Database Query Results : Auranofin, ,

AF, Auranofin: Click to Expand ⟱

Features:

Auranofin — an orally administered gold(I) coordination complex (gold–phosphine–thiolate “thiosugar” drug) originally approved as a disease-modifying antirheumatic drug (DMARD) for rheumatoid arthritis and widely studied for repurposing as a redox-targeted anticancer and anti-infective agent. It is a small-molecule metallodrug whose pharmacology is typically tracked via blood/plasma gold concentrations because intact auranofin is rapidly transformed and not reliably detected in blood. Standard abbreviation(s): AF (auranofin); primary target shorthand: TrxR/TxNRD (thioredoxin reductase).

Primary mechanisms (ranked):

Thioredoxin reductase (TXNRD1/TXNRD2; TrxR) inhibition by gold(I) → thioredoxin system suppression and loss of redox-buffering capacity
ROS and redox stress escalation (secondary to TrxR blockade; often NAC-reversible in models) → apoptosis and other regulated death programs
Mitochondrial dysfunction (Δψm collapse, bioenergetic stress) coupled to redox imbalance
Proteostasis stress (ER stress/UPR; proteasome involvement in selected contexts) → non-apoptotic death phenotypes (model-dependent)
Ferroptosis contribution in subsets of models (lipid peroxidation–dependent; context-dependent)
Radiosensitization / chemosensitization via impaired antioxidant recovery and enhanced oxidative injury (context-dependent)
Stress-response transcription (e.g., NRF2 activation as an adaptive resistance program in some settings; protective in normal cells)

Bioavailability / PK relevance: Oral absorption is incomplete; clinical PK is commonly described as ~25% of the gold content absorbed. Gold is highly protein-bound and exhibits prolonged retention/long terminal half-life, so effective exposure depends strongly on dose and dosing duration. Because “gold levels” are the main measurable surrogate, cross-study comparisons should specify matrix (whole blood vs plasma) and timing (steady-state vs short course).

In-vitro vs systemic exposure relevance: Many oncology cell studies use ~0.5–5 µM AF. Human short-course data at 6 mg/day for 7 days report plasma gold on the order of ~0.1–0.3 µg/mL (roughly sub-µM to ~1–1.5 µM range when expressed as gold equivalents), meaning lower in-vitro ranges can overlap clinically observed exposure surrogates, while higher µM regimens may exceed typical oral exposures unless higher doses/longer courses or formulation changes are used.

Clinical evidence status: Approved for rheumatoid arthritis (historical DMARD use) but oncology use remains investigational. Multiple early-phase repurposing trials exist across hematologic and solid tumors; several completed studies have limited publicly posted outcomes, and there is no established standard-of-care anticancer indication.

Pathways:
1.Thioredoxin Reductase (TrxR) Inhibition.
- Most widely recognized for potently inhibiting TrxR.
2.Induction of Reactive Oxygen Species (ROS) and Oxidative Stress.
3.MMP depolarization, release of cytochrome c
4.Endoplasmic Reticulum (ER) Stress and Unfolded Protein Response (UPR)
5.Inhibition of Pro-survival Pathways (e.g., NF-κB Signaling)

-ic50 for cancer typically 1-3uM, normal cell 5-10uM or higher.
-Several studies animal testing antitumor efficacy have used doses in the region of 5–8 mg/kg via intraperitoneal injection or oral administration.

-Auranofin’s anticancer activity is often linked to its inhibition of thioredoxin reductase, leading to increased oxidative stress.

Mechanistic axes for Auranofin (Cancer vs Normal)

