Compound Monograph
Cinnamic acid
Trans-cinnamic acid is the simple phenylpropenoic acid of cinnamon and the unsubstituted backbone from which caffeic, ferulic and p-coumaric acids derive. Studied preclinically for antidiabetic and antioxidant activity, but with no human trials of the isolate — cinnamon's human data belong to the spice and cinnamaldehyde, not to this acid.
Sources · 8
Where Does It Come From?
Cinnamic acid is a naturally occurring phenolic acid (cinnamic acid / phenylpropenoid), found in Cinnamon, Balsams, Shea butter and 5 other sources. It is well tolerated orally (low toxicity).
Source Ceylon Cinnamon Cinnamomum verum 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.
Cinnamic acid at a Glance
trans-Cinnamic acid is the simple phenylpropenoic acid of cinnamon, and the unsubstituted backbone from which caffeic, ferulic and p-coumaric acids are all derived by adding hydroxyl and methoxyl groups.
That makes it structurally foundational to the entire hydroxycinnamic acid family, and to the phenylpropanoid pathway that produces most plant phenolics.
Its own research is preclinical, covering antidiabetic and antioxidant activity, with no human trials of the isolate.
What It's Used For
Cinnamic acid is the simple phenylpropenoic acid of cinnamon and sits at a branch point in plant biochemistry — formed from phenylalanine and serving as the unsubstituted backbone from which the hydroxycinnamic acids (caffeic, ferulic, p-coumaric) derive. Two identity points matter throughout: it is distinct from cinnamaldehyde (the aldehyde that carries most of cinnamon’s pharmacology) and, lacking a ring hydroxyl, it is a weaker antioxidant than its hydroxylated relatives. Its most notable isolate signal is antidiabetic, but all of it is preclinical — cinnamon’s human glucose data belong to the spice/aldehyde, not to this acid.
Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. No human isolate trials exist, so scores stay low by design.
Oral cinnamic acid improved glucose tolerance in type-2 diabetic rats and directly stimulated glucose-induced insulin secretion in isolated islets 1Reference 1In vitroCinnamic acid exerts anti-diabetic activity by improving glucose tolerance in vivo and stimulating insulin secretion in vitroView study →; in adipocytes it raised adiponectin and the p-AMPK/AMPK ratio 3Reference 3trans-Cinnamic acid increases adiponectin and the p-AMPK/AMPK ratio in 3T3-L1 adipocytesView study →, and a dedicated review compiles insulin-secretion, reduced gluconeogenesis and enhanced glucose uptake for the acid and its derivatives 2Reference 2Cinnamic acid and its derivatives: mechanisms for prevention and management of diabetes and its complicationsView study →. (In-vitro work also reports apoptosis in melanoma cells, but only at millimolar concentrations far above achievable exposure 4Reference 4Cinnamic acid induces apoptotic cell death and cytoskeleton disruption in human melanoma cellsView study →.)
Gap: all rodent/in-vitro; no human trial of the isolate — cinnamon’s human glucose data belong to the spice and cinnamaldehyde, not to cinnamic acid 1,
Free-radical scavenging is the most consistently reported cinnamic-acid activity.
Gap: it lacks a phenolic ring hydroxyl, so it is a distinctly weaker antioxidant than its hydroxylated relatives, and most data are DPPH/ORAC-type chemical assays, not cellular or in-vivo endpoints 8,
Cinnamic acid is reviewed as an antibacterial/antifungal scaffold with membrane-permeabilizing and antibiotic-potentiating behavior 8Reference 8ReviewPharmacological potential of cinnamic acid and derivatives: a comprehensive reviewView study →.
Gap: intrinsic MICs are weak, and most potent antimicrobial activity sits in synthetic cinnamate esters/amides, not the free acid — some cited cinnamon-oil activity belongs to cinnamaldehyde 8Reference 8ReviewPharmacological potential of cinnamic acid and derivatives: a comprehensive reviewView study →.
Cinnamic acid reduces pro-inflammatory signaling (IκB phosphorylation → NF-κB) in LPS-stimulated macrophage models 9Reference 9Cinnamic acid derivatives and their biological efficacyView study →.
Gap: much of the signal comes from derivatives or nanoparticle formulations rather than the free acid, with no in-vivo isolate confirmation of note 9Reference 9Cinnamic acid derivatives and their biological efficacyView study →.
Cinnamic acid acts as a mixed-type tyrosinase inhibitor in enzyme-kinetic studies 5Reference 5Tyrosinase-inhibitory activities of cinnamic acid analoguesView study →.
Gap: purified-enzyme/in-vitro cosmetic interest only, with no skin-whitening or clinical dermatology evidence for the isolate 5Reference 5Tyrosinase-inhibitory activities of cinnamic acid analoguesView study →.
