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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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| Type: tumour-suppressor miRNA |
| miR-200c studied particularly in the regulation of epithelial-to-mesenchymal transition (EMT) and cancer metastasis. miR-200c is a member of the miR-200 family, which includes miR-200a, miR-200b, and miR-200c. These miRNAs are known to play a crucial role in maintaining epithelial cell identity and suppressing EMT, a process by which epithelial cells acquire a mesenchymal phenotype and become more migratory and invasive. miR-200c has been shown to target several genes involved in EMT and cancer progression, including: ZEB1 and ZEB2, transcription factors that promote EMT and cancer metastasis. TGF-β, a cytokine that promotes EMT and cancer progression. Vimentin, a protein that is highly expressed in mesenchymal cells and is associated with cancer metastasis. The overexpression of miR-200c has been shown to inhibit EMT and cancer metastasis in various types of cancer, including breast, lung, and ovarian cancer. Conversely, the downregulation of miR-200c has been associated with cancer progression and poor prognosis. Downregulated in: lung, CRC, GC, pancreatic, HCC (associated with poor prognosis). |
| 7092- | GAR, | Garcinol and Its Role in Chronic Diseases |
| - | Review, | Var, | NA |
| 800- | GAR, | Garcinol Regulates EMT and Wnt Signaling Pathways In Vitro and In Vivo, Leading to Anticancer Activity against Breast Cancer Cells |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | BC, | BT549 | - | in-vivo, | NA, | NA |
| 816- | GAR, | Garcinol downregulates Notch1 signaling via modulating miR-200c and suppresses oncogenic properties of PANC-1 cancer stem-like cells |
| - | in-vitro, | PC, | PANC1 |
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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