Compound Monograph
Faradiol
Faradiol is a pentacyclic triterpenediol from calendula (marigold) flowers and the principal topical anti-inflammatory constituent of the flower's lipophilic fraction — its fatty-acid monoester is roughly as potent as indomethacin in the classic mouse-ear edema assay, but the evidence is entirely preclinical, with no human trials of the isolated compound.
Sources · 4
Where Does It Come From?
Faradiol is a naturally occurring triterpene (triterpenediol), found in Marigold / Calendula flowers and 3 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.
Faradiol at a Glance
Faradiol is a pentacyclic triterpenediol from calendula (marigold) flowers, and the principal anti-inflammatory constituent of the flower’s lipophilic fraction.
Its potency is the notable fact: the fatty-acid monoester of faradiol is roughly as potent as indomethacin in topical anti-inflammatory assays — an unusually strong showing for a plant triterpene against a reference NSAID.
That makes it the compound most responsible for calendula’s traditional use on inflamed and damaged skin, and it is why calendula preparations are extracted with oil rather than water.
What It's Used For
Faradiol is a pentacyclic triterpenediol of calendula flowers — a relative of lupeol and taraxasterol — and the principal topical anti-inflammatory constituent of the flower’s lipophilic fraction. Two framing points. In the floret it occurs mainly as its C-3 fatty-acid monoesters (the pharmacopoeial QC marker), while the free diol is the more active aglycone — so keep this free-diol entry distinct from the “faradiol monoesters” marker. And its evidence, though genuinely notable, is entirely preclinical and topical: there are no human trials of the isolate, and calendula’s clinical use rests on the whole extract/ointment.
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.
The marquee application and the reason ester content is calendula’s pharmacopoeial QC marker. Della Loggia (1994) fractionated the flower’s lipophilic extract and localized the topical anti-edematous activity to the triterpenediol monoesters — free faradiol being the most active single compound, with esters and monool triterpenes weaker 1Reference 1The role of triterpenoids in the topical anti-inflammatory activity of Calendula officinalis flowersView study → — and Zitterl-Eglseer (1997) confirmed the anti-edematous ranking of the main triterpendiol esters, roughly comparable weight-for-weight to indomethacin 2Reference 2Anti-oedematous activities of the main triterpendiol esters of marigold (Calendula officinalis)View study →.
Gap: rodent topical edema models only; the indomethacin comparison is weight-for-weight in one acute assay, not therapeutic equivalence, and human anti-inflammatory use is documented only for the whole calendula preparation 1,
Marigold flower triterpenoids including the faradiol esters showed anti-tumor-promoting and cytotoxic activity in standard chemoprevention screens (EBV-EA activation / two-stage carcinogenesis) 4Reference 4Anti-inflammatory, anti-tumour-promoting and cytotoxic activities of constituents of marigold (Calendula officinalis) flowersView study →.
Gap: a single study at the in-vitro/short-term-promotion-assay level, with faradiol one of several constituents tested and no animal tumor-burden or clinical data — not an anticancer indication 4Reference 4Anti-inflammatory, anti-tumour-promoting and cytotoxic activities of constituents of marigold (Calendula officinalis) flowersView study →.
Faradiol esters mark the lipophilic anti-inflammatory triterpenoid fraction of calendula, whose ointments are used topically for wounds 1,
Gap: no isolated-faradiol wound-healing study exists — calendula’s measured fibroblast-proliferation/wound activity is largely driven by its hydrophilic flavonol-glycoside fraction, a chemically distinct part, so faradiol’s role is a plausible contributor, not demonstrated 5Reference 5New insights into the analysis of faradiol esters and related compounds in CalendulaView study →.
Chemically modified calendula triterpene derivatives were screened alongside anti-inflammatory endpoints 3Reference 3Improved anti-inflammatory activity of three new terpenoids derived by systematic chemical modification from the abundant triterpenes of Calendula officinalisView study →.
Gap: faradiol is not a notable antioxidant — calendula’s antioxidant capacity is a phenolic/flavonoid property — so this is a minor mention only 3Reference 3Improved anti-inflammatory activity of three new terpenoids derived by systematic chemical modification from the abundant triterpenes of Calendula officinalisView study →.
