Compound Monograph
Astragalin
Astragalin is kaempferol-3-O-glucoside — a widespread dietary flavonol glycoside (persimmon leaf, green tea, nettle and many plants). No human trial of the isolate exists; its evidence is a scattered preclinical set (anti-allergic airway, Nrf2 antioxidant, some neuroprotection), and much of its activity is really that of kaempferol, to which it is hydrolyzed in the gut. Unrelated to Astragalus.
Sources · 8
Where Does It Come From?
Astragalin is a naturally occurring flavonol glycoside (kaempferol-3-o-glucoside), found in Chanca Piedra, Stinging Nettle, Hops and 5 other sources. It is well tolerated orally (low toxicity).
Principal source Chanca Piedra Phyllanthus niruri Herb monograph → 
Source Arnica Arnica montana Herb monograph → 
Source Hops Humulus lupulus Herb monograph → 
Source Linden Flower Tilia spp. Herb monograph → 
Source Stinging Nettle Urtica dioica Herb monograph → 
Source Tea Camellia sinensis Herb monograph → Concentration
Content by Source
Concentrations not reported. No percent-dry-weight or mg/g figures have been published for this compound in its source plants.
Astragalin at a Glance
Astragalin is kaempferol-3-O-glucoside — a widespread dietary flavonol glycoside found in persimmon leaf, green tea, nettle and many other plants.
Like most flavonol glycosides it functions largely as a delivery form for its aglycone, kaempferol, with the attached sugar governing absorption. Its own evidence is a scattered preclinical set covering anti-allergic airway effects and Nrf2 antioxidant signalling; no human trial of the isolate exists.
What It's Used For
Astragalin is kaempferol-3-O-glucoside, a widespread dietary flavonol glycoside — cross-link its aglycone kaempferol and the analogous glycoside-prodrug rutin. Two framing points. First, despite the name it is unrelated to Astragalus and its saponins (astragaloside IV) — the name is botanical, from the genus where it was first found, not chemical. Second, much of its reported activity is really kaempferol’s, since the glucoside is hydrolyzed to the aglycone in the gut. Its own evidence is a scattered, single-lab preclinical set — the most consistent isolate signal being anti-inflammatory/anti-allergic — with no human trials.
Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. No human isolate data, so scores stay low by design.
Isolated astragalin reduced airway inflammation, eosinophil/eotaxin-1 induction and epithelial apoptosis in ovalbumin-challenged mice — acting through NF-κB restraint and oxidative-stress-responsive MAPK modulation 1,
Gap: all rodent/cell, with no human data, and the allergic-airway benefit shown only prophylactically in a single model system 1,
Astragalin promoted Nrf2 nuclear translocation and raised antioxidant defenses, reducing testicular ferroptosis 6Reference 6Astragalin alleviates oligoasthenospermia via promoting nuclear translocation of Nrf2 and reducing ferroptosis of the testisView study → and cisplatin-induced renal oxidative injury 5Reference 5Pharmacotherapeutic potentials of astragalin against cisplatin-induced renal toxicity via regulating the Nrf2/Keap1 pathwayView study →.
Gap: narrow organ-protection models, and the effect is the generic flavonol antioxidant/Nrf2 response rather than distinctively astragalin 5,
Astragalin reduced neuroinflammation and oxidative stress in an AlCl₃/D-galactose aging model 4Reference 4Astragalin attenuates AlCl₃/D-galactose-induced aging-like disorders by inhibiting oxidative stress and neuroinflammationView study →, and modulated astrocyte autophagy/apoptosis (Fas/FasL–VDAC1) in an Alzheimer’s mouse model 3Reference 3AnimalAstragalin activates autophagy and inhibits apoptosis of astrocytes in AD mice via downregulating the Fas/FasL–VDAC1 pathwayView study →.
Gap: a small, mechanistically heterogeneous preclinical set with no cross-lab replication, and poor CNS delivery expected for a glucoside 3,
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| NF-κB signaling | suppressed → ↓ cytokines/eotaxin-1 | anti-inflammatoryanti-allergic airway |
| MAPK cascade (oxidative-stress-responsive) | modulated → ↓ epithelial apoptosis | allergic airway |
| Nrf2 / Keap1 axis | Nrf2 translocation → ↑ antioxidant/anti-ferroptotic defense | antioxidantrenal/gonadal cytoprotection |
| Autophagy / apoptosis (Fas–FasL–VDAC1) | pro-autophagic, anti-apoptotic in astrocytes | neuroprotection (AD model) |
Only pathways with direct astragalin-isolate support are listed; the α-glucosidase/anti-AGE activity is class-level only 8Reference 8Analysis of the therapeutic potential of astragalin: insights into target interactions and mechanismsView study →.
