Compound Monograph
Iridin
Iridin is the isoflavone glycoside of Iris and Belamcanda rhizome (orris, She-gan) — irigenin 7-O-glucoside — a poorly-absorbed prodrug that gut flora hydrolyze to its active aglycone irigenin. Preclinical only, with no human trials of the isolate. Its plant synonym "irisin" is unrelated to the human exercise myokine irisin.
Sources · 3
Where Does It Come From?
Iridin is a naturally occurring isoflavone glycoside, found in Iris rhizome, Iris versicolor rhizome and Belamcanda chinensis. 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.
Iridin at a Glance
Iridin is the isoflavone glycoside of iris and Belamcanda rhizome — orris root and the Chinese herb she-gan — and is irigenin 7-O-glucoside.
It is a poorly absorbed prodrug: gut flora hydrolyse it to the active aglycone irigenin. Its research is preclinical, with no human data.
What It's Used For
Iridin is the isoflavone glycoside of Iris and Belamcanda rhizome — the 7-O-glucoside of irigenin — and its defining property is that it is a prodrug: as a polar glucoside it is poorly absorbed intact, and gut β-glucosidase hydrolyses it to irigenin, the aglycone that actually circulates and acts. So almost all “iridin pharmacology” is irigenin’s pharmacology after hydrolysis, and the detail sits on the irigenin page rather than restating it. One disambiguation is essential: iridin’s old synonym “irisin” collides with the human exercise myokine irisin — they are completely unrelated. All evidence is preclinical.
Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. Thin, prodrug-of-irigenin, so scores stay low by design.
The load-bearing fact. Iridin (irigenin 7-O-glucoside) is poorly absorbed intact; gut flora/glycosidases cleave the glucose to release irigenin, which is the absorbed, active species, and the aglycone is then handled by phase-II conjugation (UGT1A) 4Reference 4In vitroUGT1A1 and UGT1A9 are responsible for the phase-II metabolism of tectorigenin and irigenin in vitroView study →. A rat metabolite/pharmacokinetic study characterized this conversion directly 1Reference 1AnimalMetabolite identification of iridin in rats by UHPLC-MS/MS and pharmacokinetic study of its metabolite irigeninView study →.
Gap: the therapeutic activity is the aglycone’s, not the intact glycoside’s — read the irigenin page for the pharmacology rather than attributing it to iridin 1Reference 1AnimalMetabolite identification of iridin in rats by UHPLC-MS/MS and pharmacokinetic study of its metabolite irigeninView study →.
The isoflavone class effect (NF-κB/MAPK suppression, Nrf2/HO-1) is documented for irigenin, the released aglycone 3Reference 3The effects of iridin and irigenin on cancer: comparison with well-known isoflavones in breast, prostate and gastric cancersView study → — see that page.
Gap: there is no iridin-isolate anti-inflammatory or hepatoprotective study with a clean discrete result; the activity is inferred through hydrolysis to irigenin 3Reference 3The effects of iridin and irigenin on cancer: comparison with well-known isoflavones in breast, prostate and gastric cancersView study →.
Iridin induced G2/M cell-cycle arrest and extrinsic apoptosis via PI3K/AKT in AGS gastric-cancer cells 2Reference 2Iridin induces G2/M-phase cell-cycle arrest and extrinsic apoptotic cell death through PI3K/AKT signalling in AGS gastric-cancer cellsView study →, and a 2025 review compared iridin and irigenin against known isoflavones in breast, prostate and gastric models 3Reference 3The effects of iridin and irigenin on cancer: comparison with well-known isoflavones in breast, prostate and gastric cancersView study →.