Rank	Pathway / Axis	Cancer Cells	Normal Cells	TSF	Primary Effect	Notes / Interpretation
1	TXNRD1 TXNRD2 Thioredoxin system	↓ (primary)	↓ (primary)	P→R	Collapse of thioredoxin redox buffering	Core, proximal target of AF; downstream effects track with redox reserve and compensatory antioxidant capacity rather than tumor lineage alone.
2	ROS redox stress	↑ (often primary downstream)	↑ (dose-dependent)	P→R	Oxidative injury signaling and death pathway engagement	Frequently reversible with thiol antioxidants (e.g., NAC) in models, supporting causality; magnitude depends on baseline redox fragility.
3	Mitochondria bioenergetics	Δψm ↓, ATP stress ↑ (context-dependent)	Δψm ↓ (dose-dependent)	R	Energetic crisis and intrinsic death susceptibility	Often coupled to redox imbalance; can amplify apoptosis/regulated necrosis depending on cellular checkpoints.
4	Proteostasis ER stress UPR	↑ (model-dependent)	↔/↑ (high exposure only)	R→G	Protein-folding overload and non-apoptotic death phenotypes	Some reports implicate proteasome participation and paraptosis-like outcomes; not universal across tumor types.
5	NRF2 antioxidant response	↑ (adaptive; resistance role)	↑ (cytoprotective)	R→G	Transcriptional compensation to redox stress	NRF2 induction can blunt AF efficacy in tumors yet protect normal tissues; net effect is (context-dependent).
6	Ferroptosis lipid peroxidation	↑ (model-dependent)	↔/↑ (stress-prone contexts)	R→G	Regulated death component in subsets	Most consistent when AF-driven redox stress converges on lipid ROS handling; requires model-specific validation.
7	Radiosensitization chemosensitization	↑ sensitivity (context-dependent)	↑ toxicity risk (context-dependent)	R→G	Impaired antioxidant recovery increases treatment injury	Mechanistically coherent with TrxR blockade; best supported where oxidative damage markers and combination indices are shown.
8	Ca²⁺ stress coupling	↑/↔ (secondary)	↑/↔ (secondary)	R	Amplifies ER mitochondrial death signaling	Usually downstream of redox + organelle perturbation; include when Ca²⁺-dependent apoptosis/ER stress is explicitly demonstrated.
9	Glycolysis ATP production	↓ (context-dependent)	↔/↓ (high exposure only)	R	Metabolic stress that can reduce proliferative fitness	Reported in some models; may be secondary to mitochondrial/redox disruption rather than a primary binding target.
10	HIF-1α hypoxia programs	↔ (model-dependent)	↔	G	Context marker rather than core axis	Evaluate case-by-case; AF’s primary leverage is redox enzyme inhibition, with HIF effects emerging indirectly in some systems.
11	Clinical Translation Constraint	↔	↔	—	Exposure, tolerability, and selectivity limit window	Oral absorption is incomplete and gold is long-retained/protein-bound; many oncology studies rely on µM in-vitro dosing that may exceed typical oral exposure surrogates. Oncology trials exist but anticancer efficacy is not established as standard-of-care.

TSF legend: P: 0–30 min | R: 30 min–3 hr | G: >3 hr

Scientific Papers found: Click to Expand⟱

5462-

AF,

Repurposing Auranofin for Oncology and Beyond: A Brief Overview of Clinical Trials as Mono- and Combination Therapy

Review,

Var,

AntiTum↑, Over the last twenty years, AF has also been repurposed as an antitumor, antiviral, and antibacterial drug.
Bacteria↓,
TrxR↓, ability to inhibit thioredoxin reductase (TrxR) and disrupt redox homeostasis, leading to selective cytotoxicity in cancer cells.
ChemoSen↑, synergistic effects observed when AF is combined with chemotherapeutics, targeted therapies, or immune modulators.
Dose↝, Patients received AF orally twice daily on days 1–28. atients received AF orally, 6 mg in the morning and 6 mg in the evening.
ROS↑, AF induces oxidative stress and apoptosis in cancer cells by disrupting redox homeostasis, while sirolimus inhibits mTOR signaling.
Apoptosis↑,
mTOR↓,

5472-

AF,

Auranofin induces apoptosis and necrosis in HeLa cells via oxidative stress and glutathione depletion

in-vitro,

Cerv,

HeLa

TrxR↓, Auranofin (Au), an inhibitor of thioredoxin reductase, is a known anti‑cancer drug
AntiCan↑,
TumCG↓, Au inhibited the growth of HeLa cells with an IC50 of ~2 µM at 24 h.
Apoptosis↑, This agent induced apoptosis and necrosis, accompanied by the cleavage of poly (ADP‑ribose) polymerase and loss of mitochondrial membrane potential.
necrosis↑,
cl‑PARP↑,
MMP↓,
ROS↑, With respect to the levels of ROS and GSH, Au increased intracellular O2•- in the HeLa cells and induced GSH depletion.
GSH↓,
eff↓, The antioxidant, N‑acetyl cysteine, not only attenuated apoptosis and necrosis in the Au‑treated HeLa cells, but also decreased the levels of O2•- and GSH depletion in the cells.

