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| Hyperoside is a chemical compound and a quercetin galactoside. It is found in various plants and has antibacterial, antifungal and UV blocking properties. Hyperoside is an active ingredient in plants, such as Hypericum monogynum in Hypericaceae, Crataegus pinnatifida in Rosaceae and Polygonum aviculare in Polygonaceae. Hyperoside is a natural flavonol glycoside in various plants, such as Crataegus pinnatifida Bge, Forsythia suspensa, and Cuscuta chinensis Lam. **-Note NRF2 up in normal cells and down in cancer cells** -not currently available as supplement, but it is in Hawthorn Extract. (Natural factors lists it as hyperoside equilvalents 6.6mg/300mg) Hyperoside — also known as hyperin and quercetin-3-O-β-D-galactoside, is a naturally occurring flavonol glycoside consisting of quercetin conjugated at the 3-position to β-D-galactose. It is found in numerous medicinal and dietary plants including species of Hypericum, Crataegus, Polygonum, and Rhododendron. It is classified as a plant-derived flavonoid/polyphenolic small molecule. Hyperoside has antioxidant and cytoprotective activity in many normal-cell models but can produce cancer-selective stress responses, apoptosis, autophagy, and ferroptosis depending on tumor type and concentration. Its aglycone is quercetin. Primary mechanisms (ranked):
Bioavailability / PK relevance: Oral bioavailability of intact hyperoside appears poor. Rat studies found very low systemic exposure after intragastric administration, with substantially greater exposure after parenteral administration. Hyperoside is relatively resistant to gastrointestinal hydrolysis compared with isoquercitrin, which may limit absorption of its quercetin aglycone. Distribution studies indicate preferential accumulation in kidney relative to several other organs. Nanoparticle and liposomal formulations have therefore been investigated to improve delivery and tumor or mitochondrial accumulation. Long-term high-dose exposure warrants caution because renal toxicity has been reported preclinically. In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 µM hyperoside, while some autophagy studies have used 0.5–2 mM. These concentrations, particularly the millimolar experiments, are unlikely to represent achievable concentrations of unchanged hyperoside following conventional oral administration. Consequently, direct translation of many in-vitro anticancer effects to oral supplementation is weak without an exposure-enhancing formulation. Clinical evidence status: Preclinical. Anticancer activity has been demonstrated in multiple cancer-cell systems and several mouse xenograft or chemically induced tumor models, including lung, breast, pancreatic, skin, liver, colorectal, esophageal, and hematologic malignancy models. There is currently no established human anticancer efficacy, approved oncology indication, or convincing interventional clinical evidence for purified hyperoside. FDA substance registration identifies hyperoside chemically but does not constitute drug approval. Hyperoside Cancer-Relevant Mechanisms
Hyperoside and Alzheimer's disease: Hyperoside has significant preclinical neuroprotective evidence in Alzheimer's disease models. Long-term administration in APP/PS1 transgenic mice improved spatial learning and memory and reduced amyloid plaque deposition, tau phosphorylation, activated microglia and astrocytes, neuroinflammation, and oxidative stress. Mechanistic evidence implicates suppression of BACE1 and GSK-3β, protection of the blood-brain barrier, inhibition of mitochondrial and caspase-dependent apoptosis, and broader antioxidant/anti-inflammatory effects. Evidence remains preclinical; clinical efficacy in human Alzheimer's disease has not been established. Hyperoside Alzheimer's-Relevant Mechanisms
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| Glutathione (GSH) is a thiol antioxidant that scavenges reactive oxygen species (ROS), resulting in the formation of oxidized glutathione (GSSG). Decreased amounts of GSH and a decreased GSH/GSSG ratio in tissues are biomarkers of oxidative stress. Glutathione is a powerful antioxidant found in every cell of the body, composed of three amino acids: cysteine, glutamine, and glycine. It plays a crucial role in protecting cells from oxidative stress, detoxifying harmful substances, and supporting the immune system. cancer cells can have elevated levels of glutathione, which may help them survive in the oxidative environment created by the immune response and chemotherapy. This can make cancer cells more resistant to treatment. While glutathione can be obtained from certain foods (like fruits, vegetables, and meats), its absorption from supplements is debated. Some people take N-acetylcysteine (NAC) or other precursors to boost glutathione levels, but the effects on cancer prevention or treatment are still being studied. Depleting glutathione (GSH) to raise reactive oxygen species (ROS) is a strategy that has been explored in cancer research and therapy. Many cancer cells have altered redox states and may rely on GSH to survive. Increasing ROS levels can induce stress in these cells, potentially leading to cell death. Certain drugs and compounds can deplete GSH levels. For example, agents like buthionine sulfoximine (BSO) inhibit the synthesis of GSH, leading to its depletion. Cancer cells tend to exhibit higher levels of intracellular GSH, possibly as an adaptive response to a higher metabolism and thus higher steady-state levels of reactive oxygen species (ROS). "...intracellular glutathione (GSH) exhibits an astounding antioxidant activity in scavenging reactive oxygen species (ROS)..." "Cancer cells have a high level of GSH compared to normal cells." "...cancer cells are affluent with high antioxidant levels, especially with GSH, whose appearance at an elevated concentration of ∼10 mM (10 times less in normal cells) detoxifies the cancer cells." "Therefore, GSH depletion can be assumed to be the key strategy to amplify the oxidative stress in cancer cells, enhancing the destruction of cancer cells by fruitful cancer therapy." The loss of GSH is broadly known to be directly related to the apoptosis progression. |
| 7567- | HYP, | Hyperoside: A review on its sources, biological activities, and molecular mechanisms |
| - | Review, | Var, | NA |
| 7560- | HYP, | Hyperoside: A Review of Its Structure, Synthesis, Pharmacology, Pharmacokinetics and Toxicity |
| - | Review, | Nor, | NA | - | Review, | AD, | 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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