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Formula | C15H24O5 |
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Molecular Weight | 284.35 | CAS No. | 71939-50-9 | ||||||||
Solubility (25°C)* | In vitro | DMSO | 50 mg/mL (175.83 mM) | ||||||||
Ethanol | 7 mg/mL (24.61 mM) | ||||||||||
Water | Insoluble | ||||||||||
In vivo (Add solvents to the product individually and in order) |
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* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.) |
Description | DHA (Dihydroartemisinin) is a semi-synthetic derivative of artemisinin and isolated from the traditional Chinese herb Artemisia annua. Dihydroartemisinin induces autophagy and apoptosis by suppressing NF-κB activation. | |
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Targets |
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In vitro | Dihydroartemisinin (DHA) inhibits the growth of certain cancer cell lines and xenograft tumors such as leukemia, glioma, fibrosarcoma, and breast, cervical, ovarian, lung, oral and pancreatic cancer. DHA inhibits cell and tumor growth by modulating various tumor-suppressive pathways, such as inhibiting cell proliferation and inducing apoptosis through regulation of proliferation- and apoptosis-related proteins.DHA inhibits the proliferation and viability of cells in a dose-dependent manner and induces apoptosis.DHA-mediated cytotoxicity is tumor selective. The endoperoxide bridge of DHA is reportedly essential for its cytotoxicity because it reacts with intracellular ferrous iron to generate reactive oxygen species or carbon-centered radicals, leading to cytotoxicity[1]. |
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In vivo | DHA significantly inhibited HCC cell growth in vitro and in vivo via inducing G2/M cell cycle arrest and apoptosis[2]. DHA has been shown in the rat whole embryo culture (WEC) to primarily affect primitive red blood cells (RBCs) causing subsequent tissue damage and dysmorphogenesis[3]. |
Cell Assay: |
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Animal Study: |
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, , Oncotarget, 2015, 6(7):5275-91.
, , J Exp Clin Cancer Res, 2017, 36(1):68
, , PLoS One, 2015, 10(3):e0120426.
Data from [Data independently produced by , , Biochem Pharmacol, 2018, 150:72-85]
Dihydroartemisinin remodels tumor micro-environment and improves cancer immunotherapy through inhibiting cyclin-dependent kinases [ Int Immunopharmacol, 2024, 139:112637] | PubMed: 39033659 |
Network-based prediction of anti-cancer drug combinations [ Front Pharmacol, 2024, 15:1418902] | PubMed: 39211773 |
A pH Fingerprint Assay to Identify Inhibitors of Multiple Validated and Potential Antimalarial Drug Targets [ ACS Infect Dis, 2024, 10.1021/acsinfecdis.3c00588] | PubMed: 38499199 |
Dihydroartemisinin, a potential PTGS1 inhibitor, potentiated cisplatin-induced cell death in non-small cell lung cancer through activating ROS-mediated multiple signaling pathways [ Neoplasia, 2024, 51:100991] | PubMed: 38507887 |
Resistance to FOXM1 inhibitors in breast cancer is accompanied by impeding ferroptosis and apoptotic cell death [ Breast Cancer Res Treat, 2024, 10.1007/s10549-024-07420-9] | PubMed: 38980505 |
Protocol for analysis of intracellular conversion of artezomib molecules into new proteasome inhibitors in Plasmodium falciparum parasites [ STAR Protoc, 2024, 5(1):102896] | PubMed: 38363687 |
Circulating extracellular vesicles are monitoring biomarkers of anti-PD1 response and enhancer of tumor progression and immunosuppression in metastatic melanoma [ J Exp Clin Cancer Res, 2023, 42(1):251] | PubMed: 37759291 |
Micromolar Dihydroartemisinin Concentrations Elicit Lipoperoxidation in Plasmodium falciparum-Infected Erythrocytes [ Antioxidants (Basel), 2023, 12(7)1468] | PubMed: 37508006 |
Dihydroartemisinin-induced ferroptosis in acute myeloid leukemia: links to iron metabolism and metallothionein [ Cell Death Discov, 2023, 9(1):97] | PubMed: 36928207 |
Dihydroartemisinin-induced ferroptosis in acute myeloid leukemia: links to iron metabolism and metallothionein [ Cell Death Discov, 2023, 9(1):97] | PubMed: 36928207 |
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