5471-

AF,

Anti-Tumoral Treatment with Thioredoxin Reductase 1 Inhibitor Auranofin Fosters Regulatory T Cell and B16F10 Expansion in Mice

vitro+vivo,

Melanoma,

B16-F10

TrxR1↓, Auranofin, an FDA-approved antirheumatic drug and thioredoxin reductase 1 (TXNRD1) inhibitor, has demonstrated anti-tumoral properties
AntiTum↑,
ROS↑, TXNRD1 Inhibitors Elevated ROS Levels, Activate NRF2, and Kill B16F10 Cells In Vitro
NRF2↑,
TumCD↑,

5470-

AF,

Exploring a Therapeutic Gold Mine: The Antifungal Potential of the Gold-Based Antirheumatic Drug Auranofin

Review,

Var,

TrxR↓, mechanism of action of auranofin was correlated with thioredoxin reductase inhibition,
other↝, but other modes of action such as interference with mitochondrial protein import and NADH kinase were also described and discussed
IL6↑, Conversely, auranofin stimulated IL-6 and IL-8 secretion in monocytes,
IL8↑,
NK cell⇅, NK activation was only observed at low doses of auranofin, while high doses inhibited NK activity
COX2↓, suppression of pro-inflammatory factors such as COX-2 (cyclooxygenase-2), NOS (nitric oxide synthase), NF-κB (nuclear factor-κB), and TrxR, as well as on the activation of peroxyredoxin-1 and Nrf2 (nuclear factor erythroid 2-related factor 2) [19].
NOS2↓,
NRF2↑,
Prx↑,
Half-Life↑, plasma half-lives of 15–25 days [24]
Dose↝, To avoid frequently occurring diarrhea, oral doses of 3–6 mg per day, or below, should also be considered when repurposing auranofin for the treatment of other human diseases.
ROS↑, Imbalances in this system lead to the accumulation of cytotoxic ROS.
NF-kB↓, Auranofin can bind to IKK, which ultimately leads to NF-κB inhibition

5469-

AF,

Ligand supplementation restores the cancer therapy efficacy of the antirheumatic drug auranofin from serum inactivation

in-vitro,

CRC,

HCT116

eff↑, Synergistic effect of pantethine on auranofin
Half-Life↑, The gold ions can be maintained for a relatively long period in the blood (plasma half-lives of auranofin gold of 1.8 days in rats, 19.5 days in dogs, and 17 days in humans)37,71,72.

