|Source:||The herb of Artemisia annua L.|
|Biological Activity or Inhibitors:||1. Artemisinic acid shows antibacterial activity.
2. Artemisinic acid is a major precursor of artemisinin (an antimalaric compound), isolated as the active principles of the medicinal plant Artemisia annua L.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||4.268 mL||21.3402 mL||42.6803 mL||85.3606 mL||106.7008 mL|
|5 mM||0.8536 mL||4.268 mL||8.5361 mL||17.0721 mL||21.3402 mL|
|10 mM||0.4268 mL||2.134 mL||4.268 mL||8.5361 mL||10.6701 mL|
|50 mM||0.0854 mL||0.4268 mL||0.8536 mL||1.7072 mL||2.134 mL|
|100 mM||0.0427 mL||0.2134 mL||0.4268 mL||0.8536 mL||1.067 mL|
Food Chem Toxicol. 2013 Jan;51:225-30.
|Artemisinic acid inhibits melanogenesis through downregulation of C/EBP α-dependent expression of HMG-CoA reductase gene.[Pubmed: 23063590]|
|Cholesterol is associated with the regulation of melanogenesis which is the major physiological defense against solar irradiation. The present study was designed to determine the effects of Artemisinic acid on melanogenesis and its mechanisms of action in human epidermal melanocytes. In this study, we found that Artemisinic acid inhibited melanin content. The mRNA levels of microphthalmia-associated transcription factor (MITF) and its downstream genes tyrosinase, tyrosinase-related protein (TRP)-1, and TRP-2 were reduced by Artemisinic acid treatment. Additionally, the mRNA levels of melanogenesis-related genes (c-KIT, stem cell factor (SCF), and macrophage migration inhibitory factor (MIF)) were down-regulated by Artemisinic acid. Furthermore, cAMP production and protein kinase A (PKA) activity were suppressed by Artemisinic acid. Moreover, attempts to elucidate a possible mechanism underlying the Artemisinic acid-mediated effects revealed that Artemisinic acid regulated melanogenesis by inhibiting cholesterol synthesis through downregulation of the hydroxymethylglutaryl CoA (HMG CoA) reductase gene, which was mediated through reduced expression of the CCAAT/enhancer-binding protein (C/EBP) α gene. Taken together, these findings indicate that the inhibition of melanogenesis by Artemisinic acid occurs through reduced expression of the HMG CoA reductase gene, which is mediated by C/EBP α inhibition and suggest that Artemisinic acid may be useful as a hyperpigmentation inhibitor.|
J Cell Biochem. 2012 Jul;113(7):2488-99.
|Artemisinic acid is a regulator of adipocyte differentiation and C/EBP δ expression.[Pubmed: 22396222]|
|Adipocyte dysfunction is associated with the development of obesity. In this study, Artemisinic acid, which was isolated from Artemisia annua L., inhibited adipogenic differentiation of human adipose tissue-derived mesenchymal stem cells (hAMSCs) and its mechanism of action was determined. The mRNA levels of peroxidase proliferation-activated receptor (PPAR) γ and CCAAT/enhancer binding protein (C/EBP) α, late adipogenic factors, were reduced by Artemisinic acid. Moreover, the mRNA levels of the PPAR γ target genes lipoprotein lipase, CD36, adipocyte protein, and liver X receptor were down-regulated by Artemisinic acid. Artemisinic acid reduced expression of the C/EBP δ gene without impacting C/EBP β. In addition, attempts to elucidate a possible mechanism underlying the Artemisinic acid-mediated effects revealed that reduced expression of the C/EBP δ gene was mediated by inhibiting Jun N-terminal kinase (JNK). Additionally, Artemisinic acid also reduced the expression of the adipogenesis-associated genes glucose transporter-4 and vascular endothelial growth factor. In addition to the interference of Artemisinic acid with adipogenesis, Artemisinic acid significantly attenuated tumor necrosis factor-α-induced secretion of interleukin-6 by undifferentiated hAMSCs, thus influencing insulin resistance and the inflammatory state characterizing obesity. Taken together, these findings indicate that inhibiting adipogenic differentiation of hAMSCs by Artemisinic acid occurs primarily through reduced expression of C/EBP δ, which is mediated by the inhibition of JNK and suggest that aremisinic acid may be used as a complementary treatment option for obesity associated with metabolic syndrome.|