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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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| Cancer Stem Cells Phytochemicals (natural plant-derived compounds) that may affect CSCs: Curcumin — suppresses self-renewal and pathways (Wnt/Notch/Hedgehog). Resveratrol — shown to reduce CSC populations and sphere formation in multiple models. Sulforaphane (from broccoli sprouts) — reported to inhibit CSC properties and pathways; active in vitro and in vivo. EGCG (epigallocatechin-3-gallate, green tea) — reduces CSC markers and sphere formation in several cancer types. Quercetin — reported to inhibit CSC proliferation, self-renewal and invasiveness (breast, endometrial, others). Berberine — shown to suppress CSC “stemness” and reduce tumorigenic properties in multiple models. Genistein (soy isoflavone) — decreases CSC markers, sphere formation and stemness signaling in prostate/breast/other models. Honokiol (Magnolia bark) — shown to eliminate or suppress CSC-like populations in oral, colon, glioma models. Luteolin — inhibits stemness/EMT and reduces CSC markers and self-renewal in breast, prostate and other models. Withaferin A (from Withania somnifera / ashwagandha) — multiple preclinical reports show WA targets CSCs and reduces tumor growth/metastasis in models. Circadian disruption in cancer and regulation of cancer stem cells by circadian clock genes: An updated review Potential Role of the Circadian Clock in the Regulation of Cancer Stem Cells and Cancer Therapy Can we utilise the circadian clock to target cancer stem cells? |
| 5468- | AF, | The gold complex auranofin: new perspectives for cancer therapy |
| - | Review, | Var, | 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
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