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| Found in dried fruit rind of Garcinia Indica with anti-inflammatory, antioxidant, anticancer, and antibacterial properties Garcinia Cambogia Extract. "We conclude that patients who are T-cadherin-positive could especially benefit from a therapy with garcinol." 🔬1) NF-κB & AP-1 Suppression Garcinol inhibits NF-κB and AP-1 transcriptional activity in multiple cancer cell systems, reducing pro-inflammatory and pro-survival gene expression. 📚 2) Epigenetic Regulation Garcinol is one of the few natural products shown to inhibit p300/CBP histone acetyltransferases, shifting chromatin acetylation and influencing gene expression (differentiation, apoptosis, EMT). This is more specific than general “HDAC modulation.” 💀 3) Apoptosis Studies report modulation of the Bcl-2 family and increased caspase activity, but this is often downstream of transcription/epigenetic changes, not a direct redox trigger. 🧬 4) Cell Cycle & Proliferation Lower Cyclin D1, higher p21/p27, and G1/S arrest are common phenotypes. 🧭 5) Invasion & Angiogenesis Garcinol reduces MMP-2/9 and angiogenic markers in multiple tumor cell assays. Garcinol — a naturally occurring polyisoprenylated benzophenone and polycyclic polyprenylated acylphloroglucinol isolated principally from the dried fruit rind of Garcinia indica, commonly called kokum. It is an experimental phytochemical and pleiotropic epigenetic/signalling modulator, abbreviated GAR and also known as camboginol. Garcinol is best characterized as an inhibitor of lysine and histone acetyltransferases, particularly p300/CBP and PCAF/KAT2B, while also modulating NF-κB, STAT3, PI3K/AKT, inflammatory lipid mediators, apoptosis, and epithelial–mesenchymal plasticity. It is not an approved anticancer drug and should not be equated with whole Garcinia cambogia or hydroxycitric-acid supplements. Primary mechanisms (ranked):
Bioavailability / PK relevance: Garcinol is highly lipophilic and poorly water-soluble, making oral absorption and formulation important translational variables. Rat studies reported approximately 27–36% absolute oral bioavailability at oral doses of 22.5–45 mg/kg, with dose-dependent exposure and substantial tissue distribution. Human liver-microsome data suggest intermediate metabolic clearance, but no validated human cancer PK, therapeutic plasma range, or clinically established dose is available. Nanoparticles, phospholipid complexes, cyclodextrins, and other delivery systems may improve exposure, but remain preclinical. In-vitro vs systemic exposure relevance: Most anticancer experiments use approximately 5–50 µM garcinol, frequently around 10–25 µM. Whether these free concentrations are safely achievable in human tumors is unknown. Rat PK indicates systemic absorption, but it does not establish sustained human exposure comparable with common cell-culture concentrations. Results obtained at 25–100 µM should therefore be treated as high-concentration or mechanistic findings rather than directly clinically achievable effects. Clinical evidence status: Preclinical. Evidence consists primarily of biochemical assays, cancer-cell studies, organoid or stem-like-cell models, and rodent xenograft or genetically engineered tumor models. Combination activity has been reported with cisplatin, paclitaxel, gemcitabine, TRAIL, curcumin, and ionizing radiation, but no convincing randomized human oncology trial or established adjunctive anticancer use was identified. Garcinol is not approved by FDA, Health Canada, or EMA as a cancer therapy. Safety / deployment status: A standardized 40% garcinol preparation showed low acute and repeated-dose toxicity in rodent studies, including a reported 90-day no-observed-adverse-effect level of 100 mg/kg/day. These data do not establish long-term human safety, reproductive safety, drug-interaction risk, or safety during chemotherapy. Garcinol can inhibit platelet activation experimentally and modulates acetyltransferases and multiple drug-relevant signalling pathways, creating plausible interaction concerns. Hepatotoxicity reports involving multi-ingredient Garcinia cambogia supplements cannot be attributed specifically to purified garcinol. Garcinol Mechanistic Profile
P: 0–30 min R: 30 min–3 hr G: >3 hr |
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| TrxR is an enzyme that reduces Trx, allowing it to perform its reducing functions. It has been shown to have a role in cancer cell metabolism and survival. TrxR is overexpressed in various types of cancer, including breast, lung, colon, and prostate cancer. - Part of the thioredoxin system, which regulates reactive oxygen species (ROS). - TrxR is a major antioxidant systems that maintains the intracellular redox homeostasis. - Inhibition causes an increase in ROS. - TrxR is often upregulated in cancer cells to help manage increased oxidative stress, it is seen as a potential therapeutic target. Inhibiting TrxR may result in increased ROS in cancer cells, pushing them toward apoptosis. - TrxR is a selenoprotein—meaning it incorporates the trace element selenium in the form of the amino acid selenocysteine. TrxR inhibitors: -Piperlongumine -Withania somnifera (Ashwagandha) -Parthenolide -EGCG -Curcumin -Myricetin -Gambogic Acid |
| 7087- | GAR, | Garcinol as an Epigenetic Modulator: Mechanisms of Anti-Cancer Activity and Therapeutic Potential |
| - | 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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