Artemisinin

Antimalarial; inhibits P-type ATPase (PfATP6) of P.falciparum CAS# 63968-64-9

Artemisinin

Catalog No. BCN5814----Order now to get a substantial discount!

Product Name & Size Price Stock
Artemisinin: 5mg Please Inquire In Stock
Artemisinin: 10mg Please Inquire In Stock
Artemisinin: 20mg Please Inquire Please Inquire
Artemisinin: 50mg Please Inquire Please Inquire
Artemisinin: 100mg Please Inquire Please Inquire
Artemisinin: 200mg Please Inquire Please Inquire
Artemisinin: 500mg Please Inquire Please Inquire
Artemisinin: 1000mg Please Inquire Please Inquire

Quality Control of Artemisinin

Number of papers citing our products

Chemical structure

Artemisinin

3D structure

Chemical Properties of Artemisinin

Cas No. 63968-64-9 SDF Download SDF
PubChem ID 68827 Appearance White powder
Formula C15H22O5 M.Wt 282.3
Type of Compound Sesquiterpenoids Storage Desiccate at -20°C
Synonyms Qinghaosu
Solubility DMSO : 50 mg/mL (177.10 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)
SMILES CC1CCC2C(C(=O)OC3C24C1CCC(O3)(OO4)C)C
Standard InChIKey BLUAFEHZUWYNDE-NNWCWBAJSA-N
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Artemisinin

The herb of Artemisia annua L.

Biological Activity of Artemisinin

DescriptionArtemisinin is a sesquiterpene endoperoxide which is a potent antimalarial agent. Artemisinin is active against different bacteria and certain fungal species. It inhibits tumor necrosis factor-α-induced vascular smooth muscle cell proliferation.
TargetsTNF-α | Antifection
In vitro

Impact of Artemisinin-based Combination Therapy on falciparum malaria in urban Kolkata: a clinic based report.[Pubmed: 25720645]

Jpn J Infect Dis. 2015;68(4):321-3.

In India, Artemisinin-based combination therapy (ACT; specifically artesunate + sulfadoxine-pyrimethamine) has been implemented for uncomplicated falciparum malaria since 2010. But for vivax malaria drug policy remained unchanged i.e., chloroqine and primaquine.
METHODS AND RESULTS:
We observed the impact of this intervention in urban Kolkata by analyzing data from the Malaria Clinic from 2001 to 2013. In Kolkata, we observed that Plasmodium vivax was perennial, whereas P. falciparum infection was seasonal. Before ACT implementation, the proportion of P. falciparum was as high as 50% and it steadily decreased during 4 successive years post intervention. No change was observed in the number of P. vivax cases.
CONCLUSIONS:
ACT may be an effective measure in reducing falciparum malaria cases. Artemisinin-derivative combination therapies should be explored in vivax malaria to reduce the overall burden of malaria.

Antimicrobial activity of artemisinin and its precursors.[Reference: WebLink]

Current Science, 2000 , 78 (6) :709-713.

Artemisinic acid and Arteannuin B are biogenetic precursors of Artemisinin, an important antimalarial produced by the herb Artemisia annua. These compounds have been screened for antimicrobial activity against a range of organisms.
CONCLUSIONS:
All the three compounds are active against different bacteria and certain fungal species.

In vivo

The antimalarial agent artesunate causes sperm DNA damage and hepatic antioxidant defense in mice.[Pubmed: 25726169]

Mutat Res Genet Toxicol Environ Mutagen. 2015 Jan 1;777:1-6.

