Salmonella species are targeted by the trans-cinnamaldehyde-β-cyclodextrin complex. as well as Listeria species. According to reference [1], the lowest inhibitory doses are 10 and 20 mg/mL.

Absorption, Distribution and Excretion
Cinnamaldehyde has a skin absorption rate of 52% and has been shown to be rapidly absorbed by the intestines. It is primarily metabolized and excreted in the urine, with a small amount excreted in the feces. Following oral or intraperitoneal injection of cinnamaldehyde in rats and mice, 69%–98% of the dose was recovered in urine and feces within 24 hours. This study investigated the bioavailability of microencapsulated cinnamaldehyde (CNMA) in male F344 rats. CNMA was dissolved in corn oil and administered to rats by gavage at doses of 50, 250, and 500 mg/kg, either as a microencapsulated formulation or pure CNMA. At all doses, there were no differences in CNMA plasma concentration curves or urinary hippuric acid excretion rates between the two formulations. Both formulations showed low bioavailability (<20%) at doses of 250 and 500 mg/kg. Regardless of the formulation used, gavage administration of CNMA significantly increased urinary hippuric acid excretion. Approximately 75% of the CNMA dose is metabolized to hippuric acid and excreted in the urine. The total amount of hippuric acid recovered in 50-hour urine collection correlated well with the CNMA dose. Data indicate that CNMA is completely released from the microcapsules, and microencapsulation of CNMA does not affect its bioavailability or metabolism…
Cinnamaldehyde may be oxidized to cinnamic acid in vivo, which is excreted in the urine as benzoic acid and hippuric acid.
Intraperitoneal injection of cinnamaldehyde in rats resulted in 6.5% excretion of thioethers in the urine.
Intraperitoneal injection of cinnamaldehyde in rabbits resulted in excretion in the urine as cinnamic acid, cinnamyl glycine, benzoic acid, and hippuric acid.
For more complete data on the absorption, distribution, and excretion of cinnamaldehyde (7 types), please visit the HSDB record page. Metabolites/Metabolites Metabolism of Cinnamaldehyde This study investigated the effects of trans-[3-14C]cinnamaldehyde in male and female Fischer 344 rats and CD1 mice. Administration was administered via intraperitoneal injection (2 mg/kg body weight) and gavage (250 mg/kg body weight), respectively. In male mice, administration was via gavage. Approximately 94% of the administered dose was recovered from excrement in both animals within 72 hours, with the majority (75-81%) present in urine from 0 to 24 hours. Less than 2% of the administered dose was detected in the animal carcasses 72 hours after administration. Urinary metabolites were identified by chromatographic characterization. The major urinary metabolite in both animals was hippuric acid, accompanied by 3-hydroxy-3-phenylpropionic acid, benzoic acid, and benzoyl glucuronide. Glycine conjugates of cinnamic acid were generated in large quantities only in mice. The oxidative metabolism of cinnamaldehyde was essentially the same as that of cinnamic acid, proceeding via a β-oxidation pathway similar to that of fatty acids. In addition to the common metabolites of cinnamic acid and cinnamaldehyde, 7% of 14C in rat urinary urine from 0–24 hours was composed of two novel metabolites, while in mice it was composed of three novel metabolites. Other studies have shown that these metabolites originate from a second pathway of cinnamaldehyde metabolism involving binding to glutathione. The excretion patterns and metabolic profiles of cinnamaldehyde in rats and mice were not systematically affected by sex, dose size, or route of administration. This paper discusses the relevance of these data to the safety assessment of trans-cinnamaldehyde, particularly the effectiveness of extrapolating high-dose toxicity data to low-dose toxicity data. /trans-cinnamaldehyde/ To assess the extent of cinnamaldehyde and cinnamyl alcohol metabolism in human skin and to provide evidence of the role of skin alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in this metabolism…we investigated the extent of cinnamyl alcohol and aldehyde metabolism in human skin homogenates and subcellular fractions…in the presence and absence of the ADH/cytochrome P450 inhibitor 4-methylpyrazole and the cytoplasmic ALDH inhibitor disulfiram, respectively. Differential metabolism of cinnamyl alcohol and cinnamaldehyde was observed in different subcellular fractions: the skin cytoplasm is considered the primary site of cinnamic compound metabolism. Significant metabolic inhibition with 4-methylpyrazole and disulfiram was observed only in whole skin homogenate and cytoplasmic fractions… This study demonstrates that skin ADH and ALDH activities located in specific subcellular compartments play a crucial role in the activation and detoxification of CAlc and CAld in the skin…
Intraperitoneal injection of cinnamaldehyde into rabbits resulted in the excretion of cinnamic acid, cinnamylglycine, benzoic acid, and hippuric acid in the urine.
Two sulfur-containing cinnamaldehyde metabolites, 3-S-(N-acetylcysteine)-3-phenylpropanol and 3-S-(N-acetylcysteine)-3-phenylpropionic acid, were identified in rat urine.
For more complete data on the metabolism/metabolites of cinnamaldehyde (6 in total), please visit the HSDB record page.
Cinnamaldehyde is a known metabolite of cinnarizine in humans. Cinnamaldehyde is converted to cinnamyl-CoA by cinnamoyl-CoA reductase.

