Cinnamaldehyde

Cinnamaldehyde at a Glance

Cinnamaldehyde is what cinnamon smells and tastes of. It is a small aromatic aldehyde — a benzene ring carrying a three-carbon chain that ends in an aldehyde — and it makes up around 85% of hydro-distilled cassia bark oil and the greater part of Ceylon bark oil, which is why the two spices smell alike despite the differences elsewhere in their chemistry ^{1,2Reference 1Ooi LS et al. · 2006In vitroAntimicrobial activities of cinnamon oil and cinnamaldehyde from the Chinese medicinal herb Cinnamomum cassia Blume — in vitroView study →Reference 2Jayaprakasha GK · 2011ReviewChemistry, biogenesis, and biological activities of Cinnamomum zeylanicum — reviewView study →}. It is also one of the most widely used flavour and fragrance chemicals in the world, most of it made synthetically rather than distilled from bark.

Pharmacologically it is best known for three things. It is the most specific natural activator of TRPA1, the sensory ion channel that registers cinnamon’s burn and, in the laboratory, noxious cold ^{3Reference 3Bandell M et al. · 2004In vitroNoxious cold ion channel TRPA1 is activated by pungent compounds and bradykinin — in vitro and mouse in vivoView study →}; it is a broad-spectrum antimicrobial in vitro, inhibiting bacteria, yeasts, moulds and dermatophytes at tens to hundreds of micrograms per millilitre ^{1Reference 1Ooi LS et al. · 2006In vitroAntimicrobial activities of cinnamon oil and cinnamaldehyde from the Chinese medicinal herb Cinnamomum cassia Blume — in vitroView study →} and Helicobacter pylori at 8–16 µg/mL ^{5Reference 5Li CY et al. · 2024In vitroCinnamaldehyde: An effective component of Cinnamomum cassia inhibiting Helicobacter pylori — in vitro and mouse in vivoView study →}; and as a reactive electrophile it switches on the Nrf2 cell-protective response ^{9,10Reference 9Wondrak GT et al. · 2010In vitroThe cinnamon-derived dietary factor cinnamic aldehyde activates the Nrf2-dependent antioxidant response in human epithelial colon cells — in vitroView study →Reference 10Long M et al. · 2015AnimalNrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde — mouse in vivoView study →}.

What it does not have is a human trial. The clinical evidence that cinnamon lowers blood glucose belongs to whole powdered bark, and the fraction usually credited with that effect is the water-soluble procyanidins rather than the volatile aldehyde ^{12Reference 12Allen RW et al. · 2013Meta-analysisCinnamon use in type 2 diabetes: an updated systematic review and meta-analysis — meta-analysisView study →}. Cinnamaldehyde’s own record is chemistry, cells and rodents, plus a large body of safety data from its status as a food additive ^{15Reference 15National Toxicology Program · 2004AnimalNTP toxicology and carcinogenesis studies of trans-cinnamaldehyde (CAS NoView study →}.

Why Cinnamon Burns: TRPA1

The tingling heat of cinnamon has a molecular address. TRPA1 is a transient-receptor-potential ion channel on pain-sensing neurons, first characterised as a detector of noxious cold. In 2004 it was shown that the pungent compounds of cinnamon, wintergreen, clove, mustard and ginger oils all open it, and that cinnamaldehyde is the most specific activator of the set: it excites a subset of sensory neurons enriched in cold-sensitive cells, and injected into a mouse paw it produces pain behaviour ^{3Reference 3Bandell M et al. · 2004In vitroNoxious cold ion channel TRPA1 is activated by pungent compounds and bradykinin — in vitro and mouse in vivoView study →}. The same channel responds to the inflammatory peptide bradykinin, which is why TRPA1 became a target for new analgesics and why cinnamaldehyde is the standard tool for probing it.

