Compound Monograph
Jaceosidin
Jaceosidin (4',5,7-trihydroxy-3',6-dimethoxyflavone) is a 6-methoxyflavone of mugwort (Artemisia) and yerba santa, closely co-studied with eupatilin. Its research is a broad but cell-line-dominated anticancer literature (including HPV-16 E6/E7 inhibition) plus rodent anti-inflammatory work — all preclinical, with no human trials, and one honest counter-signal (it is pro-angiogenic in endothelial cells).
Sources · 5
Where Does It Come From?
Jaceosidin is a naturally occurring flavone (6-methoxyflavone), found in Mugwort, Yerba Santa and 3 other sources. It is well tolerated orally (low toxicity).
Principal source Mugwort Artemisia vulgaris Herb monograph → 
Source Feverfew Tanacetum parthenium Herb monograph → 
Source Yerba Santa Eriodictyon californicum 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.
Jaceosidin at a Glance
Jaceosidin is a 6-methoxyflavone of mugwort and yerba santa, and the constant companion of eupatilin — the two are almost always studied together, since both occur in Artemisia species.
Its research is a broad but cell-line-dominated anticancer literature, which is a meaningful limitation: cytotoxicity in cultured cancer cells is the easiest result to obtain and the least predictive of anything clinical.
What It's Used For
Jaceosidin is a 6-methoxyflavone (a methoxylated relative of luteolin) whose pharmacology is largely Korean Artemisia research, tightly paired with its co-flavone eupatilin. The bulk of its literature is a broad but cell-line-dominated anticancer dataset — its single most-cited result being inhibition of the HPV-16 E6/E7 oncoproteins 1Reference 1Inhibitory effect of jaceosidin from Artemisia argyi on the function of HPV-16 E6/E7 oncoproteinsView study → — alongside rodent anti-inflammatory work. Everything is preclinical, there are no human trials, and one honesty point runs through the page: in endothelial cells jaceosidin is pro-angiogenic 6Reference 6Jaceosidin promotes angiogenesis via VEGFR2/FAK/PI3K/AKT/NF-κB in endothelial cells (context caution)View study →, which cuts against a naive “anti-tumor” framing.
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.
Jaceosidin’s strongest single result is inhibition of HPV-16 E6/E7 oncoprotein function in cervical-cancer cells 1Reference 1Inhibitory effect of jaceosidin from Artemisia argyi on the function of HPV-16 E6/E7 oncoproteinsView study →; other lines show G2/M arrest via ATM–Chk1/2 in endometrial cells 2Reference 2Jaceosidin induces G2/M arrest via ATM–Chk1/2→cdc25C–cdc2 in endometrial cellsView study →, p53-dependent arrest in U87 glioblastoma 3Reference 3Jaceosidin induces p53-dependent G2/M arrest in U87 glioblastoma cellsView study →, Bax/Mcl-1/c-FLIP-mediated apoptosis in renal Caki cells 4Reference 4Jaceosidin induces apoptosis via Bax/Mcl-1/c-FLIP in renal Caki cellsView study → and ROS-driven apoptosis in ras-transformed breast epithelium 5Reference 5Jaceosidin induces apoptosis in ras-transformed breast epithelial cells via ROSView study →.
Gap: essentially all in-vitro (the HPV work extends to docking-only in-silico studies), with no in-vivo tumor efficacy and no human data — and jaceosidin is pro-angiogenic in endothelial cells (VEGFR2/FAK/PI3K/AKT/NF-κB) 6Reference 6Jaceosidin promotes angiogenesis via VEGFR2/FAK/PI3K/AKT/NF-κB in endothelial cells (context caution)View study →, a counter-signal that must be stated honestly 1,
Jaceosidin has in-vitro antioxidant and anti-inflammatory activity from A. princeps 7Reference 7In-vitro antioxidant and anti-inflammatory activities of jaceosidin from Artemisia princepsView study →, reduced carrageenan-induced paw inflammation in mice (with eupatilin) 8Reference 8AnimalEupatilin and jaceosidin inhibit carrageenan-induced inflammation in miceView study →, and benefited a mouse atopic-dermatitis model via ubiquitin-mediated JAK1 degradation 10Reference 10Jaceosidin ameliorates atopic dermatitis via ubiquitin-mediated JAK1 degradationView study →; the mechanism centers on ERK/NF-κB suppression (blocking TPA-induced COX-2 and MMP-9) 9Reference 9Jaceosidin, a pharmacologically active flavone derived from Artemisia argyi, inhibits phorbol-ester-induced upregulation of COX-2 and MMP-9 by blocking phosphorylation of ERK-1 and -2 in cultured human mammary epithelial cellsView study →.
