Diuvaretin
Diuvaretin is an antimalarial agent and a C-phenylated dihydrochalcone. Diuvaretin can be isolated from the roots of U. acuminata. Diuvaretin increases the activity of Caspase-3 and triggers Apoptosis. Diuvaretin exhibits antiparasitic activity against Plasmodium falciparum. Diuvaretin can be used in the research of promyelocytic leukemia and malaria.
For research use only. We do not sell to patients.
- CAS No.: 61463-04-5
- Formula: C30H28O6
- Molecular Weight:484.55
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
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Caspase-3 |
Plasmodium |
In Vitro
Diuvaretin (48 h) potently inhibits the proliferation of promyelocytic leukemia HL-60 cells, with an IC50 value of 6.1 μM[1].
Diuvaretin (10-20 μM; 24-48 h) induces morphological changes of apoptosis (chromatin condensation and nuclear degradation) in promyelocytic leukemia HL-60 cells[1].
Diuvaretin (5-20 μM; 6-24 h) induces G1 phase arrest and sub-G1 peak formation in promyelocytic leukemia HL-60 cells, while 5 μM Diuvaretin has no effect on cell cycle distribution[1].
Diuvaretin inhibits the growth of Plasmodium falciparum with an IC50 of 3.5 mg/mL[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:human promyelocytic leukemia HL-60 cells
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Concentration:dose-response
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Incubation Time:48 h
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Result:Exhibited dose-dependent growth inhibition of HL-60 cells, with an IC50 value of 6.1 μM.
Showed stronger cytotoxicity than isouvaretin and slightly stronger cytotoxicity than uvaretin.
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Cell Line:human promyelocytic leukemia HL-60 cells
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Concentration:5 μM, 10 μM, 20 μM
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Incubation Time:6 h, 12 h, 24 h
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Result:Induced accumulation of cells in the G1 phase and the appearance of a sub-G1 peak (indicative of apoptotic cells) at 10 μM or 20 μM for 12 h or 24 h.
Showed no cell cycle changes with 5 μM across 6-24 h incubation times.
Chemical Information
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CAS No. 61463-04-5
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Molecular Weight 484.55
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Formula C30H28O6
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SMILES
O=C(C=1C(O)=C(C(O)=C(C1OC)CC=2C=CC=CC2O)CC=3C=CC=CC3O)CCC=4C=CC=CC4
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Structure Classification
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Purity & Documentation
References
[1]. Nakatani N, et al. Induction of apoptosis in human promyelocytic leukemia cell line HL-60 by C-benzylated dihydrochalcones, uvaretin, isouvaretin and diuvaretin. Biol Pharm Bull. 2005 Jan;28(1):83-6. [Content Brief]
[2]. Makangara JJ, et al. A novel phenanthrenolide and C-benzyl dihydrochalcones from Uvaria puguensis. Nat Prod Lett. 2002;16(4):267-272. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Diuvaretin Related Classifications
HY-N13034 Related Classifications
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