K-8012
Based on 1 Customer Validation
K-8012 is a Sulindac (HY-B0008) analog and RXRα antagonist with an IC50 of 9.2 µM. K-8012 inhibits the activation of AKT. K-8012 induces Apoptosis, redirecting the TNFα signaling pathway from survival to death. K-8012 exerts anticancer activity against lung cancer, prostate cancer, and breast cancer. K-8012 can be used in research related to lung cancer, prostate cancer, breast cancer, and hepatocellular carcinoma.
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 純度 : 99.51%
- CAS 番号: 1346513-17-4
- 分子式: C23H23FN4
- 分子量:374.45
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保管条件:Powder -20°C, 3 years ; In solvent -80°C, 6 months , -20°C, 1 month
生物活性
製品説明
IC50 & Target
[1]|
RXR α 9.2 μM (IC50) |
体外実験
K-8012 (0.1-100 μM) acts as an RXRα antagonist in HCT-116 colon cancer cells, and inhibits 9-cis-RA-induced RXRα transactivation with an IC50 of 9.2 μM[1].
K-8012 (0-50 μM; 48 h) potently inhibits the growth of A549 lung cancer cells, PC3 prostate cancer cells, ZR-75-1 breast cancer cells, and MB231 breast cancer cells in vitro[1].
K-8012 (1 h) inhibits TNFα-induced AKT activation in A549 lung cancer cells and other cancer cell lines in vitro[1].
K-8012 (40 μM; 4 h) redirects the TNFα signaling pathway from survival to death in A549 lung cancer cells, and induces significant apoptosis when combined with TNFα[1].
K-8012 (0.1-100 μM) inhibits the binding of 9-cis-RA-induced coactivator peptide to purified RXRα LBD, with an IC50 of 14.5 μM[1].
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:A549 lung cancer cells, PC3 prostate cancer cells, ZR-75-1 breast cancer cells, MB231 breast cancer cells
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Concentration:0 μM, 0.2 μM, 1 μM, 5 μM, 10 μM, 25 μM, 50 μM
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Incubation Time:48 h
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Result:Inhibited the growth of all tested cancer cell lines in a concentration-dependent manner.
Was significantly more effective than Sulindac at reducing cell viability.
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Cell Line:A549 lung cancer cells
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Concentration:40 μM; 10 ng/mL TNFα (co-incubated with K-8012)
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Incubation Time:4 h
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Result:Slightly induced PARP cleavage when treated alone.
Caused significant induction of PARP cleavage when combined with TNFα, indicating apoptosis.
化学情報
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CAS 番号 1346513-17-4
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性状 Solid
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分子量 374.45
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分子式 C23H23FN4
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Color Light yellow to yellow
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SMILES
CC1=C(CCC2=NN=NN2)C3=CC(F)=CC=C3/C1=C\C4=CC=C(C=C4)C(C)C
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Powder -20°C 3 years In solvent -80°C 6 months -20°C 1 month
プロトコル
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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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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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.
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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.
純度とドキュメンテーション
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データシート (274 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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取扱説明書 (2659 KB)
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)