Toxicity Summary
Cinnamaldehyde is an allergen. Its physiological effects are achieved through increased histamine release and cell-mediated immune responses. Toxicity Data
LD50: 3400 mg/kg (rat, oral) Interactions This study used Japanese medaka (Oryzias latipes) for a MELA (Metamorphosis and Larval Experiment) to determine the potential adverse effects of ethanol and the flavoring component cinnamaldehyde (CAD) on development… Medaka were exposed to 100 mM ethanol, 10, 1.0, 0.67, or 0.50 mM CAD, a combination of ethanol and CAD, or served as an untreated control group. 100 mM ethanol had no effect. Treatment with 10 mM and 1.0 mM CAD alone was lethal within 1 day after fertilization. Embryos exposed to 100 mM ethanol and 0.67 mM cinnamaldehyde (CAD) exhibited cardiovascular and pigmentary defects, and delayed hatching. Embryos exposed to 0.50 mM cinnamaldehyde alone showed milder cardiovascular problems compared to combined ethanol and cinnamaldehyde treatment. In summary, these results indicate that the combined effect of ethanol and cinnamaldehyde is greater than their individual effects, suggesting the need to monitor wastewater discharge from fish hatcheries to protect native fish populations.

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Non-human toxicity values
Rats oral LD50 3400 mg/kg
Mice oral LD50 200 mg/kg
Mice intraperitoneal LD50 200 mg/kg
Mice intravenous LD50 75 mg/kg
For more complete non-human toxicity data for cinnamaldehyde (8 values of total), please visit the HSDB records page.

[1]. A Facile One-Pot Synthesis of Amino Furans Using Trans-Cinnamaldehyde in the Presence of Nucleophilic Isocyanides. Acta Chimica Slovenica 54(3), 341-350, (2007).

[2]. Polysaccharide-based multilayered antimicrobial edible coating enhances quality of fresh-cut papaya.LWT--Food Science and Technology 47(1), 39-45, (2012).