Artesunate is an Artemisinin derivative effective against multidrug resistant malaria.
METHODS AND RESULTS:
We analyzed the effects of artesunate 40 mg/kg b.w. as a single dose (ART1) or 13.3mg/kg b.w. for 3 days at 24h intervals (ART2) on mice spermatozoa at morphological and molecular level, and hepatic antioxidant status following 24h and 35 days following exposures in vivo. Artesunate significantly reduced epididymal sperm count and increased the frequency of sperms with abnormal head morphology following 24h of exposure. Comet assay analysis revealed significant increase in DNA strand breaks in spermatozoa evidenced by about 3-fold increase in comet tail DNA and up to 10-fold increase in Olive tail moment following 35 days of artesunate treatment. The damage index was significantly higher in the treated groups (40.27 ± 6.62 and 37.07 ± 5.35 for ART1 and ART2 respectively) as compared to the control group (16.13 ± 3.21) indicating the genotoxic effect of artesunate. The significant reduction in GSH, SOD and increase in lipid peroxidation indicate involvement of oxidative mechanisms in artesunate induced toxicity in mice.
CONCLUSIONS:
The present study suggests that artesunate has the potential to breach the testis-blood barrier and cause toxicity to male germ cells which may have implications in male reproductive toxicity.

Protocol of Artemisinin

Kinase Assay

Artemisinin inhibits tumor necrosis factor-α-induced vascular smooth muscle cell proliferation in vitro and attenuates balloon injury-induced neointima formation in rats.[Pubmed: 25707499]

Clin Exp Pharmacol Physiol. 2015 Feb 24.

The aim of this study was to evaluate the effect of Artemisinin (ART) on rat vascular smooth muscle cell (VSMC) proliferation induced by tumour necrosis factor (TNF)-α, cell cycle arrest, and apoptosis, and its effect on neointima formation after balloon injury of rat carotid artery.
METHODS AND RESULTS:
Primary rat VSMC were identified by immunofluorescence assay. The proliferation of VSMC induced by TNF-α was significantly inhibited by ART treatment in a dose-dependent manner. Treatment with 100-μM ART significantly reduced the expression of proliferating cell nuclear antigen. In contrast, the same treatment arrested the cell cycle in G0/G1 phase. Western blot analysis showed that the cell cycle-related proteins cyclin D1, cyclin E, cyclin-dependent kinase 2, and cyclin-dependent kinase 4 were downregulated by ART in TNF-α-stimulated VSMC. For apoptosis induced by ART, cleaved caspase-3/-9 was detected, and the pro-apoptotic protein Bcl-2-associated X protein was upregulated while the anti-apoptotic protein Bcl-2 was downregulated.
CONCLUSIONS:
The results suggest that ART can effectively inhibit the proliferation of VSMC induced by TNF-α through the apoptotic induction pathway and cell cycle arrest. Also, balloon injury indicated that ART significantly inhibited neointima formation in the rat carotid arteries.

Artemisinin Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Artemisinin Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Artemisinin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.5423 mL 17.7117 mL 35.4233 mL 70.8466 mL 88.5583 mL
5 mM 0.7085 mL 3.5423 mL 7.0847 mL 14.1693 mL 17.7117 mL
10 mM 0.3542 mL 1.7712 mL 3.5423 mL 7.0847 mL 8.8558 mL
50 mM 0.0708 mL 0.3542 mL 0.7085 mL 1.4169 mL 1.7712 mL
100 mM 0.0354 mL 0.1771 mL 0.3542 mL 0.7085 mL 0.8856 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Organizitions Citing Our Products recently

 
 
 

Calcutta University

University of Minnesota

University of Maryland School of Medicine

University of Illinois at Chicago

The Ohio State University

University of Zurich

Harvard University

Colorado State University

Auburn University

Yale University

Worcester Polytechnic Institute

Washington State University

Stanford University

University of Leipzig

Universidade da Beira Interior

The Institute of Cancer Research

Heidelberg University

University of Amsterdam

University of Auckland
TsingHua University
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University

Background on Artemisinin

Artemisinin, a natural product that is widely used as an anti-malarial drug, is an inhibitor of HCV subgenomic replicon replication.

