Home Transmembrane Transporters TRP Channel agonist Cinnamaldehyde

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Cinnamaldehyde TRP Channel agonist

Cat.No.S3763

Cinnamaldehyde is a flavonoid that is naturally synthesized by the shikimate pathway. Its supplementation can improve glucose and lipid homeostasis in diabetic animals; a TRPA1 agonist.
Cinnamaldehyde TRP Channel agonist Chemical Structure

Chemical Structure

Molecular Weight: 132.16

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Quality Control

Chemical Information, Storage & Stability

Molecular Weight 132.16 Formula

C9H8O

 Storage (From the date of receipt) 2 years  -20°C  liquid
CAS No. 14371-10-9 Download SDF Storage of Stock Solutions

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Mechanism of Action

Targets/IC50/Ki
TRPA1 [2]
In vitro
Cinnamaldehyde (40 μM) could enhance the expression of hormone-sensitive lipase (HSL), and suppress the expression of perilipin and glycerol-3-phosphate dehydrogenase as well as reduce adipocyte genes expression of peroxisome proliferator-activated receptor (PPAR)-γ and CCAAT/enhancer-binding protein-α (CEBP-α) in 3T3-L1 pre-adipocytes. It also increases expression of PPARδ and PPARγ as well as its targeted genes such as aP2 and CD36 in 3T3-L1 differentiated adipocytes. This compound treatment increases GLUT4 expression via activating peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) and triggering its downstream effector myocyte enhancer factors 2 (MEF2) in C2C12 cells. Its treatment regulates oxidative metabolism through increasing expressions of 5'-adenosine monophosphate-activated protein kinase (AMPK), NAD+-dependent deacetylases sirtuin 1, PGC-1α and cytochrome C as well as improving PPARα and PPARβ/δ expression, which contributes to mitochondrial biogenesis. However, it is demonstrated to inhibit mitochondrial metabolism by reducing basal and chemically-induced peak myotube oxidative metabolism in C2C12 cells[1]. This chemical exerts cytotoxic effects on human leukemia K562 cells by inducing apoptosis and synergizing the cytotoxicity of CIK cells against K562 cells[3].
In vivo
Cinnamaldehyde exhibits glucolipid lowering effects in diabetic animals by increasing glucose uptake and improving insulin sensitivity in adipose and skeletal muscle tissues, improving glycogen synthesis in liver, restoring pancreatic islets dysfunction, slowing gastric emptying rates, and improving diabetic renal and brain disorders. This compound exerts these effects through its action on multiple signaling pathways, including PPARs, AMPK, PI3K/IRS-1, RBP4-GLUT4, and ERK/JNK/p38MAPK, TRPA1-ghrelin and Nrf2 pathways. In addition, this compound seems to regulate the activities of PTP1B and α-amylase. Oral administration of this chemical ranging from 20mg/kg to 40 mg/kg per day for a duration lasting from 21 to 60 days results in a significant improvement in the levels of blood glucose and glycosylated hemoglobin (HbA1C) as well as insulin sensitivity in STZ-induced diabetic rats. It is not stable in the body, with the possibility of metabolizing into cinnamic acid and transforming into cinnamyl alcohol. Excessive doses of this compound may generate the toxic response. In human, 3% of this substance may cause skin irritation. It is demonstrated to decrease serum IL-1β and inhibit inflammatory gene expression (COX-2, MCP-1, TNF-α, and IL-6) in WAT of HFD insulted male Swiss albino mice and C57BLKS db/db mice, while increased expression of Cpt1a protects against pro-inflammatory adipokines release and promotes fatty acid oxidation, which contributes to an improvement in insulin resistance[1].
References

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT05654298 Completed
Migraine
Universitaire Ziekenhuizen KU Leuven
 March 15 2022 Not Applicable
NCT04183283 Completed
Healthy
Eli Lilly and Company
 December 12 2019 Phase 1
NCT04415892 Unknown status
Chemotherapy-induced Peripheral Neuropathy
Universitaire Ziekenhuizen KU Leuven
 October 1 2019 Not Applicable

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