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| Isovitexin - Apigenin-6-C-Glucoside Alternative Names: Apigenin-6-C-glucoside, apigenin-6-C-β-D-glucopyranoside Type: Flavone C-glycoside / apigenin derivative Function: Isovitexin is a naturally occurring C-glycosylated flavone and positional isomer of vitexin, with glucose attached to apigenin at the C-6 position. It exhibits antioxidant, anti-inflammatory, metabolic, neuroprotective, and antiproliferative activities and can influence NF-κB, Nrf2, MAPK, PI3K/AKT, AMPK, apoptotic, and oxidative-stress signaling. -similar to VitexinIsovitexin — Isovitexin (IVT; ISV; IVX), also known as apigenin-6-C-glucoside or 6-C-β-D-glucopyranosylapigenin, is a naturally occurring C-glycosylated flavone and positional isomer of vitexin, in which glucose is attached to apigenin at carbon 6 rather than carbon 8. It occurs in food and medicinal plants including mung bean, rice, passionflower, and other botanical sources. It is formally classified as a flavone C-glycoside / apigenin derivative. Compared with vitexin, isovitexin has a smaller but distinct experimental literature and should be maintained as a separate compound. Anticancer activity remains preclinical. Primary mechanisms (ranked):
Bioavailability / PK relevance: Oral exposure is a significant translational limitation. C-glycosylation gives isovitexin greater chemical stability than many O-glycosides, but direct intestinal absorption is limited and substantial material reaches the intestine for microbial metabolism. Rat studies demonstrate absorption and broad tissue distribution after oral plant-extract administration, while intravenous isovitexin has a plasma half-life of approximately 1 hour and distributes particularly to kidney, intestine, and liver. Human isovitexin-specific PK data are not established. In-vitro vs systemic exposure relevance: Many mechanistic experiments use micromolar concentrations that may be difficult to reproduce as circulating unchanged isovitexin after ordinary dietary or oral exposure. Consequently, high-concentration cell-culture findings should not be interpreted as demonstrating clinically achievable anticancer activity. Intestinal exposure and metabolites may be more pharmacologically relevant after oral administration. Clinical evidence status: Preclinical. Anticancer evidence consists primarily of cell studies and rodent/xenograft experiments. No established human anticancer efficacy, randomized clinical trial evidence, or approved oncology indication was identified. Isovitexin has an FDA substance identifier but this does not constitute drug approval. Long-term human safety, therapeutic dosing, drug interactions, and cancer-specific pharmacokinetics remain insufficiently defined. Mechanistic Profile
Alzheimer's disease relevance: Isovitexin has meaningful but entirely preclinical AD relevance. Direct evidence includes inhibition of AChE and BChE in biochemical assays, protection against Aβ-induced neuronal toxicity, and improvement of cognition, Aβ burden, neuroinflammation, and autophagic dysfunction in an STZ-induced mouse model. The latter study links benefit to miR-107-mediated suppression of PI3K/AKT/mTOR signaling. These findings justify retaining AD as a disease category, but they do not establish clinical efficacy. Primary mechanisms (ranked):
Clinical evidence status: Preclinical only. No human Alzheimer's disease efficacy data or validated therapeutic dosing were identified. Alzheimer's Disease Mechanisms
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| Source: TCGA |
| Type: Antiapoptotic |
| Nrf2 is responsible for regulating an extensive panel of antioxidant enzymes involved in the detoxification and elimination of oxidative stress. Thought of as "Master Regulator" of antioxidant response. -One way to estimate Nrf2 induction is through the expression of NQO1. NQO1, the most potent inducer: SFN 0.2 μM, quercetin (2.5 μM), curcumin (2.7 μM), Silymarin (3.6 μM), tamoxifen (5.9 μM), genistein (6.2 μM ), beta-carotene (7.2μM), lutein (17 μM), resveratrol (21 μM), indol-3-carbinol (50 μM), chlorophyll (250 μM), alpha-cryptoxanthin (1.8 mM), and zeaxanthin (2.2 mM) 1. Raising Nrf2 enhances the cell's antioxidant defenses and ↓ROS. This strategy is used to decrease chemo-radio side effects. 