That tool status has produced one of the few controlled human experiments on the molecule. Painting 10% cinnamaldehyde on the skin of healthy volunteers produces a reproducible local increase in dermal blood flow, and an oral TRPA1 antagonist reduced that response dose-dependently in 16 volunteers, establishing the cinnamaldehyde flare as a target-engagement biomarker for the channel ^{4Reference 4Bamps D et al. · 2023Clinical trialTRPA1 Antagonist LY3526318 Inhibits the Cinnamaldehyde-Evoked Dermal Blood Flow Increase: Translational Proof of Pharmacology — human volunteersView study →}. It is a pharmacology experiment, not a therapeutic one — but it is direct evidence that topical cinnamaldehyde engages TRPA1 in people at the concentrations that also cause irritation.

The Cinnamyl Relatives: Acetate & Alcohol

Cinnamon bark oil is not only cinnamaldehyde. Alongside it sit three small molecules that share its carbon skeleton and differ only at the end of the side chain: cinnamyl acetate (the ester), cinnamyl alcohol (the alcohol) and cinnamic acid (the acid) ^{1Reference 1Ooi LS et al. · 2006In vitroAntimicrobial activities of cinnamon oil and cinnamaldehyde from the Chinese medicinal herb Cinnamomum cassia Blume — in vitroView study →}. In cassia and Ceylon bark oil all three are minor components measured in low single-digit percentages; cinnamyl acetate becomes the major volatile only in Ceylon cinnamon’s fruits, flowers and fruit stalks, which are not the spice ^{2Reference 2Jayaprakasha GK · 2011ReviewChemistry, biogenesis, and biological activities of Cinnamomum zeylanicum — reviewView study →}.

They travel together in the body as well as the plant. Cinnamyl alcohol and cinnamaldehyde are interconverted by the same oxidoreductases, and the aldehyde is oxidised onward to cinnamic acid, so the three form one metabolic series with cinnamic acid as the common exit ^{13Reference 13Peters MM · 1994AnimalStudies on trans-cinnamaldehydeView study →}. In flavour and fragrance use they are handled as a family: cinnamyl acetate and cinnamyl alcohol are perfumery materials in their own right, milder and sweeter than the aldehyde.

The point where they part company is the skin. Cinnamyl alcohol has long been treated as a “prohapten” — a molecule with no reactivity of its own that sensitises only after the skin oxidises it to cinnamaldehyde. Reconstructed human epidermis says otherwise: incubated with carbon-13-labelled cinnamyl alcohol, the tissue formed no cinnamaldehyde at all, and the reactive species were an epoxy-alcohol and an allylic sulfate. Cinnamyl alcohol is therefore a skin sensitiser by its own route, not merely as a cinnamaldehyde precursor ^{17Reference 17Moss E et al. · 2016In vitroIn Situ Metabolism of Cinnamyl Alcohol in Reconstructed Human Epidermis: New Insights into the Activation of This Fragrance Skin Sensitizer — in vitroView study →}. Neither the acetate nor the alcohol has a pharmacology worth separating from the aldehyde’s; their appearance in the cinnamon literature is as composition markers and as co-allergens in the fragrance mix.

Cinnamaldehyde Is Not Cinnamon

Two distinctions keep the cinnamon literature honest, and both run against the grain of the marketing.

The glucose evidence is for bark, not for the aldehyde. A meta-analysis of ten randomised trials (543 patients with type 2 diabetes, 120 mg to 6 g of cinnamon a day for 4–18 weeks) found fasting glucose lower by about 25 mg/dL, with reductions in total cholesterol, LDL and triglycerides, but no significant change in HbA1c and very high heterogeneity between trials ^{12Reference 12Allen RW et al. · 2013Meta-analysisCinnamon use in type 2 diabetes: an updated systematic review and meta-analysis — meta-analysisView study →}. Every one of those trials gave powdered bark or an aqueous extract. Cinnamaldehyde is volatile and poorly represented in a water extract, and the fraction most often credited with the insulin-sensitising activity is the non-volatile type-A procyanidin tannin, not the oil. The rodent studies of pure cinnamaldehyde do show glucose lowering ^{11Reference 11Subash Babu P et al. · 2007AnimalCinnamaldehyde—a potential antidiabetic agent — rat in vivoView study →}, but they are a separate line of evidence, not the mechanism behind the human trials.

