/Copper Combined with Irradiation Induces Immunogenic Cell Death in Melanoma
- in-vivo, Melanoma, B16-F10
Apoptosis↑, ICD↑, HMGB1↑, ATP↓, TumCG↓,
5011- DSF,  Cu,    Leveraging disulfiram to treat cancer: Mechanisms of action, delivery strategies, and treatment regimens
- Review, Var, NA
BioAv↓, eff↓, ChemoSen↑, RadioS↑,
5012- DSF,  Cu,    Advancing Cancer Therapy with Copper/Disulfiram Nanomedicines and Drug Delivery Systems
ROS↑, ALDH↓, TumCP↓, CSCs↓, angioG↓, TumMeta↓, DNAdam↑, Proteasome↓, SOD1↓, GSR↓, ox-GSSG↑, GSH/GSSG↓, MMP↓, Akt↓, cycD1/CCND1↓, NF-kB↓, CSCs↓, MAPK↓, angioG↓, DrugR↓, EMT↓, Vim↓, BioAv↑, eff↑,
5013- DSF,  Cu,  Z,    Disulfiram inhibits activating transcription factor/cyclic AMP-responsive element binding protein and human melanoma growth in a metal-dependent manner in vitro, in mice and in a patient with metastatic disease
- vitro+vivo, Melanoma, NA - Case Report, Melanoma, NA
P-gp↓, NF-kB↓, ChemoSen↑, angioG↓, TumCG↓, TumMeta↓, Remission↑, toxicity↓, ATF2↓, CREB↓, cycA1/CCNA1↓, TumCG↓, angioG↓, Dose↝, toxicity↝,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned ⓘ

DrugR↓, 1,  

Redox & Oxidative Stress ⓘ

Ferroptosis↑, 2,   GSH/GSSG↓, 1,   GSR↓, 1,   ox-GSSG↑, 1,   HO-1↓, 1,   ICD↑, 1,   Iron↑, 2,   Keap1↓, 1,   lipid-P↑, 2,   NRF2↓, 3,   ROS↑, 7,   SOD↓, 2,   SOD1↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

CREB↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 4,   ATF2↓, 1,   Ferroptosis↑, 2,   JNK↑, 2,   p‑JNK↑, 1,   MAPK↓, 2,   Myc↑, 1,   Proteasome?, 1,   Proteasome↓, 1,   TumCD↑, 4,  

Transcription & Epigenetics ⓘ

tumCV↑, 1,  

Autophagy & Lysosomes ⓘ

p‑p62↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,  

Cell Cycle & Senescence ⓘ

cycA1/CCNA1↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ALDH↓, 2,   CSCs↓, 5,   EMT↓, 2,   FOXO↑, 1,   TumCG↓, 3,  

Migration ⓘ

MMP1↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 3,   TumCP↑, 1,   TumMeta↓, 3,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 6,  

Barriers & Transport ⓘ

P-gp↓, 2,  

Immune & Inflammatory Signaling ⓘ

HMGB1↑, 1,   Imm↑, 2,   NF-kB↓, 6,   NF-kB↑, 1,   p65↓, 1,   PD-L1↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   BioAv↝, 1,   ChemoSen↑, 6,   Dose↝, 3,   eff↓, 4,   eff↑, 9,   Half-Life↓, 1,   Half-Life↑, 1,   RadioS↑, 5,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

Myc↑, 1,   PD-L1↑, 1,  

Functional Outcomes ⓘ

antiNeop↑, 1,   AntiTum↑, 3,   chemoP↑, 1,   OS↑, 1,   OS∅, 1,   Remission↑, 1,   toxicity↓, 2,   toxicity↑, 1,   toxicity↝, 2,  

Infection & Microbiome ⓘ

Sepsis↓, 1,  
Total Targets: 78

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  
Total Targets: 1

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:387  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

Home Page