Harmalol
Harmalol is a β-carbazine alkaloid with anticancer activity. Harmalol binds and interacts with several natural and synthetic nucleic acids of different motifs, including DNA and RNA. In addition, harmalol has an apoptosis-inducing effect on human hepatoma cells in vitro.
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- CAS No.: 525-57-5
- 화학식: C12H12N2O
- 분자량:200.24
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| Platelet | IC50 |
>130 μM
Compound: Harmalol
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Antiplatelet aggregation activity against collagen-induced platelet
Antiplatelet aggregation activity against collagen-induced platelet
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[PMID: 20329729] |
| Platelet | IC50 |
130 μM
Compound: Harmalol
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Antiplatelet activity in rabbit platelets assessed as inhibition of collagen-induced platelet aggregation
Antiplatelet activity in rabbit platelets assessed as inhibition of collagen-induced platelet aggregation
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[PMID: 21983333] |
Chemical Information
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CAS No. 525-57-5
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분자량 200.24
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화학식 C12H12N2O
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SMILES
CC1=NCCC2=C1NC3=C2C=CC(O)=C3
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Structure Classification
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Initial Source
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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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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Liver Cancer Modeling
Liver cancer can be classified into primary liver cancer and secondary liver cancer. Secondary liver cancer is the metastatic liver cancer. Primary liver cancer includes hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC) and fibrolamellar HCC, of which HCC is the most common form, accounting for approximately 90% of primary liver cancers[1]. HCC mouse models include chemical agent-induced models, transplanted tumor models, and genetic engineered models.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)