The coumarin problem is cassia’s, not cinnamaldehyde’s. Cassia bark carries variable and sometimes large amounts of the hepatotoxic lactone coumarin, which is why cassia has an intake cap and Ceylon does not. Cinnamaldehyde is not coumarin, does not turn into it, and is present in both species; the daily-intake advice on the cassia page is about a different molecule.

What It's Used For

Cinnamaldehyde’s evidence is almost entirely in vitro and rodent, but it is unusually mechanistic — a small electrophilic molecule with well-mapped targets rather than a diffuse “antioxidant”. No human trial of the isolated compound exists for any indication.

Evidence by IndicationStrength of support · Beta

01Antimicrobial & H. pyloriShaky34%Broad in-vitro MIC panels; H. pylori MIC 8–16 µg/mL + mouse gastritis model ^{1,5,7Reference 1Ooi LS et al. · 2006In vitroAntimicrobial activities of cinnamon oil and cinnamaldehyde from the Chinese medicinal herb Cinnamomum cassia Blume — in vitroView study →Reference 5Li CY et al. · 2024In vitroCinnamaldehyde: An effective component of Cinnamomum cassia inhibiting Helicobacter pylori — in vitro and mouse in vivoView study →Reference 7Vasconcelos NG et al. · 2018ReviewAntibacterial mechanisms of cinnamon and its constituents: A review — reviewView study →}

02Anti-InflammatoryShaky30%Gastric-cell NF-κB/IL-8; adjuvant-arthritis mice (i.p.) ^{6,8Reference 6Muhammad JS et al. · 2015In vitroAnti-inflammatory effect of cinnamaldehyde in Helicobacter pylori induced gastric inflammation — in vitroView study →Reference 8El-Tanbouly GS · 2022AnimalNovel anti-arthritic mechanisms of trans-cinnamaldehyde against complete Freund’s adjuvant-induced arthritis in mice: involvement of NF-кB/TNF-α and IL-6/IL-23/ IL-17 pathways in the immuno-inflammatory responses — mouse in vivoView study →}

03Nrf2 Activation & Colon ChemopreventionShaky28%Human colon cells; AOM/DSS mice with Nrf2-knockout control ^{9,10Reference 9Wondrak GT et al. · 2010In vitroThe cinnamon-derived dietary factor cinnamic aldehyde activates the Nrf2-dependent antioxidant response in human epithelial colon cells — in vitroView study →Reference 10Long M et al. · 2015AnimalNrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde — mouse in vivoView study →}

04Glycaemic ControlShaky26%STZ-diabetic rats (isolate); human RCTs are whole bark ^{11,12Reference 11Subash Babu P et al. · 2007AnimalCinnamaldehyde—a potential antidiabetic agent — rat in vivoView study →Reference 12Allen RW et al. · 2013Meta-analysisCinnamon use in type 2 diabetes: an updated systematic review and meta-analysis — meta-analysisView study →}

05Anticancer (Cell Biology)Shaky18%Cell-line apoptosis / anti-angiogenesis literature, reviewed ^{18Reference 18Peng J et al. · 2024ReviewThe role and mechanism of cinnamaldehyde in cancer — reviewView study →}

Mechanisms

The thread through the table is the aldehyde group: a reactive electrophile that opens TRPA1, modifies Keap1, damages bacterial membranes and haptenates skin proteins. Cinnamaldehyde’s benefits and its irritancy are the same chemistry.