5468-

AF,

The gold complex auranofin: new perspectives for cancer therapy

Review,

Var,

TrxR↓, Auranofin mainly targets the anti-oxidative system catalyzed by thioredoxin reductase (TrxR), which protects the cell from oxidative stress and death in the cytoplasm and the mitochondria.
ROS↑, Inhibiting TrxR dysregulates the intracellular redox state causing increased intracellular reactive oxygen species levels, and stimulates cellular demise
eff↑, TrxR is over-expressed in many cancers as an adaptive mechanism for cancer cell proliferation, rendering it an attractive target for cancer therapy, and auranofin as a potential therapeutic agent for cancer.
Apoptosis↑, promotion of ASK-induced apoptosis, and blockage of cell growth, proliferation, and survival due to reduced AKT activity and NF-kB- and p53-mediated transcription.
TumCG↓,
TumCP↓,
Akt↓,
NF-kB↓,
DNAdam↑, DNA damage
eff↝, auranofin inhibits TrxR1 in a p53-independent manner
eff↓, Pre-treatment with NAC counteracted the cancer cell killing effects of auranofin,
PI3K↓, auranofin induces cytotoxicity in human pancreatic adenocarcinoma and non-small cell lung cancer via the inhibition of the PI3K/AKT/mTOR pathway
Akt↓,
mTOR↓,
Hif1a↓, auranofin inhibits the cancer cell response to hypoxia, demonstrated by a decrease in HIF-1 𝛼 expression and VEGF secretion upon auranofin treatment under hypoxic conditions
VEGF↓,
Casp3↑, auranofin was shown to induce caspase-3-mediated apoptosis in human ovarian carcinoma SKOV-3 cells
CSCs↓,
ATP↓, it was found that auranofin inhibits ABCG2 function by depleting cellular ATP via inhibition of glycolysis [96]
Glycolysis↓,
eff↑, auranofin synergizes with another Trx1 inhibitor, piperlongumine, in killing gastric cancer cells in association with ROS-mediated ER stress response and mitochondrial dysfunction.
eff↑, when the gold complex is combined with either selenite or tellurite [104]
MMP↓, Increased ROS induced by AUR causes decreased membrane potential in the mitochondrial membrane, resulting in a decrease in anti-apoptotic proteins, caspase-dependent cell death, and translocation of apoptosis-inducing factor (AIF)
AIF↑,
toxicity↓, Auranofin is considered safe for human use in treating rheumatoid arthritis; thus, this gold derivative can reach the clinic for other diseases relatively quickly and at a low cost

5467-

AF,

Auranofin Inhibition of Thioredoxin Reductase Sensitizes Lung Neuroendocrine Tumor Cells (NETs) and Small Cell Lung Cancer (SCLC) Cells to Sorafenib as well as Inhibiting SCLC Xenograft Growth

in-vitro,

Lung,

DMS53 human small cell lung cancer cells

TrxR↓, AF treatment decreased TrxR activity and clonogenic survival in small cell lung cancer (SCLC) cell lines (DMS273 and DMS53) as well as the lung atypical (neuroendocrine tumor) NET cell line H727.
eff↑, AF treatment also significantly sensitized DMS273 and H727 cell lines in vitro to sorafenib, a multi-kinase inhibitor that was shown to decrease intracellular glutathione.
Dose↝, AF was administered intraperitoneally at 2 mg/kg or 4 mg/kg (IP) once (QD) or twice daily (BID) for 1 to 5 days in mice with DMS273 xenografts.
OS↑, When this daily AF treatment was extended for 14 days a significant prolongation of median survival from 19 to 23 days (p=0.04, N=30 controls, 28 AF) was observed without causing changes in animal bodyweight, CBCs, bone marrow toxicity, blood urea ni
eff↑, We also demonstrated that suppressing TrxR with AF can sensitize breast cancer stem cells to ROS induced stem cell transitions associated with EMT and cytotoxicity associated with 2-deoxyglucose treatment.

5466-

AF,

Auranofin Inhibition of Thioredoxin Reductase in a Preclinical Model of Small Cell Lung Cancer

in-vivo,

Lung,

AF was administered intraperitoneal, daily or twice daily for 1 to 5 days in mice bearing DMS273 xenografts.

TrxR↓, TrxR is viable target in clinical trials using the anti-rheumatic drug, auranofin (AF).
Dose↝, 4 mg/kg once daily resulting in 18 μM gold in the plasma and 50% inhibition of TrxR activity in DMS273 SCLC tumors.
RadioS↑, effective inhibitor of TrxR and suggest that AF could be used as an adjuvant in radio-chemotherapy protocols to enhance therapeutic efficacy.
ChemoSen↑,
ROS↑, We also demonstrated the suppressing TrxR with AF can sensitize breast cancer stem cells to ROS induced differentiation and cytotoxicity.16
Diff↑,
toxicity↓, These results suggest that this dosing regimen is nontoxic to kidneys, liver, and bone marrow as well as demonstrating a trend toward a survival advantage in tumor bearing animals.

