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| 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):
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)
TSF legend: P: 0–30 min | R: 30 min–3 hr | G: >3 hr |
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| ATF2 (Activating Transcription Factor 2) -ATF2 is a member of the ATF/CREB (cyclic AMP response element‐binding protein) family of transcription factors. -It functions by binding to specific DNA sequences to regulate the transcription of a variety of target genes involved in cell proliferation, stress response, apoptosis, and differentiation. -ATF2 activity is regulated through phosphorylation by stress-activated protein kinases such as JNK, p38, and ERK, integrating signals from various cellular stressors. -Increased ATF2 activity in certain lung cancer subtypes has been linked with increased invasiveness and metastatic potential. |
| 5463- | AF, | Will Auranofin Become a Golden New Treatment Against COVID-19? |
| - | Review, | Covid, | NA |
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#:1295 State#:% Dir#:1
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