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Carnosic acid

$118

  • Brand : BIOFRON

  • Catalogue Number : BD-P0010

  • Specification : 95.0%(HPLC)

  • CAS number : 3650-09-7

  • Formula : C20H28O4

  • Molecular Weight : 332.43

  • PUBCHEM ID : 65126

  • Volume : 25mg

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Catalogue Number

BD-P0010

Analysis Method

Specification

95.0%(HPLC)

Storage

-20℃

Molecular Weight

332.43

Appearance

Powder

Botanical Source

This product is isolated and purified from the herb of Rosmarinus officinalis L.

Structure Type

Category

SMILES

CC(C)C1=C(C(=C2C(=C1)CCC3C2(CCCC3(C)C)C(=O)O)O)O

Synonyms

Salvin/4a(2H)-Phenanthrenecarboxylic acid, 1,3,4,9,10,10a-hexahydro-5,6-dihydroxy-1,1-dimethyl-7-(1-methylethyl)-, (4aR,10aS)-/Carnosic acid/RoseOx/11,12-Dihydroxyabieta-8,11,13-trien-20-oic acid/Carnosic acid/(4aR,10aS)-5,6-dihydroxy-1,1-dimethyl-7-propan-2-yl-2,3,4,9,10,10a-hexahydrophenanthrene-4a-carboxylic acid/Carsonic acid/Carnosolic Acid

IUPAC Name

Density

1.2±0.1 g/cm3

Solubility

Methanol; Dichloromethane

Flash Point

274.2±26.6 °C

Boiling Point

506.4±50.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

QRYRORQUOLYVBU-VBKZILBWSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:3650-09-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

31631173

Abstract

BACKGROUND Lung cancer is one of the leading causes of cancer-related mortalities worldwide and majority of these deaths result from non-small cell lung cancer (NSCLC). The primary objective of this research was to determine the anticancer potential of carnosic acid, a plant derived abietane diterpene, against human lung cancer cells, as well as to determine its effects on cell migration and invasion, apoptosis, and the PI3K/AKT/m-TOR signaling pathway. MATERIAL AND METHODS Cell viability was evaluated by Cell Counting Kit-8 (CCK-8) assay; fluorescence microscopy using acridine orange/ethidium bromide stain and Comet assay were used to study cellular apoptosis. In vitro wound healing assay was used to study effects on cell migration; Transwell assay was used to study cell invasion after drug treatment. Western blot assay was used to study effects of carnosic acid on the PI3K/AKT/m-TOR signaling pathway. RESULTS It was shown that carnosic acid could inhibit the growth of A-549 human non-small cell lung carcinoma cells dose-dependently showing an IC₅₀ value of 12.5 μM. This growth inhibition of A-549 cells was mediated via apoptotic cell death as observed by fluorescence microscopy showing nuclear fragmentation and chromatin condensation. Carnosic acid, dose-dependently, also inhibited cell migration and invasion. Finally, western blot assay revealed that carnosic acid also led to inhibition of the PI3K/AKT/m-TOR signaling pathway. CONCLUSIONS In conclusion, our results showed that Carnosic acid has the potential to inhibit cancer cell growth in A-549 lung cancer cells by activating apoptotic death, inhibiting cell migration and invasion and suppressing PI3K/AKT/m-TOR signaling pathway.

Title

Antiproliferative Activity of Carnosic Acid is Mediated via Inhibition of Cell Migration and Invasion, and Suppression of Phosphatidylinositol 3-Kinases (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) Signaling Pathway.

Author

Zhao L1, Zhang J2, Fan Y3, Li Y4.

Publish date

2019 Oct 21

PMID

31408993

Abstract

The phenolic compounds of methanolic extracts of Salvia pomifera and Salvia fruticosa were identified by liquid chromatography tandem mass spectrometry. Carnosic acid and its metabolite carnosol were the most abundant terpene phenolic compounds of S. fruticosa, while they were completely absent in S. pomifera. The main terpene phenolic constituent of S. pomifera was 12-O-methylcarnosic acid and its mass/mass fragmentation pathway was explained. The detailed mechanism of carnosic acid oxidation to carnosol was suggested. The effects of Salvia extracts and/or carnosic acid, the main diterpene phenolic component of S. fruticosa, on the proliferation and cell cycle of two melanoma cell lines (A375, Mel JuSo) and human fibroblast cell line (HFF) were investigated by MTT assay, PI-exclusion assay and flow cytometry cell cycle analysis. Extract of S. fruticosa more efficiently than S. pomifera extract reduced the proliferation of the human melanoma cells. Carnosic acid showed the most significant effect. The first evidence that carnosic acid affects microtubule dynamics and arrests the cell cycle in the G2/M phase was provided. Collectively, our results demonstrate that these two Salvia species are plants of medicinal interest with perspective for further investigation. Carnosic acid could be the compound responsible for the biological activities of S. fruticosa extracts.

KEYWORDS

12-O-methylcarnosic acid; LC-MS; Salvia fruticosa; Salvia pomifera; cancer; carnosic acid; cell cycle; cytotoxicity; melanoma; microtubules

Title

Characterization of Phenolic Compounds and Antiproliferative Effects of Salvia pomifera and Salvia fruticosa Extracts.

Author

Koutsoulas A1, carnecka M2, Slanina J2, Toth J3, Slaninova I4.

Publish date

2019 Aug 12

PMID

31356939

Abstract

Inhibition the activity of glycosidase is an effective method for the treatment and prevention of diabetes. In this study, enzymatic kinetics, fluorescence spectrum experiment, starch granule digestion, molecular docking studies and animal’s studies were used to investigate the interaction mechanism of carnosic acid against two glycosidase (α-amylase and α-glucosidase). Enzymatic kinetics showed that carnosic acid inhibited α-amylase activity in a competitive manner and α-glucosidase activity in a non-competitive manner. The half inhibitory concentrations (IC50) of carnosic acid to α-amylase and α- glucosidase were (1.12 ± 0.31) and (0.08 ± 0.17), respectively. The fluorescence quenching experiments showed that the intrinsic fluorescence of α-amylase or α-glucosidase was quenched by forming a complex with carnosic acid, and there was only one binding site between carnosic acid and glycosidase. The starch granules were no longer hydrolyzed by α-amylase after the addition of carnosic acid, which indicated that carnosic acid inhibited the activity of α-amylase. Molecular docking study showed that carnosic acid binds to the amino acid residues of glycosidase through hydrogen bond and van der Waals force, which leads to the change of the molecular conformation of glycosidase and thus reduces the activity of glycosidase. The experiment on mice showed that carnosic acid could effectively reduce postprandial blood glucose in mice.

Copyright © 2019 Elsevier B.V. All rights reserved.

KEYWORDS

Carnosic acid; Interaction mechanism; α-Amylase; α-Glucosidase

Title

Interaction mechanism of carnosic acid against glycosidase (α-amylase and α-glucosidase).

Author

Wang H1, Wang J2, Liu Y2, Ji Y2, Guo Y3, Zhao J4.

Publish date

2019 Oct 1


Description :

Carnosic acid inhibits the proliferation and migration capacity of human colorectal cancer cells.[Pubmed: 22246562 ]Oncol Rep. 2012 Apr;27(4):1041-8. Cell lines:Human colon carcinoma cell lines, Caco-2, HT29 and LoVo Concentrations: 0 to 388 μM Incubation Time: 24 h Method: Cells (1×104) are seeded in 96-well microplates in complete medium. After 48 h, cells are washed twice with PBS and treated with RE, RA and CA (concentration range from 0 to 388 μM) in complete medium for 24 h. Cell viability is assessed.