Pharmacokinetics

Cinnamaldehyde is absorbed rapidly and cleared almost as fast. In rats and mice given radiolabelled trans-cinnamaldehyde, about 94% of the dose was recovered in excreta within 72 hours, 75–81% of it in the first day’s urine, with less than 2% left in the carcass; the pattern was the same whether the dose was 2 or 250 mg/kg, by injection or by mouth, and in either sex ^{13Reference 13Peters MM · 1994AnimalStudies on trans-cinnamaldehydeView study →}. The aldehyde is oxidised to cinnamic acid and then β-oxidised like a fatty acid to benzoic acid, so the major urinary metabolite is hippuric acid (benzoylglycine), with 3-hydroxy-3-phenylpropionic acid, benzoic acid and benzoyl glucuronide alongside; a second pathway, conjugation with glutathione, accounted for about 7% of urinary radioactivity ^{13Reference 13Peters MM · 1994AnimalStudies on trans-cinnamaldehydeView study →}. In rats dosed orally at 5–500 mg/kg, 81–85% of the label was in the urine at 24 hours and only 3–5% in faeces; tissue residue was mainly gut, liver and kidney, with a small fraction in fat, and at repeated 500 mg/kg the metabolite profile shifted toward benzoic acid, suggesting glycine conjugation saturates at high dose ^{14Reference 14Sapienza PP et al. · 1993AnimalTissue distribution and excretion of 14C-labelled cinnamic aldehyde following single and multiple oral administration in male Fischer 344 rats — rat in vivoView study →}. There is no human pharmacokinetic study, but the rodent picture — near-complete absorption, one-day elimination, no accumulation — is consistent with decades of use as a flavour.

Clinical Trials

No trial has given isolated cinnamaldehyde to people for any indication. The human data touching it are the TRPA1 dermal-flare studies, in which 10% topical cinnamaldehyde is the probe rather than the treatment ^{4Reference 4Bamps D et al. · 2023Clinical trialTRPA1 Antagonist LY3526318 Inhibits the Cinnamaldehyde-Evoked Dermal Blood Flow Increase: Translational Proof of Pharmacology — human volunteersView study →}, and the whole-cinnamon glucose trials, which did not measure or standardise the aldehyde ^{12Reference 12Allen RW et al. · 2013Meta-analysisCinnamon use in type 2 diabetes: an updated systematic review and meta-analysis — meta-analysisView study →}.

Last checked: September 2026.

Isolate vs. Plant Studies

The mechanistic evidence is mostly isolate and transfers well to the oil: cassia oil and pure cinnamaldehyde were interchangeable against microbes ^{1Reference 1Ooi LS et al. · 2006In vitroAntimicrobial activities of cinnamon oil and cinnamaldehyde from the Chinese medicinal herb Cinnamomum cassia Blume — in vitroView study →}, and a cassia extract standardised for cinnamaldehyde matched the pure compound as an Nrf2 inducer ^{9Reference 9Wondrak GT et al. · 2010In vitroThe cinnamon-derived dietary factor cinnamic aldehyde activates the Nrf2-dependent antioxidant response in human epithelial colon cells — in vitroView study →}. In those settings the aldehyde is the active, and the cinnamon essential oil can be read as a cinnamaldehyde preparation.

The reverse is not true for the spice. Powdered bark is only a few percent volatile oil, aqueous cinnamon extracts carry little aldehyde, and the human glucose trials therefore say nothing about cinnamaldehyde ^{12Reference 12Allen RW et al. · 2013Meta-analysisCinnamon use in type 2 diabetes: an updated systematic review and meta-analysis — meta-analysisView study →}. The clean division is: essential oil and topical use — cinnamaldehyde pharmacology; bark powder and tea — a different, tannin-led chemistry. The cassia coumarin caution belongs to the second category and not to the molecule at all.

Its Role in Plants

Cinnamaldehyde is a phenylpropanoid, made from the amino acid phenylalanine: phenylalanine ammonia-lyase gives cinnamic acid, which is activated to its CoA thioester and reduced to the aldehyde by cinnamoyl-CoA reductase — the same first steps the plant uses to build lignin, from which cinnamon’s bark oil branches off ^{2Reference 2Jayaprakasha GK · 2011ReviewChemistry, biogenesis, and biological activities of Cinnamomum zeylanicum — reviewView study →}. Its concentration in the bark, its broad antimicrobial activity and its irritant pungency all fit a defensive role against microbes and browsing animals, though this has been inferred from its chemistry rather than tested ecologically.