Gap: small models, often co-dosed with eupatilin, with no human trials 8,
Jaceosidin’s flavone hydroxyl pattern gives in-vitro radical-scavenging activity 7Reference 7In-vitro antioxidant and anti-inflammatory activities of jaceosidin from Artemisia princepsView study →.
Gap: generic scavenging with no isolate clinical relevance 7Reference 7In-vitro antioxidant and anti-inflammatory activities of jaceosidin from Artemisia princepsView study →.
Jaceosidin (with other Eriodictyon californicum flavonoids) antagonizes the human bitter receptor hTAS2R31 in a cell assay 14Reference 14Flavonoids from Eriodictyon californicum as hTAS2R31 bitter-receptor antagonistsView study → — a plausible contributor to yerba santa’s traditional “bitter-blocking” reputation.
Gap: one in-vitro report, and a flavor-science curiosity rather than a health claim — no confirmation that whole-plant exposure produces a meaningful taste effect in people 14Reference 14Flavonoids from Eriodictyon californicum as hTAS2R31 bitter-receptor antagonistsView study →.
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| HPV-16 E6 / E7 oncoproteins | inhibits function (cell; docking-predicted binding) | anticancer (cervical/HPV) |
| ATM–Chk1/2; p53; Bax↑/Mcl-1↓/c-FLIP↓ | cell-cycle arrest and intrinsic apoptosis | anticancer (various lines) |
| ERK1/2 → COX-2, MMP-9; NF-κB / MAPK | suppressed | anti-inflammatory / anti-invasion |
| JAK1 | ubiquitin-mediated degradation | atopic-dermatitis model |
| VEGFR2/FAK/PI3K/AKT/NF-κB | activated → pro-angiogenic (context caution) | endothelial counter-signal |
| hTAS2R31 (bitter receptor) | antagonist (cell assay) | taste / bitter-masking |
Pharmacokinetics
Jaceosidin shows typical flavone pharmacokinetics — poor. Systemic levels are low enough to require tandem MS for quantitation in rat plasma 11Reference 11AnimalLC-MS/MS determination of jaceosidin in rat plasmaView study →, and human-liver-microsome work shows it is metabolized by cytochrome P450 with rapid phase-II UGT glucuronidation 12Reference 12In-vitro metabolism of jaceosidin: CYP and UGT characterisation in human liver microsomesView study →; both jaceosidin and eupatilin also inhibit several CYP activities in vitro, a theoretical herb–drug-interaction signal at high exposure 13Reference 13Effects of eupatilin and jaceosidin on CYP450 activities in human liver microsomesView study →. The expected profile is low oral bioavailability, extensive first-pass conjugation and short plasma exposure, with no human pharmacokinetics for the isolate.
Clinical trials
There are no human clinical trials of isolated jaceosidin (efficacy, PK or safety); all evidence is in-vitro or rodent.
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| —(none, isolate) | — | — | Moderate(cell-line-dominated) |
Last checked: July 2026.
Toxicity & Safety
No toxicology of concern has surfaced for jaceosidin, but there is one counter-signal worth knowing: it is pro-angiogenic in endothelial cells, which cuts against any assumption that a broadly “anticancer” flavone is safe to self-medicate with.
- No isolated-compound toxicology of concern. It shows the usual flavone preference for transformed over normal cells.
- Do not import wormwood toxicity. Thujone is a chemically unrelated monoterpene ketone; jaceosidin carries none of its convulsant profile.
- Avoid in pregnancy and lactation. No reproductive data, and mugwort carries a traditional uterine-stimulant reputation.
- Pro-angiogenic in endothelial cells. This argues against self-medication framing in cancer or vascular-sensitive contexts.
- Possible herb-drug interaction at high doses. In-vitro CYP inhibition flags it, though it is untested in people.