Pharmacokinetics
There is no dedicated human pharmacokinetic study of the isolate. As a flavonol 3-O-glucoside, astragalin behaves like its class: modest oral absorption of the intact glycoside, with substantial gut-microbial and brush-border (lactase-phlorizin hydrolase) hydrolysis releasing the aglycone kaempferol, which is then rapidly conjugated (glucuronidation/sulfation). The net effect is low, non-sustained systemic exposure to the intact parent, with circulating material dominated by kaempferol conjugates — so most in-vivo activity attributed to dietary astragalin should be read as kaempferol-equivalent exposure (see kaempferol) 8Reference 8Analysis of the therapeutic potential of astragalin: insights into target interactions and mechanismsView study →.
Clinical trials
There are no randomized or open-label human trials of isolated astragalin for any indication. Human relevance is limited to dietary intake as one of many flavonol glycosides in persimmon leaf, green tea, nettle and numerous other plants.
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| —(none, isolate) | — | — | Scattered |
Last checked: July 2026.
Toxicity & Safety
People eat astragalin routinely in tea and leafy plants with no sign of harm — the uncertainty is entirely about concentrated supplements, for which no human data exist at all.
- Routinely consumed in the diet with no signal of harm. Preclinical studies use it as a protective agent, not a toxin.
- No isolate toxicology or human safety dataset. Cautions here are theoretical, not observed.
- Generic concentrated-polyphenol cautions apply. Possible additive effects alongside antiplatelet or anticoagulant use.
- Avoid isolated supplements in pregnancy. Dietary amounts are a different matter.
Full Safety & Interactions Detail
Astragalin is a widespread dietary flavonol glycoside consumed routinely in teas and leafy plants with no signal of dietary harm, and preclinical studies use it as a protective agent — so the low flag is appropriate. No isolate toxicology, genotoxicity or human safety dataset exists; cautions are theoretical and generic to concentrated polyphenol supplements (possible additive effects with antiplatelet/anticoagulant use, and the general uncertainty of taking any isolated flavonoid at supraphysiologic doses without human data).
Dosage
There is no efficacy dose established (no human trials) and no standard supplemental dose — astragalin is obtained incidentally through diet and herbal preparations rather than dosed on its own, and any oral efficacy target is undermined by its hydrolysis to kaempferol, so a meaningful “astragalin dose” cannot honestly be stated.
References
- Kim YH, Choi YJ, Kang MK, et al. (2017). Astragalin inhibits allergic inflammation and airway thickening in ovalbumin-challenged mice. Journal of Agricultural and Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/28064485/
- Cho IH, Gong JH, Kang MK, et al. (2014). Astragalin inhibits airway eotaxin-1 induction and epithelial apoptosis through modulating oxidative-stress-responsive MAPK signalling. BMC Pulmonary Medicine. https://pubmed.ncbi.nlm.nih.gov/25069610/
- Wang S, Yang Y, Lin J, et al. (2025). Astragalin activates autophagy and inhibits apoptosis of astrocytes in AD mice via downregulating the Fas/FasL–VDAC1 pathway. Free Radical Biology and Medicine. https://pubmed.ncbi.nlm.nih.gov/40032030/
- Hu Y, Fang X, Wang J, et al. (2022). Astragalin attenuates AlCl₃/D-galactose-induced aging-like disorders by inhibiting oxidative stress and neuroinflammation. Neurotoxicology. https://pubmed.ncbi.nlm.nih.gov/35537655/
- Ijaz MU, Furqan R, Salar MZ, et al. (2025). Pharmacotherapeutic potentials of astragalin against cisplatin-induced renal toxicity via regulating the Nrf2/Keap1 pathway. Archives of Physiology and Biochemistry. https://pubmed.ncbi.nlm.nih.gov/40418170/
- Cai J, Song L, Hu Z, et al. (2024). Astragalin alleviates oligoasthenospermia via promoting nuclear translocation of Nrf2 and reducing ferroptosis of the testis. Heliyon. https://pubmed.ncbi.nlm.nih.gov/39444397/
- Tang P, Wang Y, Huang X, et al. (2026). Protective effects of astragalin against acute ultraviolet-B-induced photodamage in HaCaT cells and mouse skin. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/42123424/
- Duc Nguyen H (2025). Analysis of the therapeutic potential of astragalin: insights into target interactions and mechanisms. Xenobiotica. https://pubmed.ncbi.nlm.nih.gov/40934094/