Prevalence in Nature

Cinnamaldehyde is a Cinnamomum signature. In cassia (C. cassia) bark it is the overwhelming volatile — 85% of a hydro-distilled oil in a direct GC-MS analysis, with 70–90% the usual range ^{1Reference 1Ooi LS et al. · 2006In vitroAntimicrobial activities of cinnamon oil and cinnamaldehyde from the Chinese medicinal herb Cinnamomum cassia Blume — in vitroView study →} — accompanied by cinnamyl acetate, cinnamic acid, cinnamyl alcohol, a little eugenol and caryophyllene. Ceylon cinnamon (C. verum) bark oil is also cinnamaldehyde-dominated, at a somewhat lower share (roughly 50–75%) with proportionally more eugenol and a characteristic linalool note; in that species the leaf oil is eugenol-dominated, the root-bark oil camphor-dominated, and cinnamyl acetate leads in the fruits and flowers, so which part is distilled decides whether the oil is a cinnamaldehyde oil at all ^{2Reference 2Jayaprakasha GK · 2011ReviewChemistry, biogenesis, and biological activities of Cinnamomum zeylanicum — reviewView study →}. Indonesian (C. burmannii) and Saigon (C. loureiroi) cinnamons, the other commercial barks, carry it in comparable proportions. Outside the genus it appears only in traces.

Discovery & Synthesis

Cinnamaldehyde was isolated from cinnamon oil in 1834 by Jean-Baptiste Dumas and Eugène Péligot, and it became one of the earliest natural products to be made in the laboratory when Luigi Chiozza synthesised it in 1854 by condensing benzaldehyde with acetaldehyde — the aldol-type reaction now called the Claisen–Schmidt condensation. That reaction remains the industrial route, and synthetic cinnamaldehyde dominates the flavour and fragrance market; natural material is obtained by fractionating cassia bark or leaf oil, and is sold at a premium for “natural flavour” labelling. Its regulatory identity is as a food additive: it is an approved flavouring in the United States and was nominated for the full National Toxicology Program bioassay on the strength of that use ^{15Reference 15National Toxicology Program · 2004AnimalNTP toxicology and carcinogenesis studies of trans-cinnamaldehyde (CAS NoView study →}.

Toxicity & Safety

Cinnamaldehyde carries a low flag. It has one of the more complete safety dossiers of any flavour compound, and the two real hazards — skin sensitisation and mucosal irritation — are concentration-dependent effects of undiluted or concentrated material, not of the spice.

The Two-Year Bioassay

The National Toxicology Program fed microencapsulated trans-cinnamaldehyde to rats and mice for two years at 1,000–4,100 ppm — about 50–200 mg/kg/day in rats and 125–550 mg/kg/day in mice, many hundred times a human flavour intake. There was no evidence of carcinogenic activity in either species or sex. In mice the only exposure-related finding was pigmentation of the olfactory epithelium; three-month studies at far higher doses (up to 4,000–5,000 mg/kg/day) produced forestomach hyperplasia and inflammation, consistent with a local irritant rather than a systemic toxin ^{15Reference 15National Toxicology Program · 2004AnimalNTP toxicology and carcinogenesis studies of trans-cinnamaldehyde (CAS NoView study →}. The genetic-toxicology package was mixed in the way reactive aldehydes often are: mutagenic in one Salmonella strain only with mouse-liver activation, positive for sister-chromatid exchange in hamster cells, negative for chromosomal aberrations, and negative in the mouse micronucleus test in vivo ^{15Reference 15National Toxicology Program · 2004AnimalNTP toxicology and carcinogenesis studies of trans-cinnamaldehyde (CAS NoView study →}. Rapid metabolism to hippuric acid is the plausible reason in-vitro reactivity does not translate into in-vivo genotoxicity ^{13Reference 13Peters MM · 1994AnimalStudies on trans-cinnamaldehydeView study →}.