In Vitro:Artemisinin (3.125-100 μM) concentration-dependently suppresses Aβ25-35 induced cytotoxicity in PC12 cells. Artemisinin (25 μM) suppresses Aβ25-35-induced LDH release, apoptosis and ROS production, attenuates Aβ-induced mitochondrial membrane potential loss and caspase 3/7 activity increase, and stimulates the phosphorylation of ERK1/2 in a time- and concentration-dependent manner in PC12 cell. ERK 1/2 pathway mediates the protect effects of artemisinin in PC12 cells[1]. Artemisinin shows cytotoxic activity in MCF-7/Dox cell line with IC50 of 3.7±0.4 μg/mL after 24 h treatment. Besides, Artemisinin treatment of MCF-7 cells, sensitive and resistant to Dox and DDP, causes a decrease in expression of proteins such as LF, FTH1, and HEP. Artemisinin activates p38 MAPK-kinase cascade regardless of the oxidative stress due to inhibition of VEGF expression and cell migration[2]. Artemisinin (50, 100 or 200 mg) significantly inhibits isoflurane-induced hippocampal neuronal loss, decreases caspase-3-positive cell counts and also cleaves caspase-3 expression, and modulates the expression of apoptosis pathway proteins. Artemisinin modulates JNK/ERK 1/2 signalling and histone acetylation[3]. Artemisinin inhibits HCV replication in a dose-dependent manner with EC50 value of 167±38 µM. Artemisinin and its most potent analogues partially inhibit the in vitro replication of HCV by induction of reactive oxygen species (ROS)[4]. Artemisinin significantly inhibits VSMC proliferation in a dose-dependent manner. Artemisinin (1 mM) for 72 h significantly reduces the expression of proliferating cell nuclear antigen messenger RNA[5].

In Vivo:Artemisinin (50, 100 or 200 mg/kg b.wt/day, p.o.) prevents isoflurane-induced working memory impairments as observed in T-maze test. Artemisinin enhances spatial navigation and memory of rats exposed to isoflurane. Artemisinin-treated rats exhibit markedly better performance in comparison with isoflurane-alone-exposed rats[3].

References:
[1]. Zeng Z, et al. Artemisinin protects PC12 cells against β-amyloid-induced apoptosis through activation of the ERK1/2 signaling pathway. Redox Biol. 2017 Apr 4;12:625-633. [2]. Chekhun VF, et al. Artemisinin modulating effect on human breast cancer cell lines with different sensitivity to cytostatics. Exp Oncol. 2017 Mar;39(1):25-29. [3]. Xu G, et al. Neuroprotective effects of artemisinin against isoflurane-induced cognitive impairments and neuronal cell death involve JNK/ERK1/2 signalling and improved hippocampal histone acetylation in neonatal rats. J Pharm Pharmacol. 2017 Mar 12. [4]. Obeid S, et al. Artemisinin analogues as potent inhibitors of in vitro hepatitis C virus replication. PLoS One. 2013 Dec 11;8(12):e81783. [5]. Wang HY, et al. The effects of artemisinin on the proliferation and apoptosis of vascular smooth muscle cells of rats. Cell Biochem Funct. 2013 Sep 17.

Featured Products
New Products
 

References on Artemisinin

The antimalarial agent artesunate causes sperm DNA damage and hepatic antioxidant defense in mice.[Pubmed:25726169]

Mutat Res Genet Toxicol Environ Mutagen. 2015 Jan 1;777:1-6.