Gap: a single cell line, with no in-vivo tumor efficacy or clinical signal, and the standard isoflavone-anticancer caveats apply 2,
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| Gut β-glucosidase / microbiota | hydrolyses iridin → irigenin (aglycone) | pharmacokinetics (the defining step) |
| UGT1A (glucuronidation of the aglycone) | phase-II conjugation | low systemic exposure |
| PI3K / AKT | inhibited (G2/M arrest, extrinsic apoptosis) | anticancer (gastric cells) |
| NF-κB / MAPK; Nrf2 / HO-1 | modulated — via released irigenin | anti-inflammatory / antioxidant — see irigenin |
Pharmacokinetics
Iridin is a glucoside prodrug. As the polar 7-O-glucoside it is poorly absorbed intact; oral iridin is deglycosylated by gut β-glucosidase to the aglycone irigenin, the absorbed and pharmacologically active species. In rats given oral iridin, thirteen metabolites were identified across plasma, urine and feces — the principal pathway being demethylation followed by glucuronidation — and the pharmacokinetics of the metabolite irigenin were characterized 1Reference 1AnimalMetabolite identification of iridin in rats by UHPLC-MS/MS and pharmacokinetic study of its metabolite irigeninView study →; the aglycone is a UGT1A1/1A9 substrate in vitro 4Reference 4In vitroUGT1A1 and UGT1A9 are responsible for the phase-II metabolism of tectorigenin and irigenin in vitroView study →. The net picture is low intact-glycoside exposure, gut-microbiota-dependent conversion to irigenin, then heavy phase-II conjugation, with no human pharmacokinetic data.
Clinical trials
There are no human clinical trials of isolated iridin. Human exposure occurs only incidentally through Iris/orris/Belamcanda (She-gan) preparations, and all evidence is in-vitro or rodent.
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| —(none, isolate) | — | — | Thin |
Last checked: July 2026.
Toxicity & Safety
There is essentially no toxicology for purified iridin — the emetic, purgative reputation people associate with it belongs to the whole orris/blue-flag rhizome and its glycoside-and-resin mixture, not to the isolated compound.
- Low isolate-toxicity signal. No organ-toxicity finding specific to purified iridin appears in the literature.
- Avoid in pregnancy and lactation. No reproductive or developmental data for the isolate.
- No isolate toxicology at all. No genotoxicity or repeat-dose data exists for the purified compound.
- The rhizome’s acrid action is not the isolate’s. Orris and blue flag are emetic, purgative and mucous-membrane irritant; iridin is only one of several constituents.
- Theoretical hormonal caveat. Generic and weakly supported, on isoflavone class membership alone.
Full Safety & Interactions Detail
Iridin has a low isolate-toxicity signal — there is no isolated-compound toxicology, genotoxicity or repeat-dose data for purified iridin, and as an isoflavone glycoside it carries only the generic, weakly-supported theoretical hormonal caveat. One context point matters: the whole-rhizome orris/blue-flag reputation for emetic, purgative and mucous-membrane-irritant action is a property of the whole rhizome and its glycoside/resin mixture (iridin is one of several constituents), not clean toxicology demonstrated for purified iridin — so the herb’s acrid GI action should not be attributed to the isolate as if characterized.
Dosage
There is no established human dose — iridin is not sold or used as a standardized isolate and appears only within Iris/orris/Belamcanda herbal material. Figures in the literature (e.g. the 100 mg/kg rat pharmacokinetic dose) are preclinical, not recommendations.
References
- Hu T, Ge X, Wang J, et al. (2021). Metabolite identification of iridin in rats by UHPLC-MS/MS and pharmacokinetic study of its metabolite irigenin. Journal of Chromatography B. https://pubmed.ncbi.nlm.nih.gov/34492510/
- Bhosale PB, Vetrivel P, Ha SE, et al. (2021). Iridin induces G2/M-phase cell-cycle arrest and extrinsic apoptotic cell death through PI3K/AKT signalling in AGS gastric-cancer cells. Molecules. https://pubmed.ncbi.nlm.nih.gov/34068568/
- Won Y, Kim HH, Jeong SH, et al. (2025). The effects of iridin and irigenin on cancer: comparison with well-known isoflavones in breast, prostate and gastric cancers. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/40141034/
- Li J, Xu Z, Gu J (2022). UGT1A1 and UGT1A9 are responsible for the phase-II metabolism of tectorigenin and irigenin in vitro. Molecules. https://pubmed.ncbi.nlm.nih.gov/35807350/