Contact Allergy

The clinically important hazard. Cinnamaldehyde is a direct hapten — its aldehyde binds skin proteins — and “cinnamal” is a constituent of the fragrance-mix patch test and a labelled allergen in cosmetics. Its prevalence has fallen sharply as the fragrance industry limited it: in 25,545 patients patch-tested in London from 1980 to 1996, positive reactions to the fragrance mix ran at 8.5% of women and 6.7% of men, but sensitivity to cinnamic aldehyde declined by 18% a year and to cinnamic alcohol by 9% a year over the period, making both uncommon fragrance allergens by the end of it ^{16Reference 16Buckley DA et al. · 2000ObservationalThe frequency of fragrance allergy in a patch-test population over a 17-year period — observationalView study →}. Cinnamyl alcohol is a sensitiser by its own metabolic route rather than through conversion to the aldehyde ^{17Reference 17Moss E et al. · 2016In vitroIn Situ Metabolism of Cinnamyl Alcohol in Reconstructed Human Epidermis: New Insights into the Activation of This Fragrance Skin Sensitizer — in vitroView study →}. Practical implications: neat cinnamon oil should not go on skin; diluted oil can still sensitise in the predisposed; and an established cinnamaldehyde allergy is a reason to check toothpaste, chewing gum and flavoured foods, which are the commonest sources of oral and perioral reactions.

Irritation and Overdose

Undiluted cinnamon oil irritates skin and mucous membranes, and cinnamaldehyde’s TRPA1 agonism is the reason: the same channel that gives the flavour its warmth gives the concentrate its burn ^{3,4Reference 3Bandell M et al. · 2004In vitroNoxious cold ion channel TRPA1 is activated by pungent compounds and bradykinin — in vitro and mouse in vivoView study →Reference 4Bamps D et al. · 2023Clinical trialTRPA1 Antagonist LY3526318 Inhibits the Cinnamaldehyde-Evoked Dermal Blood Flow Increase: Translational Proof of Pharmacology — human volunteersView study →}. The rodent oral LD₅₀ of about 1,850 mg/kg ^{11Reference 11Subash Babu P et al. · 2007AnimalCinnamaldehyde—a potential antidiabetic agent — rat in vivoView study →} places acute toxicity far from any realistic ingestion. Drug-interaction data specific to cinnamaldehyde are lacking; the coumarin-related hepatotoxicity and anticoagulant cautions attached to cassia are not cinnamaldehyde effects. No reproductive or developmental toxicity has been attributed to the molecule at flavour levels; decisions about cinnamon in pregnancy belong on the herb pages.

Safety at a Glance

✅ Low / no toxicity

• Low intrinsic toxicity. Two-year NTP feed studies in rats and mice found no carcinogenic activity at up to 550 mg/kg/day; cleared as hippuric acid within a day.
• Skin sensitiser. A direct hapten and fragrance-mix allergen; neat cinnamon oil should never be applied to skin, and diluted oil can sensitise.
• Mucosal irritant. TRPA1 agonism makes concentrated cinnamaldehyde a burn hazard on lips, mouth and eyes; flavoured products are the usual trigger for oral reactions in the sensitised.
• Not the coumarin story. Cassia’s hepatotoxicity cap is about coumarin, a different molecule; cinnamaldehyde is present in Ceylon and cassia alike.

Dosage

There is no human dose of isolated cinnamaldehyde. Figures below are research doses in animals and the whole-spice doses used in the cinnamon trials; none is a personal recommendation.

