Deacetyltanghinin
Deacetyltanghinin is a selective inhibitor targeting Na+/K+ ATPase, acting through non-covalent binding but is highly cardiotoxic. Deacetyltanghinin inhibits Na+/K+ ATPase activity, induces cancer cell apoptosis (involving caspase pathway activation), and at the same time affect the TXA2-PGI2 balance in the rabbit heart. Deacetyltanghinin has significant anti-cancer activity and is mainly used in the research field of targeted therapy of malignant tumors such as breast cancer and lung cancer. At the same time, attention should be paid to the regulation of its cardiotoxicity.
For research use only. We do not sell to patients.
- CAS No.: 4589-95-1
- Formula: C30H44O9
- Molecular Weight:548.66
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Caspase Isoforms
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Biological Activity
Description
IC50 & Target
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TXA2 |
Chemical Information
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CAS No. 4589-95-1
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Molecular Weight 548.66
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Formula C30H44O9
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SMILES
O[C@@]12[C@@]34[C@@](C[C@@]5([H])[C@@]([C@@]4([H])CC[C@@]1([C@@H](C(CO6)=CC6=O)CC2)C)(CC[C@@H](C5)O[C@H]7[C@H]([C@@H]([C@H]([C@@H](O7)C)O)OC)O)C)([H])O3
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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
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)