5465-

AF,

The Thioredoxin Reductase Inhibitor Auranofin Suppresses Pulmonary Metastasis of Osteosarcoma, But Not Local Progression

in-vitro,

OS,

TrxR↓, Auranofin (AUR), a thioredoxin reductase (TXNRD) inhibitor, shows anticancer activity against several cancers.
ROS↑, AUR induced apoptosis of OS cells via the oxidative stress-MAPK-Caspase 3 pathway, and suppressed the migration of OS cells.
TumCMig↓,

5464-

AF,

Inhibition of Thioredoxin-Reductase by Auranofin as a Pro-Oxidant Anticancer Strategy for Glioblastoma: In Vitro and In Vivo Studies

vitro+vivo,

GBM,

TrxR↓, Gold derivatives are irreversible inhibitors of TrxR. Among them, auranofin (AF), a selective TrxR inhibitor, has proven its effectiveness as a drug for the treatment of rheumatoid arthritis
BioAv↓, further clinical application of AF could be challenging due to the low solubility and insufficient delivery to glioblastoma.
ROS↑, The inhibition of TrxR1, which leads to increased ROS levels, is currently recognized as the primary mechanism of AF cytotoxicity [106]. In vitro studies have also shown that AF inhibits other thioredoxin reductases, such as TrxR2 and TrxR3
eff↝, The literature indicates that not all cancer tumors exhibit the same level of TrxR expression, affecting their sensitivity to AF.
TET1?, AF was shown to inhibit TET1 in T-ALL models
BioAv↑, Encapsulating AF into nanoparticles or combining it with other pharmaceutical excipients can minimize its potential adverse effects, preserve its interaction with serum proteins, and result in greater stability.

5463-

AF,

Will Auranofin Become a Golden New Treatment Against COVID-19?

Review,

Covid,

IL6↓, This gold(I) compound has anti-inflammatory properties because it reduces IL-6 expression via inhibition of the NF-κB-IL-6-STAT3 signaling pathway.
NF-kB↓,
ATF2↓,
TrxR↓, by inhibiting redox enzymes such as thioredoxin reductase, auranofin increases cellular oxidative stress and promotes apoptosis.
ROS↑,
Apoptosis↑,
IL6↓, Recently, it was reported that auranofin reduced by 95% SARS-CoV-2 RNA in infected human cells in vitro and decreased SARS-CoV-2-induced cytokine expression, including IL-6.
Dose↑, After 14 days of treatment with 21 mg/day auranofin, plasma gold concentration reached 1.18 µM to 2.21 µM ‘auranofin equivalent’

5461-

AF,

Dual inhibition of thioredoxin reductase and proteasome is required for auranofin-induced paraptosis in breast cancer cells

in-vitro,

BC,

MDA-MB-231

in-vitro,

Nor,

MCF10

Paraptosis↑, We show here that 4~5 µM AF induces paraptosis, a non-apoptotic cell death mode characterized by dilation of the endoplasmic reticulum (ER) and mitochondria, in breast cancer cells.
ER Stress↑,
TrxR↓, covalent inhibition of thioredoxin reductase (TrxR)
selectivity↑, subtoxic doses of AF and Bz induced paraptosis selectively in breast cancer cells, sparing non-transformed MCF10A cells
toxicity↝, whereas 4~5 μM AF killed both cancer and MCF10A cells
ROS↑, We found that treatment with 5 μM AF very weakly and transiently increased ROS levels at 2~4 h and then again at 24 h
mt-TrxR1↓, AF inhibits cytosolic and mitochondrial TrxR (TrxR1 and TrxR2), two selenoenzymes for the Trx pathway [3]
mt-TrxR2↓,

5460-

AF,

Auranofin radiosensitizes tumor cells through targeting thioredoxin reductase and resulting overproduction of reactive oxygen species

vitro+vivo,

Var,

4T1

RadioS↑, AF at 3–10 μM is a potent radiosensitizer in vitro
ROS↑, . The first one is linked to an oxidative stress, as scavenging of reactive oxygen species (ROS)
eff↓, N-acetyl cysteine counteracted radiosensitization. (NAC)
mt-OCR↓, We also observed a decrease in mitochondrial oxygen consumption with spared oxygen acting as a radiosensitizer under hypoxic conditions.
DNAdam↑, Overall, radiosensitization was accompanied by ROS overproduction, mitochondrial dysfunction, DNA damage and apoptosis
Apoptosis↑,
TrxR↓, targeting thioredoxin reductase (TrxR)
eff↑, a simultaneous disruption of the thioredoxin and glutathione systems by the combination of AF and buthionine sulfoximine was shown to significantly improve tumor radioresponse.

