Ly101-4B
Ly101-4B is an apoptosis inducer and multi-target inhibitor with antiproliferative, antitumor and cycytotoxic effects. Ly101-4B reduces HSF1 expression, inhibits microRNA-214 synthesis, downregulates HSP27, HSP70 and HSP90 expression, while suppressing E2F-dependent transcriptional activity and downregulating its target genes. Ly101-4B induces caspase 3/7-mediated apoptosis by reducing DNA synthesis, inhibiting the cell cycle and G1/S phase transition, without affecting RNA synthesis or inducing necrosis. Ly101-4B is selective for pancreatic ductal adenocarcinoma cells with different genotypes and varying degrees of E2F dependence. Ly101-4B can be used in research related to epithelial ovarian cancer and pancreatic ductal adenocarcinoma.
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- CAS. Nr.: 1415728-94-7
- Formel: C23H30N4O5
- Molecular Weight:442.51
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
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- Verweise
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Help & FAQs
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Biologische Aktivität
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Caspase-3 |
Caspase-7 |
HSP70 |
HSP90 |
HSF1 |
Ly101-4B (20-100 μM; 24-48 h) inhibits the proliferation of human epithelial cisplatin-resistant ovarian cancer cell line SKOV3, induces its apoptosis, and downregulates the expression of HSF1, HSP27, HSP70 and HSP90 in these cells[1].
Ly101-4b (20-100 μM; 48 h) reduces the viability of primary Nupr1-deficient and Nupr1 wt; KIC pancreatic cancer cells, and exerts a significantly differential effect at the concentration of 100 μM[2].
Ly101-4B (1-25 μM; 12-72 h) inhibits E2F activity in MiaPaCa2 cells in luciferase activity assays using E2F-dependent reporter gene vectors[3].
Ly101-4B (25 μM; 12-72 h) reduces the viability of MiaPaCa2 cells, induces caspase 3/7-mediated apoptosis, and inhibits DNA synthesis, without affecting RNA synthesis or triggering necrosis[3].
Ly101-4B exhibits greater potency against primary PDAC cells with high E2F expression (CRCM93, CRCM08, CRCM17) than against those with low E2F expression (CRCM10, CRCM12, CRCM110, CRCM92), with a lower 72 h IC50 value (19.4 μM vs 44.1 μM)[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:SKOV3 human epithelial cisplatin-resistant ovarian cancer cells
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Concentration:60 μM (HSF1 protein depletion); 20-100 μM (cell viability assessment)
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Incubation Time:48 h (HSF1 protein depletion, cell viability assessment); 24 h (HSF1 mRNA measurement)
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Result:Efficiently inhibited cell proliferation with greater efficiency than cisplatin. Decreased HSF1 mRNA levels after 24 h of treatment.
Considerably depleted HSF1 protein expression after 48 h of treatment. Increased the percentage of early apoptotic cells from 5.0% to 19.0%. Accumulated the cleaved form of caspase9 (p35 segment).
Considerably decreased protein expression of HSP27, HSP70, and HSP90.
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Cell Line:primary Nupr1-deficient pancreatic cancer cells, primary Nupr1wt;KIC pancreatic cancer cells
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Concentration:20, 50, 100 μM
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Incubation Time:48 h
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Result:Induced a reduction in cell viability in both Nupr1-deficient and Nupr1wt; KIC cells starting from 20 μM. Showed activity comparable to that of gemcitabine from 50 μM.
Observed a significant differential response at 100 μM.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c-nu/nu (female, 4-week old)[1]
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Dosage:100 mg/kg
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Administration:i.p.; twice a week; 4 weeks
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Result:Significantly retarded tumor growth compared to control;
Detected few Ki-67-positive cells in treated tumors;
Sharply decreased HSF1-positive cells and staining intensity;
Depleted HSF1 mRNA and miR-214 levels in treated tumors.
Chemical Information
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CAS. Nr. 1415728-94-7
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Molecular Weight 442.51
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Formel C23H30N4O5
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SMILES
O[C@H]1[C@@H](O)[C@H](N2C(C(N)=O)=NC(C#CC3=CC=C(CCCCCCC)C=C3)=N2)O[C@@H]1CO
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
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Data Sheet (274 KB)
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SDS (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Handling Instructions (2659 KB)
Verweise
[1]. Chen YF, et al. Nucleoside analog inhibits microRNA-214 through targeting heat-shock factor 1 in human epithelial ovarian cancer. Cancer Sci. 2013;104(12):1683-1689. [Content Brief]
[2]. Cano CE, et al. Genetic inactivation of Nupr1 acts as a dominant suppressor event in a two-hit model of pancreatic carcinogenesis. Gut. 2014;63(6):984-995. [Content Brief]
[3]. Lan W, et al. E2F signature is predictive for the pancreatic adenocarcinoma clinical outcome and sensitivity to E2F inhibitors, but not for the response to cytotoxic-based treatments. Sci Rep. 2018;8(1):8330. Published 2018 May 29. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
Ly101-4B Related Classifications
HY-164184 Related Classifications
Powered by Bioz
- Ly101-4B
- 1415728-94-7
- Apoptosis
- Caspase
- HSP
- Early 2 Factor (E2F)
- DNA/RNA Synthesis
- epithelial ovarian cancer
- E2F transcription factor family
- apoptosis
- HSP70
- HSP27
- SKOV3 human epithelial cisplatin-resistant ovarian cancer cells
- MiaPaCa2 cells
- HO8910 human ovarian cancer cells
- pancreatic ductal adenocarcinoma cells
- heat shock factor 1 (HSF1)
- Inhibitor
- inhibitor
- inhibit