References

1. Ooi LS, Li Y, Kam SL, et al. (2006). Antimicrobial activities of cinnamon oil and cinnamaldehyde from the Chinese medicinal herb Cinnamomum cassia Blume — in vitro. Am J Chin Med. https://pubmed.ncbi.nlm.nih.gov/16710900/
2. Jayaprakasha GK, Rao LJ (2011). Chemistry, biogenesis, and biological activities of Cinnamomum zeylanicum — review. Crit Rev Food Sci Nutr. https://pubmed.ncbi.nlm.nih.gov/21929331/
3. Bandell M, Story GM, Hwang SW, et al. (2004). Noxious cold ion channel TRPA1 is activated by pungent compounds and bradykinin — in vitro and mouse in vivo. Neuron. https://pubmed.ncbi.nlm.nih.gov/15046718/
4. Bamps D, Blockeel AJ, Dreesen E, et al. (2023). TRPA1 Antagonist LY3526318 Inhibits the Cinnamaldehyde-Evoked Dermal Blood Flow Increase: Translational Proof of Pharmacology — human volunteers. Clin Pharmacol Ther. https://pubmed.ncbi.nlm.nih.gov/37562824/
5. Li CY, Liao LJ, Yang SX, et al. (2024). Cinnamaldehyde: An effective component of Cinnamomum cassia inhibiting Helicobacter pylori — in vitro and mouse in vivo. J Ethnopharmacol. https://pubmed.ncbi.nlm.nih.gov/38663778/
6. Muhammad JS, Zaidi SF, Shaharyar S, et al. (2015). Anti-inflammatory effect of cinnamaldehyde in Helicobacter pylori induced gastric inflammation — in vitro. Biol Pharm Bull. https://pubmed.ncbi.nlm.nih.gov/25744466/
7. Vasconcelos NG, Croda J, Simionatto S (2018). Antibacterial mechanisms of cinnamon and its constituents: A review — review. Microb Pathog. https://pubmed.ncbi.nlm.nih.gov/29702210/
8. El-Tanbouly GS, Abdelrahman RS (2022). Novel anti-arthritic mechanisms of trans-cinnamaldehyde against complete Freund’s adjuvant-induced arthritis in mice: involvement of NF-кB/TNF-α and IL-6/IL-23/ IL-17 pathways in the immuno-inflammatory responses — mouse in vivo. Inflammopharmacology. https://pubmed.ncbi.nlm.nih.gov/35648328/
9. Wondrak GT, Villeneuve NF, Lamore SD, et al. (2010). The cinnamon-derived dietary factor cinnamic aldehyde activates the Nrf2-dependent antioxidant response in human epithelial colon cells — in vitro. Molecules. https://pubmed.ncbi.nlm.nih.gov/20657484/
10. Long M, Tao S, Rojo de la Vega M, et al. (2015). Nrf2-dependent suppression of azoxymethane/dextran sulfate sodium-induced colon carcinogenesis by the cinnamon-derived dietary factor cinnamaldehyde — mouse in vivo. Cancer Prev Res (Phila). https://pubmed.ncbi.nlm.nih.gov/25712056/
11. Subash Babu P, Prabuseenivasan S, Ignacimuthu S (2007). Cinnamaldehyde—a potential antidiabetic agent — rat in vivo. Phytomedicine. https://pubmed.ncbi.nlm.nih.gov/17140783/
12. Allen RW, Schwartzman E, Baker WL, et al. (2013). Cinnamon use in type 2 diabetes: an updated systematic review and meta-analysis — meta-analysis. Ann Fam Med. https://pubmed.ncbi.nlm.nih.gov/24019277/
13. Peters MM, Caldwell J (1994). Studies on trans-cinnamaldehyde. 1. The influence of dose size and sex on its disposition in the rat and mouse — animal in vivo. Food Chem Toxicol. https://pubmed.ncbi.nlm.nih.gov/7959441/
14. Sapienza PP, Ikeda GJ, Warr PI, et al. (1993). Tissue distribution and excretion of 14C-labelled cinnamic aldehyde following single and multiple oral administration in male Fischer 344 rats — rat in vivo. Food Chem Toxicol. https://pubmed.ncbi.nlm.nih.gov/8477915/
15. National Toxicology Program (2004). NTP toxicology and carcinogenesis studies of trans-cinnamaldehyde (CAS No. 14371-10-9) in F344/N rats and B6C3F1 mice (feed studies) — animal in vivo. Natl Toxicol Program Tech Rep Ser. https://pubmed.ncbi.nlm.nih.gov/15146216/
16. Buckley DA, Wakelin SH, Seed PT, et al. (2000). The frequency of fragrance allergy in a patch-test population over a 17-year period — observational. Br J Dermatol. https://pubmed.ncbi.nlm.nih.gov/10730761/
17. Moss E, Debeuckelaere C, Berl V, et al. (2016). In Situ Metabolism of Cinnamyl Alcohol in Reconstructed Human Epidermis: New Insights into the Activation of This Fragrance Skin Sensitizer — in vitro. Chem Res Toxicol. https://pubmed.ncbi.nlm.nih.gov/27281158/
18. Peng J, Song X, Yu W, et al. (2024). The role and mechanism of cinnamaldehyde in cancer — review. J Food Drug Anal. https://pubmed.ncbi.nlm.nih.gov/38934689/

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