5459-

AF,

Auranofin Induces Lethality Driven by Reactive Oxygen Species in High-Grade Serous Ovarian Cancer Cells

in-vitro,

Ovarian,

ROS↑, AF primarily functions as a pro-oxidant by inhibiting thioredoxin reductase (TrxR), an antioxidant enzyme overexpressed in ovarian cancer.
TrxR↓, The primary mechanism of action of auranofin is to act as a pro-oxidative agent, increasing the production of reactive oxygen species (ROS) as a consequence of inhibiting the thioredoxin reductase (TrxR) anti-oxidant system
MMP↓, triggers the depolarization of the mitochondrial membrane, and kills HGSOC cells by inducing apoptosis.
Apoptosis↑,
eff↓, Notably, AF-induced cell death was abrogated by the ROS-scavenger N-acetyl cysteine (NAC).
Casp3↑, lethality of AF was associated with the activation of caspases-3/7 and the generation of DNA damage
Casp7↑,
DNAdam↑,
eff↑, Finally, when AF and L-BSO were combined, we observed synergistic lethality against HGSOC cells, which was mediated by a further increase in ROS and a decrease in the levels of the antioxidant GSH.
GSH↓,
angioG↓, Additionally, auranofin has been shown to inhibit angiogenesis
ChemoSen↑, In this study, we identified the mechanisms of cytotoxicity induced by auranofin in HGSOC cells that have different clinical sensitivities to platinum.
cl‑PARP↑, the cleavage of poly-ADP ribose polymerase (PARP), and the polyubiquitination of proteins
eff↑, synergistic lethal interaction between auranofin and a second pro-oxidant agent, the glutathione (GSH) inhibitor, L-buthionine sulfoximine (L-BSO);

5458-

AF,

Auranofin reveals therapeutic anticancer potential by triggering distinct molecular cell death mechanisms and innate immunity in mutant p53 non-small cell lung cancer

in-vitro,

NSCLC,

TrxR↓, Auranofin (AF) is an FDA-approved antirheumatic drug with anticancer properties that acts as a thioredoxin reductase 1 (TrxR) inhibitor.
AntiCan↓,
GPx4↓, Although functionally AF appeared a potent inhibitor of GPX4 in all NCI–H1299 cell lines, the induction of lipid peroxidation and consequently ferroptosis was limited to the p53 R273H expressing cells.
DNAdam↑, AF mainly induced large-scale DNA damage and replication stress, leading to the induction of apoptotic cell death rather than ferroptosis.
toxicity↓, AF is an orally available, lipophilic, organogold compound with a well-known safety profile that was approved by the U.S. Food and Drug Administration (FDA) for the treatment of rheumatoid arthritis (RA).
eff↝, AF represents a potential novel therapeutic strategy to efficiently kill mutant p53 NSCLC tumor cells through distinct immunogenic cell death pathways.

5457-

AF,

Clinical pharmacokinetics of oral and injectable gold compounds

Human,

Nor,

*BioAv↝, intramuscularly administered gold is greater than 95% bioavailable, whereas only 20 to 30% of an orally administered dose of auranofin is absorbed.
*Dose↝, 50mg intramuscular injection of GST, serum gold concentrations rise sharply, peaking between 4 and 8 mg/L in approximately 2 hours and declining to an average of 3 mg/L by 7 days.
*Half-Life↑, Both compounds are retained within the body for prolonged periods.
*BioAv↝, In human subjects, parenterally administered gold is widely distributed among bodily tissues, showing a predilection for tissues of the reticuloendothelial system as well as the kidney and adrenal cortex.
*other↝, auranofin but animal studies have shown comparatively less affinity for the liver, kidney and spleen.