(E)-Cinnamaldehyde is the E (trans) stereoisomer of cinnamaldehyde, which is the parent compound of the cinnamaldehyde class of compounds. It has multiple functions, including lowering blood sugar, acting as an EC 4.3.1.24 (phenylalanine ammonia-lyase) inhibitor, a vasodilator, an antifungal agent, a flavoring agent, a plant metabolite, and a sensitizer. It is a 3-phenylprop-2-enal, belonging to the cinnamaldehyde class of compounds. Cinnamaldehyde is a naturally occurring flavonoid compound that gives the spice cinnamon its unique flavor and aroma. It is naturally found in the bark of the cinnamon tree, as well as in plants of the genus Cinnamomum (such as camphor trees and cinnamon bark). Sensitivity to cinnamaldehyde can be detected through clinical patch testing. Cinnamaldehyde is a standardized chemical allergen. The physiological effects of cinnamaldehyde are achieved through increased histamine release and cell-mediated immunity. Cinnamaldehyde has been reported in turmeric (Curcuma xanthorrhiza), ginger (Alpinia latilabris), and several other organisms with relevant data. Cinnamaldehyde is the aldehyde that gives cinnamon its unique flavor and aroma. It is naturally found in the bark of cinnamon trees, as well as the bark of other cinnamon species such as camphor and cassia. These trees are the natural source of cinnamon, and cinnamon bark essential oil is approximately 90% cinnamaldehyde. Cinnamaldehyde is also used as a fungicide. It has been shown to be effective on more than 40 different crops and is typically applied to the plant roots. Its low toxicity and well-known properties make it ideal for agriculture. Cinnamaldehyde is also an effective insecticide to some extent, and its odor repels animals such as cats and dogs. It can also be used as a corrosion inhibitor for steel and other ferrous alloys in corrosive liquids. It can be mixed with other ingredients such as dispersants, solvents, and other surfactants. Concentrated cinnamaldehyde can irritate the skin, and large doses are toxic, but no organization currently suspects the compound is carcinogenic or poses a long-term health hazard. Most cinnamaldehyde is excreted in urine as cinnamic acid (the oxidized form of cinnamaldehyde). Cinnamaldehyde is a metabolite of Saccharomyces cerevisiae. Drug Indications Cinnamaldehyde has been approved by the U.S. Food and Drug Administration (FDA) for use in allergic skin patch testing, an auxiliary diagnostic test for allergic contact dermatitis (ACD) in individuals aged 6 years and older. Therapeutic Uses /EXPL THER/ Cinnamonum zeylanicum is widely used in traditional Indian medicine to treat diabetes. This study aimed to isolate and identify potential anti-diabetic compounds… Male diabetic Wistar rats induced by streptozotocin (STZ) (60 mg/kg body weight) were administered different doses (5, 10, and 20 mg/kg body weight) of cinnamaldehyde for 45 consecutive days. The results showed that plasma glucose concentrations were significantly reduced in a dose-dependent manner compared to the control group (p<0.05, a reduction of 63.29%). Furthermore, oral administration of cinnamaldehyde (20 mg/kg body weight) significantly reduced glycated hemoglobin (HbA1c), serum total cholesterol, and triglyceride levels, while significantly increasing plasma insulin, liver glycogen, and high-density lipoprotein cholesterol levels. In addition, cinnamaldehyde restored abnormal plasma enzyme levels (aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, alkaline phosphatase, and acid phosphatase) to near-normal levels. Administration of the reference drug glibenclamide (0.6 mg/kg body weight) also significantly reduced blood glucose concentration in streptozotocin (STZ)-induced diabetic rats (p < 0.05). These results indicate that cinnamaldehyde has hypoglycemic and lipid-lowering effects in STZ-induced diabetic rats.

C₉H₈O

132.16

132.057

14371-10-9

637511

Colorless to light yellow liquid

1.0±0.1 g/cm3

246.8±9.0 °C at 760 mmHg

−9-−4 °C(lit.)

71.1±0.0 °C

0.0±0.5 mmHg at 25°C

1.577

2.12

0

1

2

10

121

0

O=C([H])/C(/[H])=C(\[H])/C1C([H])=C([H])C([H])=C([H])C=1[H]

KJPRLNWUNMBNBZ-QPJJXVBHSA-N

InChI=1S/C9H8O/c10-8-4-7-9-5-2-1-3-6-9/h1-8H/b7-4+

(E)-3-phenylprop-2-enal

transCinnamaldehyde; trans Cinnamaldehyde

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL (~378.33 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (18.92 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (18.92 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (18.92 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)