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| Pancreatic β-cell insulin secretion | ↑ glucose-stimulated insulin release (isolated islets) | antidiabetic |
| Adiponectin / AMPK (adipocytes) | ↑ adiponectin, ↑ p-AMPK/AMPK | antidiabetic / metabolic |
| ROS / free radicals | radical scavenging (weak, no ring -OH) | antioxidant |
| NF-κB / IκB phosphorylation | ↓ pro-inflammatory transcription | anti-inflammatory |
| Tyrosinase | mixed-type enzyme inhibition | skin / cosmetic |
Pharmacokinetics
Cinnamic acid is orally absorbed and rapidly metabolized by hepatic/mitochondrial β-oxidation: activation to cinnamoyl-CoA, conversion to benzoyl-CoA and benzoic acid, then glycine conjugation to hippuric acid — the dominant urinary metabolite, accounting for the majority of an oral dose in humans 6,
Clinical trials
There are no human trials of purified trans-cinnamic acid for any indication. Human cinnamon trials test the whole spice or extract and reflect cinnamaldehyde and other constituents — they cannot be attributed to cinnamic acid. The evidence base is preclinical (rodent, in-vitro, enzyme-kinetic) plus reviews.
| Completed | Planned | Terminated | Preclinical |
|---|---|---|---|
| —(none, isolate) | — | — | Moderate |
Last checked: July 2026.
Toxicity & Safety
You already eat this compound daily and the body has an efficient route for clearing it — there are no notable safety concerns at dietary or flavor-use levels. What is missing is any dedicated human data on the isolate.
- A widespread dietary phenolic acid. Found in fruits, vegetables, cinnamon, balsams and honey, and a long-standing GRAS flavor and fragrance ingredient.
- Efficiently detoxified. β-oxidation to benzoic and hippuric acid clears it; animal acute toxicity is low.
- Limited isolate human toxicology. No dedicated dataset exists for the purified compound.
- Cell-study doses are not dietary doses. The millimolar concentrations used in some in-vitro work are far above real exposure.
Full Safety & Interactions Detail
Cinnamic acid is a widespread dietary phenolic acid (fruits, vegetables, cinnamon, balsams, honey) and a long-standing GRAS flavor/fragrance ingredient. Its efficient β-oxidation to benzoic and hippuric acid is a detoxication route, and animal acute toxicity is low, with no notable safety concerns at dietary or flavor-use levels. A dedicated isolated-compound human toxicology dataset is limited, and the millimolar concentrations used in some cell studies are far above dietary exposure. No reproductive-toxicity study of isolated cinnamic acid was located. It is a normal constituent of food and spice at dietary levels; concentrated or supplemental doses have not been assessed.
Dosage
There is no established therapeutic human dose — cinnamic acid is not used as a stand-alone supplement, and human exposure is dietary (milligram quantities from cinnamon, fruit and other plant foods). Preclinical antidiabetic effects used rodent oral doses (roughly 5–30 mg/kg in the source studies) that do not translate to a validated human regimen; treat it as a dietary/flavor constituent and biochemical precursor, not a dosed intervention.
References
- Hafizur RM, et al. (2015). Cinnamic acid exerts anti-diabetic activity by improving glucose tolerance in vivo and stimulating insulin secretion in vitro. Phytomedicine. https://pubmed.ncbi.nlm.nih.gov/25765836/
- Adisakwattana S (2017). Cinnamic acid and its derivatives: mechanisms for prevention and management of diabetes and its complications. Nutrients. https://pubmed.ncbi.nlm.nih.gov/28230764/
- Kopp T, et al. (2014). trans-Cinnamic acid increases adiponectin and the p-AMPK/AMPK ratio in 3T3-L1 adipocytes. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/24557583/
- Niero EL, Machado-Santelli GM (2013). Cinnamic acid induces apoptotic cell death and cytoskeleton disruption in human melanoma cells. Journal of Experimental & Clinical Cancer Research. https://pubmed.ncbi.nlm.nih.gov/23701745/
- Takahashi T, Miyazawa M, et al. (2010). Tyrosinase-inhibitory activities of cinnamic acid analogues. Pharmazie. https://pubmed.ncbi.nlm.nih.gov/21284262/
- Hoskins JA, Holliday SB, et al. (1984). The metabolism of cinnamic acid by healthy and phenylketonuric adults: a kinetic study. Biomedical Mass Spectrometry. https://pubmed.ncbi.nlm.nih.gov/6743769/
- Nutley BP, et al. (1994). Metabolism of trans-cinnamic acid in the rat and mouse and its variation with dose. Food and Chemical Toxicology. https://pubmed.ncbi.nlm.nih.gov/7959442/
- Tian Y, Jiang X, Guo J, et al. (2025). Pharmacological potential of cinnamic acid and derivatives: a comprehensive review. Pharmaceuticals (Basel). https://pubmed.ncbi.nlm.nih.gov/40872532/
- Ruwizhi N, Aderibigbe BA (2020). Cinnamic acid derivatives and their biological efficacy. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/32784935/