5456-

AF,

Phase I Clinical Trial Results of Auranofin, a Novel Antiparasitic Agent

Trial,

Nor,

*Dose?, Subjects received orally 6 mg (p.o.) of auranofin daily, the recommended dose for rheumatoid arthritis, for 7 days and were followed for 126 days.
*Half-Life↝, The mean gold maximum concentration in plasma (Cmax) at day 7 was 0.312 μg/ml and the half-life (t1/2) 35 days, so steady-state blood levels would not be reached in short-term therapy.
*Dose↑, The highest concentration of gold, 13 μM (auranofin equivalent), or more than 25× the 50% inhibitory concentration (IC50) for E. histolytica and 4× that for Giardia, was in feces at 7 days.
*toxicity↝, Long-term (months to years) auranofin therapy was linked to side effects, including diarrhea (40% of subjects), skin rashes (2% to 5%), hematologic abnormalities (rare), and proteinuria (5%)
*Bacteria↓, Higher doses of auranofin will clearly be required for some infections.
*Dose↑, The FDA has approved clinical trials using auranofin at up to 21 mg/day for treatment of relapsed chronic lymphocytic leukemia after daily doses of 9 and 12 mg for at least 28 days were well tolerated

5455-

AF,

Ridaura

Study,

PSA,

Dose↝, 6mg dose(equivalent to 1.74mg of gold) radioactive
Half-Life↝, plasma terminal half-life was 17days

1900-

AF,

Potential Anticancer Activity of Auranofin

Review,

Var,

TrxR↓, Auranofin inhibits the activity of thioredoxin reductase (TrxR
ROS↑, TrxR inhibition leads to an increase in cellular oxidative stress and induces apoptosis
Apoptosis↓,
TumCP↓, TrxR1 knockdown also inhibits cancer cell proliferation and DNA replication
eff↑, cytotoxicity of cisplatin is increased in cells expressing high levels of TrxR1 compared with cells expressing low levels

2951-

PL,

AF,

Synergistic Dual Targeting of Thioredoxin and Glutathione Systems Irrespective of p53 in Glioblastoma Stem Cells

in-vitro,

GBM,

U87MG

GSH↓, natural product piperlongumine (PPL) inhibit the GSH system.
eff↑, subsequent efficacy of PLL in combination with Au within a nanomolar range in GSCs. Auranofin (Au), a known TrxR1 inhibitor
GSTP1/GSTπ↓, PPL is a natural alkaloid found in the plant Piper longum Linn that directly inhibits GSTP-1 and exhibits anti-cancer properties

1459-

SFN,

AF,

Auranofin Enhances Sulforaphane-Mediated Apoptosis in Hepatocellular Carcinoma Hep3B Cells through Inactivation of the PI3K/Akt Signaling Pathway

in-vitro,

Liver,

Hep3B

 auranofin (0.5, 1, 1.5, and 2 μM) or sulforaphane (2.5, 5, 7.5, and 10 μM)

in-vitro,

Liver,

HepG2

eff↑, sulforaphane significantly enhanced auranofin-induced apoptosis by inhibiting TrxR activity and cell proliferation compared to either single treatment
TumCCA↑, Sub-G1 cells
Apoptosis↑,
MMP↓,
BAX↑,
cl‑PARP↑,
Casp3↑,
Casp8↑,
Casp9↑,
ROS↑, combined treatment induced excessive generation of reactive oxygen species (ROS)
eff↓, treatment with N-acetyl-L-cysteine, a ROS scavenger, reduced combined treatment-induced ROS production and apoptosis.
PI3K↓,
Akt↓,
TrxR↓, treatment with either sulforaphane or auranofin alone at low concentrations weakly inhibit TrxR activity Combined treatment significantly reduced TrxR activity and cell viability
BAX↑,
Bcl-2∅,

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 21

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 72

Pathway results for Effect on Normal Cells:

Transcription & Epigenetics ⓘ

other↝, 1,

Drug Metabolism & Resistance ⓘ

BioAv↝, 2, Dose?, 1, Dose↑, 2, Dose↝, 1, Half-Life↑, 1, Half-Life↝, 1,

Functional Outcomes ⓘ

toxicity↝, 1,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 9

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#:273  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Database Query Results : Auranofin, ,

Mechanistic axes for Auranofin (Cancer vs Normal)

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Transcription & Epigenetics ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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