Compound Monograph
Arctiin
Arctiin is the glucoside prodrug of arctigenin — the major dibenzylbutyrolactone lignan of burdock (Arctium lappa) seed and a marker constituent of Forsythia fruit. Gut bacteria hydrolyze it to the more-active aglycone arctigenin, so most of its reported activity is arctigenin's after conversion; arctiin itself is the less-active precursor, with only preclinical data and no human trials of the isolate.
Sources · 6
Where Does It Come From?
Arctiin is a naturally occurring lignan glucoside (dibenzylbutyrolactone; arctigenin 4'-o-glucoside), found in Burdock — seed/fruit and 5 other sources. It is well tolerated orally (low toxicity).
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.
Arctiin at a Glance
Arctiin is the glucoside prodrug of arctigenin — the major lignan of burdock seed and a marker constituent of forsythia fruit.
Its pharmacology is largely its conversion: gut bacteria hydrolyse the sugar to release the far more active aglycone, so most of what arctiin does in a body is done by arctigenin. That dependence on the microbiome makes the effective dose person-dependent in a way the compound’s own chemistry cannot predict.
What It's Used For
Arctiin is the glucoside prodrug of arctigenin — the 4’-O-glucoside of the burdock lignan — and a sibling of matairesinol in the burdock dibenzylbutyrolactone lignan complex (distinct from the mammalian enterolignans). The accuracy point that governs the page: arctiin is a prodrug/reservoir. Gut β-glucosidase hydrolyses it to arctigenin, the more-active aglycone, so most systemic activity is arctigenin’s and arctiin itself is directly “less active” — in DSS colitis, arctigenin but not arctiin was the effective constituent. Its own evidence is a handful of preclinical reports; full pharmacology, PK and safety live on the arctigenin page.
Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. Thin, preclinical-only, with activity largely re-attributable to arctigenin, so scores stay low by design.
Arctiin itself inhibits COX-2 expression via NF-κB pathways in vitro 4Reference 4Anti-inflammatory function of arctiin by inhibiting COX-2 expression via NF-κB pathwaysView study →, but in DSS colitis arctigenin — not arctiin — was the effective constituent 2Reference 2AnimalArctigenin but not arctiin is the major effective constituent of Arctium lappa fruit for attenuating DSS-induced colonic inflammation in miceView study →, underscoring that most of the anti-inflammatory signal is the hydrolysis product’s, not the intact glucoside’s.
Gap: cell/rodent only, with no human data, and the direct arctiin evidence is thin while the aglycone outperforms it 2,
A 2024 review compiles arctiin’s reported pro-apoptotic, anti-proliferative and cell-cycle effects across cancer cell lines 5Reference 5ReviewAn insight into the anticancer potentials of the lignan arctiin: a comprehensive review of molecular mechanismsView study →, much of which overlaps mechanisms attributed to arctigenin after deglycosylation.
Gap: in-vitro/animal only, frequently at supraphysiologic concentrations, with no isolate clinical work and effects largely re-attributable to the aglycone 5Reference 5ReviewAn insight into the anticancer potentials of the lignan arctiin: a comprehensive review of molecular mechanismsView study →.
Arctiin induced a UVB-protective effect in human dermal fibroblasts via microRNA-expression changes 3Reference 3Arctiin induces a UVB-protective effect in human dermal fibroblast cells through microRNA-expression changesView study → — one of the few genuinely arctiin-specific (not arctigenin-attributed) findings.
Gap: a single in-vitro study in cultured fibroblasts, with no in-vivo skin or topical human data 3Reference 3Arctiin induces a UVB-protective effect in human dermal fibroblast cells through microRNA-expression changesView study →.
Arctiin enhanced adipose-tissue browning and energy expenditure by activating the adenosine A2A receptor in a preclinical model 6Reference 6Arctiin, a lignan compound, enhances adipose-tissue browning and energy expenditure by activating the adenosine A2A receptorView study →.
Gap: rodent-only, a single report, with no human metabolic data 6Reference 6Arctiin, a lignan compound, enhances adipose-tissue browning and energy expenditure by activating the adenosine A2A receptorView study →.