2. Downregulating Nrf2 lowers antioxidant defenses and ↑ROS. In cancer cells this leads to DNA damage, and cell death. 3. However there are some cases where increasing Nrf2 paradoxically causes an increase in ROS (cancer cells). Such as cases of Mitochondial overload, signal crosstalk, reductive stress -In some cases, Nrf2 is overexpressed in cancer cells, which can lead to the activation of genes involved in cell proliferation, angiogenesis, and metastasis. This can contribute to the development of resistance to chemotherapy and targeted therapies. -Increased Nrf2 expression: Lung, Breast, Colorectal, Prostrate. Decreased Nrf2 expression: Skine, Liver, Pancreatic. -Nrf2 is a cytoprotective transcription factor which demonstrated both a negative effect as well as a positive effect on cancer - "promotes Nrf2 translocation from the cytoplasm to the nucleus," means facilitates the movement of Nrf2 into the nucleus, thereby enhancing the cell's antioxidant and cytoprotective responses. -Major regulator of Nrf2 activity in cells is the cytosolic inhibitor Keap1. Nrf2 Inhibitors and Activators Nrf2 Inhibitors: Brusatol, Luteolin, Trigonelline, VitC, Retinoic acid, Chrysin Nrf2 Activators: SFN, OPZ EGCG, Resveratrol, DATS, CUR, CDDO, Api - potent Nrf2 inducers from plants include sulforaphane, curcumin, EGCG, resveratrol, caffeic acid phenethyl ester, wasabi, cafestol and kahweol (coffee), cinnamon, ginger, garlic, lycopene, rosemany Nrf2 plays dual roles in that it can protect normal tissues against oxidative damage and can act as an oncogenic protein in tumor tissue. – In healthy tissues, NRF2 activation helps protect cells from oxidative damage and maintains cellular homeostasis. – In many cancers, constitutive activation of NRF2 (often through mutations in NRF2 itself or loss-of-function mutations in KEAP1) leads to an enhanced antioxidant capacity. – This upregulation can promote tumor cell survival by enabling cancer cells to thrive under oxidative stress, resist chemotherapeutic agents, and sustain metabolic reprogramming. – Elevated NRF2 levels have been implicated in promoting tumor growth, metastasis, and resistance to therapy in various malignancies. – High or sustained NRF2 activity is frequently associated with aggressive tumor phenotypes, poorer prognosis, and decreased overall survival in several cancer types. – While its activation is essential for protecting normal cells from oxidative stress, aberrant or sustained NRF2 activation in tumor cells can lead to enhanced survival, therapeutic resistance, and tumor progression. NRF2 inhibitors: (to decrease antioxidant defenses and increase cell death from ROS). -Brusatol: most cited natural inhibitors of Nrf2. -Luteolin: luteolin can reduce Nrf2 activity in specific cancer models and may enhance cell sensitivity to chemotherapy. However, luteolin is also known as an antioxidant, and its influence on Nrf2 can sometimes be context dependent. -Apigenin: certain studies to down‑regulate Nrf2 in cancer cells: Dose and context dependent . -Oridonin: -Wogonin: although its effects might be cell‑ and dose‑specific. - Withaferin A |
| 7911- | IVT, | Isovitexin Depresses Osteoarthritis Progression via the Nrf2/NF-κB Pathway: An in vitro Study |
| - | in-vitro, | Arthritis, | NA |
| 7904- | IVT, | Isovitexin alleviates myocardial oxidative stress injury in diabetic mice by enhancing myocardial SIRT3 expression and reducing oxidative stress |
| - | in-vivo, | Nor, | NA |
| 7897- | IVT, | VT, | Vitexin and isovitexin delayed ageing and enhanced stress-resistance through the activation of the SKN-1/Nrf2 signaling pathway |
| - | in-vitro, | Nor, | NA |
| 7890- | IVT, | Isovitexin protects against cisplatin-induced kidney injury in mice through inhibiting inflammatory and oxidative responses |
| - | in-vivo, | Nor, | NA |
| 7888- | IVT, | Isovitexin Exerts Anti-Inflammatory and Anti-Oxidant Activities on Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting MAPK and NF-κB and Activating HO-1/Nrf2 Pathways |
| - | vitro+vivo, | Nor, | NA |
| 7887- | VT, | IVT, | Dietary Flavonoids Vitexin and Isovitexin: New Insights into Their Functional Roles in Human Health and Disease Prevention |
| - | Review, | AD, | NA | - | 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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