Artesunate is an Artemisinin derivative effective against multidrug resistant malaria. We analyzed the effects of artesunate 40 mg/kg b.w. as a single dose (ART1) or 13.3mg/kg b.w. for 3 days at 24h intervals (ART2) on mice spermatozoa at morphological and molecular level, and hepatic antioxidant status following 24h and 35 days following exposures in vivo. Artesunate significantly reduced epididymal sperm count and increased the frequency of sperms with abnormal head morphology following 24h of exposure. Comet assay analysis revealed significant increase in DNA strand breaks in spermatozoa evidenced by about 3-fold increase in comet tail DNA and up to 10-fold increase in Olive tail moment following 35 days of artesunate treatment. The damage index was significantly higher in the treated groups (40.27 +/- 6.62 and 37.07 +/- 5.35 for ART1 and ART2 respectively) as compared to the control group (16.13 +/- 3.21) indicating the genotoxic effect of artesunate. The significant reduction in GSH, SOD and increase in lipid peroxidation indicate involvement of oxidative mechanisms in artesunate induced toxicity in mice. The present study suggests that artesunate has the potential to breach the testis-blood barrier and cause toxicity to male germ cells which may have implications in male reproductive toxicity.

Impact of Artemisinin-Based Combination Therapy on Falciparum Malaria in Urban Kolkata: A Clinic-Based Report.[Pubmed:25720645]

Jpn J Infect Dis. 2015;68(4):321-3.

In India, Artemisinin-based combination therapy (ACT; specifically artesunate + sulfadoxine-pyrimethamine) has been implemented for uncomplicated falciparum malaria since 2010. But for vivax malaria drug policy remained unchanged i.e., chloroqine and primaquine. We observed the impact of this intervention in urban Kolkata by analyzing data from the Malaria Clinic from 2001 to 2013. In Kolkata, we observed that Plasmodium vivax was perennial, whereas P. falciparum infection was seasonal. Before ACT implementation, the proportion of P. falciparum was as high as 50% and it steadily decreased during 4 successive years post intervention. No change was observed in the number of P. vivax cases. ACT may be an effective measure in reducing falciparum malaria cases. Artemisinin-derivative combination therapies should be explored in vivax malaria to reduce the overall burden of malaria.

Artemisinin inhibits tumour necrosis factor-alpha-induced vascular smooth muscle cell proliferation in vitro and attenuates balloon injury-induced neointima formation in rats.[Pubmed:25707499]

Clin Exp Pharmacol Physiol. 2015 May;42(5):502-9.

The aim of this study was to evaluate the effect of Artemisinin (ART) on rat vascular smooth muscle cell (VSMC) proliferation induced by tumour necrosis factor (TNF)-alpha, cell cycle arrest, and apoptosis, and its effect on neointima formation after balloon injury of rat carotid artery. Primary rat VSMC were identified by immunofluorescence assay. The proliferation of VSMC induced by TNF-alpha was significantly inhibited by ART treatment in a dose-dependent manner. Treatment with 100-muM ART significantly reduced the expression of proliferating cell nuclear antigen. In contrast, the same treatment arrested the cell cycle in G0/G1 phase. Western blot analysis showed that the cell cycle-related proteins cyclin D1, cyclin E, cyclin-dependent kinase 2, and cyclin-dependent kinase 4 were downregulated by ART in TNF-alpha-stimulated VSMC. For apoptosis induced by ART, cleaved caspase-3/-9 was detected, and the pro-apoptotic protein Bcl-2-associated X protein was upregulated while the anti-apoptotic protein Bcl-2 was downregulated. The results suggest that ART can effectively inhibit the proliferation of VSMC induced by TNF-alpha through the apoptotic induction pathway and cell cycle arrest. Also, balloon injury indicated that ART significantly inhibited neointima formation in the rat carotid arteries.

Artemisinins target the SERCA of Plasmodium falciparum.[Pubmed:12931192]

Nature. 2003 Aug 21;424(6951):957-61.