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| Gut β-glucosidase (intestinal bacteria) | hydrolyses arctiin → arctigenin (→ onward metabolites) | defining prodrug PK — the aglycone is the systemic actor |
| NF-κB → COX-2 | suppressed COX-2 expression (in vitro) | anti-inflammatory |
| DSS colitis model | arctigenin, not arctiin, effective | confirms arctiin is the less-active precursor |
| microRNA expression (dermal fibroblasts) | UVB-protective response | dermal/photoprotective (in vitro) |
| Adenosine A2A receptor | ↑ adipose browning, energy expenditure (preclinical) | metabolic |
Pharmacokinetics
Arctiin is a glucoside prodrug with low intact oral bioavailability. Human intestinal bacteria transform it — via β-glucosidase deglycosylation — to the aglycone arctigenin, and thereafter toward downstream metabolites 1Reference 1Transformation of arctiin to estrogenic and antiestrogenic substances by human intestinal bacteriaView study →. The absorbed, systemically relevant species is therefore arctigenin, not intact arctiin, and conversion depends on gut-microbiota composition. Arctiin is quantifiable alongside arctigenin in Arctii Fructus preparations, and processing (e.g. stir-frying) shifts the arctiin/arctigenin ratio and its pharmacokinetics 7Reference 7A UHPLC-MS/MS method for evaluating the influence of stir-frying on the pharmacokinetics of seven compounds in Arctii FructusView study →. Full disposition of the active aglycone (extensive first-pass glucuronidation, poor systemic exposure) is covered on the arctigenin page.
Clinical trials
There are no human interventional trials of arctiin. The only burdock-lignan human data are early-phase trials of an arctigenin-rich burdock-seed extract (GBS-01) — a multi-component preparation reported on the arctigenin page — not of arctiin.
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| —(none, isolate) | — | — | Modest(in-vitro + rodent) |
Last checked: July 2026.
Toxicity & Safety
Arctiin has no toxicity signal of its own at dietary levels — but because the body hydrolyses it to arctigenin, the cautions that matter are the aglycone’s, not the glucoside’s.
- A dietary lignan with no toxicity signal at food levels. Ordinary burdock-seed and Forsythia exposure supports the low flag.
- Avoid the isolated compound in pregnancy and breastfeeding. No human safety data.
- Read arctigenin’s cautions as arctiin’s. It is hydrolyzed in vivo, so the aglycone’s phytoestrogenic and interaction cautions carry over.
- No isolate toxicology in humans. Preclinical work simply treats it as a benign lignan glucoside.
Full Safety & Interactions Detail
Arctiin is a dietary burdock-seed lignan (also in Forsythia fruit) with ordinary dietary exposure and no signal of toxicity at food levels — hence low. There is no isolate toxicology in humans, and preclinical work uses it as a benign lignan glucoside. Because arctiin is hydrolyzed to arctigenin in vivo, arctigenin’s own cautions (poor bioavailability, theoretical UGT/CYP interactions, phytoestrogenic/antiproliferative activity) are the relevant safety considerations — those are documented on arctigenin, not restated here.
Dosage
There is no established therapeutic dose and no isolate trials. Arctiin functions as a prodrug reservoir for arctigenin; relevant exposure comes from burdock-seed (Niu Bang Zi / Arctii Fructus) and Forsythia fruit preparations, with the body converting arctiin to arctigenin at a rate set by individual gut flora. Any figures would be research references, not recommendations.
References
- Xie LH, et al. (2003). Transformation of arctiin to estrogenic and antiestrogenic substances by human intestinal bacteria. Chemical & Pharmaceutical Bulletin (Tokyo). https://pubmed.ncbi.nlm.nih.gov/12672988/
- Wu X, et al. (2014). Arctigenin but not arctiin is the major effective constituent of Arctium lappa fruit for attenuating DSS-induced colonic inflammation in mice. International Immunopharmacology. https://pubmed.ncbi.nlm.nih.gov/25284342/
- Lee GT, Cha HJ, Lee KS, et al. (2014). Arctiin induces a UVB-protective effect in human dermal fibroblast cells through microRNA-expression changes. International Journal of Molecular Medicine. https://pubmed.ncbi.nlm.nih.gov/24398562/
- Lee JY, Kim CJ (2011). Anti-inflammatory function of arctiin by inhibiting COX-2 expression via NF-κB pathways. Journal of Inflammation (London). https://pubmed.ncbi.nlm.nih.gov/21733191/
- Chowdhury R, Bhuia MS, Wilairatana P, et al. (2024). An insight into the anticancer potentials of the lignan arctiin: a comprehensive review of molecular mechanisms. Heliyon. https://pubmed.ncbi.nlm.nih.gov/38988539/
- Gu Y, He W, Li W, et al. (2025). Arctiin, a lignan compound, enhances adipose-tissue browning and energy expenditure by activating the adenosine A2A receptor. Molecular Medicine. https://pubmed.ncbi.nlm.nih.gov/40369420/
- Shi Y, Hu J, Wang H, et al. (2022). A UHPLC-MS/MS method for evaluating the influence of stir-frying on the pharmacokinetics of seven compounds in Arctii Fructus. RSC Advances. https://pubmed.ncbi.nlm.nih.gov/36276052/