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| Croton-oil / TPA acute edema (topical) | suppressed; faradiol/monoester most active of the fraction, ≈ indomethacin w/w | topical anti-inflammatory (the only well-supported mechanism) |
| Arachidonic-acid / eicosanoid cascade (inferred) | anti-edematous action consistent with, but not molecularly mapped to, eicosanoid modulation | topical anti-inflammatory (mechanism unresolved) |
| EBV-EA activation / carcinogenesis promotion | inhibited; cytotoxic to some tumor lines | anti-tumor-promotion (screen only) |
Honest note: only the topical anti-edematous effect is genuinely supported; the upstream molecular target for faradiol has not been pinned down — the classic work is phenotypic (edema assay), not target-level.
Pharmacokinetics
There is no dedicated pharmacokinetic study of isolated faradiol. It is a highly lipophilic pentacyclic triterpenediol (class-typical of lupeol/taraxasterol: very low aqueous solubility, high logP), so topical delivery is the pharmacologically relevant route — the entire evidence base is topical/local, matching calendula ointment use — and oral bioavailability is expected to be poor, meaning in-vitro/topical potencies should not be read as oral human efficacy. In the plant it exists mainly esterified (C-3 myristate/palmitate/laurate), and this ester-versus-free-diol distinction matters for both QC and any absorption assumptions; no human ADME, metabolism or half-life data exist.
Clinical trials
There are no trials of isolated faradiol or its monoesters. All human evidence is for whole calendula preparations (extracts/ointments), where faradiol esters are a standardized marker but not an isolated intervention — no trial should be attributed to faradiol itself.
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| —(none, isolate) | — | — | Modest(topical anti-inflammatory) |
Last checked: July 2026.
Toxicity & Safety
Faradiol inherits calendula’s benign topical record and shows no acute-toxicity signal, but the pure isolate has no toxicology behind it at all — no genotoxicity, carcinogenicity or repeat-dose data.
- A benign topical record. No acute-toxicity signal in the calendula bioassays, consistent with a dietary and topical plant triterpene.
- Avoid the isolate in pregnancy and lactation. No isolate data, and oral calendula is traditionally cautioned.
- No toxicology data on the pure compound. Genotoxicity, carcinogenicity and repeat-dose studies are all absent.
- Do not read cytotoxicity as toxicity. The reported tumor-cell cytotoxicity is an anticancer-screening readout, not evidence of systemic harm.
- Asteraceae contact sensitization is possible. That risk belongs to the whole plant (sesquiterpene lactones), not to faradiol itself.
Full Safety & Interactions Detail
Faradiol has a low toxicity verdict — consistent with a dietary/topical plant triterpene, with no signal of acute toxicity in the calendula bioassays and a benign topical safety record for calendula, of which the faradiol esters are constituents. There are no genotoxicity, carcinogenicity or repeat-dose toxicology data on the pure isolate (the reported tumor-cell cytotoxicity is an anticancer-screening readout, not evidence of systemic toxicity). Contact sensitization to calendula/Asteraceae is possible at the whole-plant level (sesquiterpene lactones, not faradiol), and is relevant to the source herb rather than to faradiol specifically.
Dosage
There is no established human dose — there is no isolated-faradiol dosing in humans, the evidence is topical and preclinical, and the ”≈ indomethacin” figure is a weight-for-weight comparison in the mouse-ear edema assay, not a therapeutic dose. In practice faradiol is delivered within standardized calendula preparations, where faradiol-monoester content is the pharmacopoeial QC parameter rather than a dosed active.
References
- Della Loggia R, et al. (1994). The role of triterpenoids in the topical anti-inflammatory activity of Calendula officinalis flowers. Planta Medica. https://pubmed.ncbi.nlm.nih.gov/7809203/
- Zitterl-Eglseer K, et al. (1997). Anti-oedematous activities of the main triterpendiol esters of marigold (Calendula officinalis). Journal of Ethnopharmacology. https://pubmed.ncbi.nlm.nih.gov/9254116/
- Neukirch H, et al. (2005). Improved anti-inflammatory activity of three new terpenoids derived by systematic chemical modification from the abundant triterpenes of Calendula officinalis. Chemistry & Biodiversity. https://pubmed.ncbi.nlm.nih.gov/17192009/
- Ukiya M, et al. (2006). Anti-inflammatory, anti-tumour-promoting and cytotoxic activities of constituents of marigold (Calendula officinalis) flowers. Journal of Natural Products. https://pubmed.ncbi.nlm.nih.gov/17190444/
- Zimmermann BF, Häberle E (2025). New insights into the analysis of faradiol esters and related compounds in Calendula. Journal of Pharmaceutical and Biomedical Analysis. https://pubmed.ncbi.nlm.nih.gov/40120297/