Full Safety & Interactions Detail
Jaceosidin has a low isolate-toxicity signal on thin data — no isolated-compound toxicology of concern surfaced, and it shows the usual flavone preference for transformed over normal cells in several studies. Two discipline points: do not import wormwood/thujone toxicity onto this molecule — thujone is a chemically and toxicologically unrelated monoterpene ketone from Artemisia, and jaceosidin carries none of that convulsant profile; and two honest caveats belong on the page — in-vitro CYP inhibition flags a possible herb–drug interaction at high doses 13Reference 13Effects of eupatilin and jaceosidin on CYP450 activities in human liver microsomesView study →, and the pro-angiogenic endothelial finding 6Reference 6Jaceosidin promotes angiogenesis via VEGFR2/FAK/PI3K/AKT/NF-κB in endothelial cells (context caution)View study → argues against self-medication framing in cancer or vascular-sensitive contexts.
Dosage
There is no established human dose — jaceosidin has never been given to humans as an isolate. All dosing is preclinical (µM in vitro; mg/kg in rodent models) and not translatable, so no human figure should be inferred.
References
- Kim MK, et al. (2005). Inhibitory effect of jaceosidin from Artemisia argyi on the function of HPV-16 E6/E7 oncoproteins. Journal of Ethnopharmacology. https://pubmed.ncbi.nlm.nih.gov/15814270/
- Lee HG, et al. (2013). Jaceosidin induces G2/M arrest via ATM–Chk1/2→cdc25C–cdc2 in endometrial cells. Food and Chemical Toxicology. https://pubmed.ncbi.nlm.nih.gov/23274058/
- Khan M, et al. (2011). Jaceosidin induces p53-dependent G2/M arrest in U87 glioblastoma cells. Asian Pacific Journal of Cancer Prevention. https://pubmed.ncbi.nlm.nih.gov/22471459/
- Woo SM, Kwon TK, et al. (2016). Jaceosidin induces apoptosis via Bax/Mcl-1/c-FLIP in renal Caki cells. Chemico-Biological Interactions. https://pubmed.ncbi.nlm.nih.gov/27729209/
- Lee HG, et al. (2007). Jaceosidin induces apoptosis in ras-transformed breast epithelial cells via ROS. Annals of the New York Academy of Sciences. https://pubmed.ncbi.nlm.nih.gov/17404061/
- Lee TH, Jung H, Park KH, et al. (2014). Jaceosidin promotes angiogenesis via VEGFR2/FAK/PI3K/AKT/NF-κB in endothelial cells (context caution). Experimental Biology and Medicine. https://pubmed.ncbi.nlm.nih.gov/24939823/
- Kim MJ, Han JM, Jin YY, et al. (2008). In-vitro antioxidant and anti-inflammatory activities of jaceosidin from Artemisia princeps. Archives of Pharmacal Research. https://pubmed.ncbi.nlm.nih.gov/18449499/
- Min SW, et al. (2009). Eupatilin and jaceosidin inhibit carrageenan-induced inflammation in mice. Journal of Ethnopharmacology. https://pubmed.ncbi.nlm.nih.gov/19505561/
- Jeong MA, et al. (2007). Jaceosidin, a pharmacologically active flavone derived from Artemisia argyi, inhibits phorbol-ester-induced upregulation of COX-2 and MMP-9 by blocking phosphorylation of ERK-1 and -2 in cultured human mammary epithelial cells. Annals of the New York Academy of Sciences. https://pubmed.ncbi.nlm.nih.gov/17404058/
- Wei R, Cheng W, Zhang J, et al. (2026). Jaceosidin ameliorates atopic dermatitis via ubiquitin-mediated JAK1 degradation. Phytomedicine. https://pubmed.ncbi.nlm.nih.gov/42341525/
- Song WY, Kim NJ, Kim SY, et al. (2009). LC-MS/MS determination of jaceosidin in rat plasma. Journal of Pharmaceutical and Biomedical Analysis. https://pubmed.ncbi.nlm.nih.gov/19070985/
- Song WY, Ji HY, Baek NI, et al. (2010). In-vitro metabolism of jaceosidin: CYP and UGT characterisation in human liver microsomes. Archives of Pharmacal Research. https://pubmed.ncbi.nlm.nih.gov/21191764/
- Ji HY, Kim SY, Kim DK, et al. (2010). Effects of eupatilin and jaceosidin on CYP450 activities in human liver microsomes. Molecules. https://pubmed.ncbi.nlm.nih.gov/20877236/
- Fletcher JN, et al. (2011). Flavonoids from Eriodictyon californicum as hTAS2R31 bitter-receptor antagonists. Journal of Agricultural and Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/22059530/
