Artemisinin B
Artemisinin B is an orally active sesquiterpene natural product with anti-neuroinflammatory activity, which can be found in Artemisia annua Linn.. Artemisinin B suppresses the TLR4-MyD88-NF-κB signaling pathway by reducing the protein levels of TLR4 and MyD88, as well as inhibiting the mRNA expression of NF-κB p65. Artemisinin B reduces the expression of pro-inflammatory cytokines and attenuates synaptic loss, which can be used for the research of cognitive and behavioral impairments in Alzheimer's disease. Artemisinin B shows no cytotoxicity against human cardiomyocytes and exhibits very weak binding to hERG, suggesting its potential for cardioprotective property research.
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- CAS No.: 145941-07-7
- Formule: C15H22O4
- Masse moléculaire:266.33
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Artemisinin B (1-128 μM; 24 h) shows no obvious cytotoxicity in BV2 cells at low concentrations (≤8 μM), but exhibits concentration-dependent cytotoxicity at higher concentrations (>16 μM)[1].
Artemisinin B (1-128 μM; 24 h) reduces nitric oxide (NO) production in LPS(HY-D1056)-stimulated BV2 cells in a dose-dependent manner[1].
Artemisinin B (1-8 μM; 2 h pretreatment followed by 24 h co-incubation) decreases the mRNA expression levels of inflammatory cytokines (IL-1β, IL-6, and TNF-α) and key signaling molecules (MyD88 and NF-κB p65) in LPS-stimulated BV2 cells[1].
Artemisinin B (1-8 μM; 4 h pretreatment followed by 30 min co-incubation) inhibits the TLR4-MyD88-NF-κB signaling pathway by reducing the protein levels of TLR4 and MyD88 in LPS-stimulated BV2 cells[1].
Artemisinin B exhibits very weak binding affinity for the hERG channel (LBE = -4.467 kcal/mol) in a molecular docking assay and shows no obvious cytotoxicity in AC16 cardiomyocytes (≤100 μM; 24 h), indicating good cardiac safety[2].
Artemisinin B (10 μM; 24 h) produces a transcriptomic profile highly similar to that of the cardioprotective agent Dexrazoxane (HY-B0581) in AC16 cardiomyocytes and significantly upregulates the expression of seven cardiotoxicity-related marker genes, including APP and CCND1[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:BV2 cells
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Concentration:1, 2, 4, 8, 16, 32, 48, 64, and 128 μM
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Incubation Time:24 h
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Result:Showed no obvious cytotoxicity at low concentrations (≤ 8 μM), but exhibited dose-dependent cytotoxicity at higher concentrations (> 16 μM).
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Cell Line:AC16 cardiomyocytes
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Concentration:Up to 100 μM (with serial dilutions)
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Incubation Time:24 h
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Result:Showed no cellular cytotoxicity, maintaining cell viability comparable to the cardioprotective control compound dexrazoxane.
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Cell Line:BV2 cells
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Concentration:1, 2, 4, and 8 μM
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Incubation Time:Pretreated for 2 h, followed by LPS stimulation for 24 h
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Result:Dose-dependently decreased the mRNA expression of inflammatory cytokines (IL-1β, IL-6, and TNF-α) and key signaling molecules (MyD88 and NF-κB p65).
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Cell Line:BV2 cells
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Concentration:1, 2, 4, and 8 μM
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Incubation Time:Pretreated for 4 h, followed by LPS stimulation for 30 min
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Result:Alleviated the LPS-induced upregulation of TLR4 and MyD88 protein levels.
Artemisinin B (0.0625-1.0 pg/mL; yolk sac microinjection; single injection at 48 h post-fertilization) shows good safety in zebrafish larvae with no obvious toxicity, causing only slight cardiotoxicity, while the mortality rate and incidence of pericardial edema remain below 10%[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:KM mice (male, 17-20 g) [1]
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Dosage:20, 40, and 80 mg/kg
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Administration:Oral gavage (p.o.); once daily for 3 weeks
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Result:Significantly improved learning and memory in Aβ25-35-induced dementia mice, as shown by increased escape rate, platform crossings, and target quadrant swimming distance in the Morris water maze, as well as prolonged dark chamber latency and reduced error times in the step-through test.
Showed no significant effects on mental state or spontaneous locomotor activity in the open field test.
Preserved hippocampal CA1 neuronal morphology, preventing loss of Nissl bodies and synaptophysin-1.
Inhibited microglial activation in hippocampal CA1 by significantly reducing IBA-1 expression.
Alleviated neuroinflammation by increasing IL-10 and decreasing TNF-α levels in both cortical and hippocampal tissues.
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Animal Model:Zebrafish Larvae Model[2]
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Dosage:0.0625, 0.125, 0.25, 0.5, and 1.0 pg/ml
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Administration:Yolk sac microinjection; single injection at 48 h post-fertilization
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Result:Demonstrated an excellent safety profile with no toxic effects at doses up to 1.0 pg/mL.
Showed only slight cardiotoxicity in the picomolar range, with mortality and pericardial edema incidence remaining below 10%, within the range of normal biological variation or experimental error.
Chemical Information
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CAS No. 145941-07-7
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Masse moléculaire 266.33
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Formule C15H22O4
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SMILES
O[C@@]12[C@@H](CC[C@H]([C@]1([H])CC=C([C@H]2O)C)C)C(C(O)=O)=C
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Structure Classification
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Initial Source
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Pureté et documentation
Références
[1]. Qiang W, et al. Artemisinin B Improves Learning and Memory Impairment in AD Dementia Mice by Suppressing Neuroinflammation. Neuroscience. 2018 Dec 15;395:1-12. [Content Brief]
[2]. Kadioglu O, et al. Selection of safe artemisinin derivatives using a machine learning-based cardiotoxicity platform and in vitro and in vivo validation. Arch Toxicol. 2021 Jul;95(7):2485-2495. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Artemisinin B Related Classifications
HY-125447 Related Classifications
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