Artemisinins are extracted from sweet wormwood (Artemisia annua) and are the most potent antimalarials available, rapidly killing all asexual stages of Plasmodium falciparum. Artemisinins are sesquiterpene lactones widely used to treat multidrug-resistant malaria, a disease that annually claims 1 million lives. Despite extensive clinical and laboratory experience their molecular target is not yet identified. Activated Artemisinins form adducts with a variety of biological macromolecules, including haem, translationally controlled tumour protein (TCTP) and other higher-molecular-weight proteins. Here we show that Artemisinins, but not quinine or chloroquine, inhibit the SERCA orthologue (PfATP6) of Plasmodium falciparum in Xenopus oocytes with similar potency to thapsigargin (another sesquiterpene lactone and highly specific SERCA inhibitor). As predicted, thapsigargin also antagonizes the parasiticidal activity of Artemisinin. DesoxyArtemisinin lacks an endoperoxide bridge and is ineffective both as an inhibitor of PfATP6 and as an antimalarial. Chelation of iron by desferrioxamine abrogates the antiparasitic activity of Artemisinins and correspondingly attenuates inhibition of PfATP6. Imaging of parasites with BODIPY-thapsigargin labels the cytosolic compartment and is competed by Artemisinin. Fluorescent Artemisinin labels parasites similarly and irreversibly in an Fe2+-dependent manner. These data provide compelling evidence that Artemisinins act by inhibiting PfATP6 outside the food vacuole after activation by iron.

The antimalaria agent artemisinin exerts antiangiogenic effects in mouse embryonic stem cell-derived embryoid bodies.[Pubmed:14615418]

Lab Invest. 2003 Nov;83(11):1647-55.

Artemisinin is widely used as an agent to treat malaria; the possible antiangiogenic effects of this compound are unknown. In the present study, the antiangiogenic effects of Artemisinin were investigated in mouse embryonic stem cell-derived embryoid bodies, which are a model system for early postimplantation embryos and which efficiently differentiate capillaries. Artemisinin dose dependently inhibited angiogenesis in embryoid bodies and raised the level of intracellular reactive oxygen species. Furthermore impaired organization of the extracellular matrix component laminin and altered expression patterns of matrix metalloproteinases 1, 2, and 9 were observed during the time course of embryoid body differentiation. Consequently accelerated penetration kinetics of the fluorescent anthracycline doxorubicin occurred within the tissue, indicating increased tissue permeability. Artemisinin down-regulated hypoxia-inducible factor-1alpha and vascular endothelial growth factor (VEGF) expression, which control endothelial cell growth. The antiangiogenic effects and the inhibition of hypoxia-inducible factor-1alpha and VEGF were reversed upon cotreatment with the free radical scavengers mannitol and vitamin E, indicating that Artemisinin may act via reactive oxygen species generation. Furthermore, capillary formation was restored upon coadministration of exogenous VEGF. The data of the present study suggest that the antiangiogenic activity of Artemisinin and the increase in tissue permeability for cytostatics may be exploited for anticancer treatment.

Artemisinin and its derivatives: an important new class of antimalarial agents.[Pubmed:11578659]

Pharmacol Ther. 2001 May-Jun;90(2-3):261-5.

Artemisinin and its derivatives are a potent new class of antimalarials, originated from Artemisia annua, L. The clinical efficacy of these drugs is characterized by an almost immediate onset and rapid reduction of parasitaemia. Their efficacy is high in such areas as well where multidrug-resistance is rampant, but in these areas, their combination with other (effective) antimalarials (e.g., mefloquine) is highly recommended. In this short review, the chemical structures, pharmacological properties, and clinical uses of Artemisinin drugs are discussed.

Description

Artemisinin (Qinghaosu), a sesquiterpene lactone, is an anti-malarial drug isolated from the aerial parts of Artemisia annua L. plants. Artemisinin inhibits AKT signaling pathway by decreasing pAKT in a dose-dependent manner. Artemisinin reduces cancer cell proliferation, migration, invasion, tumorigenesis and metastasis and has neuroprotective effects.

Keywords:

Artemisinin,63968-64-9,Qinghaosu,Natural Products, buy Artemisinin , Artemisinin supplier , purchase Artemisinin , Artemisinin cost , Artemisinin manufacturer , order Artemisinin , high purity Artemisinin

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: