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| Found in roots, leaves, nut-hulls, bark and wood of walnut trees. Juglone (5-hydroxy-1,4-naphthoquinone) Juglans nigra refers to the black walnut tree, which is one of the most well-known sources of juglone -Research has focused on the hulls (the green outer covering of the walnut) because they have the highest concentrations. -Fresh hulls can contain juglone levels in the range of approximately 1–5% of the dry weight -Juglone can redox cycle to generate reactive oxygen species (ROS). -Increasing Bax, decreasing Bcl‑2, caspase activation, and MMP depolarization. -Modulation of MAPK pathways (including ERK, JNK, and p38) -May inhibit NF‑κB signaling -Cause DNA damage or stress that, in turn, leads to p53 pathway activation— Pin1 Inhibition –Pin1, a peptidyl-prolyl cis/trans isomerase, is frequently overexpressed in cancer. -ic50 maybe 5-10uM -For matching 5uM, crude estimate is 5mg consumption of juglone required which might be 1.5 g of black walnut hull material Juglone — Juglone (5-hydroxy-1,4-naphthoquinone; JG) is a naturally occurring redox-active naphthoquinone found in plants of the Juglans genus, including black walnut (Juglans nigra), with particularly high concentrations reported in green walnut hulls. It is best classified as a natural small-molecule quinone and experimental anticancer agent rather than an established therapeutic drug. Its anticancer activity is strongly concentration-dependent and reflects electrophilic thiol reactivity, redox cycling, oxidative stress, mitochondrial injury, ferroptosis, apoptosis, and modulation of several oncogenic signaling pathways. Juglone is also widely used experimentally as a Pin1 inhibitor, although this designation should not imply high target selectivity because juglone can covalently modify protein sulfhydryl groups and affect transcription and other cellular proteins. Primary mechanisms (ranked):
Bioavailability / PK relevance: Free juglone has unfavorable drug-delivery characteristics, including hydrophobicity, high chemical reactivity, rapid disposition, and substantial renal exposure. In an animal intravenous PK study, free juglone had a plasma half-life of approximately 2 hours and showed prominent kidney localization; sterically stabilized liposomal delivery increased plasma half-life approximately 12-fold, improved tumor localization, and reduced renal toxicity. Robust human oral pharmacokinetic data are lacking. Consequently, dietary or walnut-hull intake cannot presently be converted reliably into a systemic micromolar juglone exposure. In-vitro vs systemic exposure relevance: Most direct anticancer studies use approximately low-to-tens-of-micromolar juglone, commonly around 5–20 µM. Whether these free-drug concentrations can be maintained safely in human tumors is not established. Recent quantitative work also demonstrates limited intracellular accumulation despite extracellular juglone exposure. Thus, common in-vitro concentrations should not be assumed to be achievable through oral walnut or black-walnut-hull consumption. Clinical evidence status: Preclinical. Juglone has substantial cell-culture evidence and multiple mouse/xenograft studies showing antitumor activity, including apoptosis, ferroptosis, anti-metastatic, and anti-angiogenic effects. There is no established anticancer dose, regulatory approval, or convincing human clinical efficacy evidence for juglone itself. Translation is limited by nonspecific electrophilic/redox chemistry, systemic toxicity risk, formulation and pharmacokinetic limitations, and the uncertain therapeutic window between cancer and normal tissues. Juglone Mechanistic Profile
P: 0–30 min R: 30 min–3 hr G: >3 hr > |
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| Type: Protein Coding gene |
| Beclin 1, an autophagy and haploinsufficient tumor-suppressor protein, is frequently monoallelically deleted in breast and ovarian cancers. However, the precise mechanisms by which Beclin 1 inhibits tumor growth remain largely unknown. A key biomarker of autophagy is Beclin-1. Beclin-1 stimulates LC3-I’s lipidation to produce LC3-II, which localizes to the autophagosome membrane to activate the development of autophagosomes. -BECN1 = the official gene symbol (human gene name) -Beclin-1 = the protein name encoded by the BECN1 gene BECN1 - Beclin 1 Abbreviation: BECN1, Beclin 1 Alternative Names: ATG6, VPS30 Type: Autophagy regulator / class III PI3K complex component Function: Beclin 1 is a core component of the VPS34/class III PI3K complex and promotes phosphatidylinositol-3-phosphate production required for autophagosome nucleation and membrane trafficking. Cancer: ↕ Context-dependent. Reduced BECN1 expression can contribute to tumor initiation and genomic instability, supporting a tumor-suppressive role in some tissues. However, established cancers can also exploit Beclin 1-dependent autophagy for survival under metabolic and therapeutic stress. |
| 5118- | JG, | Juglone induces apoptosis and autophagy via modulation of mitogen-activated protein kinase pathways in human hepatocellular carcinoma cells |
| - | in-vitro, | HCC, | HepG2 |
| 1917- | JG, | Inhibition of human leukemia cells growth by juglone is mediated via autophagy induction, endogenous ROS production, and inhibition of cell migration and invasion |
| - | in-vitro, | AML, | HL-60 |
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#:105 Target#:30 State#:% Dir#:2
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