BYBC-1
BYBC‑1 is a selective G4‑RNA‑targeting ligand with high affinity forKRAS and NRAS G4‑RNAs (Kd = 0.05-0.28 μM). BYBC‑1 stabilizes G4‑RNA structures in KRAS and NRAS mRNA, blocks thePI3K/AKT and MAPK/ERK pathways, activates the DNA damage response (DDR), suppresses energy metabolism, and induces S‑phase arrest and apoptosis. BYBC‑1 exhibits high selectivity over non‑malignant fibroblasts and significantly inhibits the growth of HCT‑116 xenograft tumors in vivo. BYBC‑1 can be used for the study of colorectal cancer.
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- CAS No.: 2563902-57-6
- 화학식: C25H23BrN2O2S
- 분자량:495.43
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보관:
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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Biological Activity
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Chemical Information
- 순도&문서
- References
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Help & FAQs
Biological Activity
BYBC-1 shows potent antiproliferative activity against cancer cells at 48 h with IC50 values of 1.09 μM (HCT-116), 2.88 μM (SW480), 1.38 μM (PANC-1), 2.19 μM (A549), 2.88 μM (MDA-MB-231), 4.74 μM (SK-MEL-2), 4.13 μM (HepG2), and 3.56 μM (HeLa), while exhibiting > 20-fold selectivity over nonmalignant HFF1 and BJ fibroblasts (IC50 > 20 μM)[1]
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BYBC-1 (0.5-2 μM; 48 h) downregulates KRAS and NRAS protein expression in HCT-116 cells[1]
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BYBC-1 (0.5-2 μM; 48 h) inhibits PI3K/AKT and MAPK/ERK pathways in HCT-116 cells[1]
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BYBC-1 (0.5-2 μM; 48 h) reactivates the DNA damage response, inhibits HR, BER, NER and MMR repair pathways, increases phosphorylation of CHK1 and CHK2, and induces S‑phase arrest in HCT‑116 cells[1]
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BYBC-1 (0.5-2 μM; 3 h) suppresses mitochondrial respiration and glycolysis in HCT-116 cells[1]
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BYBC-1 (0.5-2 μM; 48 h) inhibits migration and induces apoptosis in HCT‑116 cells[1]
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BYBC-1 (0.5-2 μM; 8 days) inhibits growth of HCT-116 multicellular tumor spheroids[1]
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MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HCT-116 (colorectal cancer), PANC-1 (pancreatic cancer), MDA-MB-231 (breast cancer), HFF1 (human fibroblast), BJ (human fibroblast)
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:48 h
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Result:Exhibited potent antiproliferative activity with > 20-fold selectivity over nonmalignant fibroblast cells.
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Cell Line:HCT-116 (colorectal cancer))
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:48 h
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Result:Dose-dependently reduced colony formation and cell proliferation.
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Cell Line:HCT-116 (colorectal cancer)
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:48 h
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Result:Dose-dependently reduced protein levels of KRAS, NRAS, VEGF, and TRF2 without affecting their mRNA expression. Decreased phosphorylation levels of PI3K, AKT, MEK, and ERK.
Increased phosphorylation of ATM, ATR, CHK1, CHK2, p53, and γ-H2A.x.
Promoted cleavage of caspase 3 and caspase 9.
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Cell Line:HCT-116 (colorectal cancer), HFF1 (human fibroblast), BJ (human fibroblast)
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Concentration:0.5 μM, 1 μM, 2 μM, >20 μM
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Incubation Time:48 h
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Result:Showed low cytotoxicity to nonmalignant fibroblast cells (IC50 > 20 μM) while exerting potent cytotoxicity to colorectal cancer cells.
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Cell Line:HCT-116 (colorectal cancer)
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:48 h
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Result:Dose-dependently increased apoptotic rate. Upregulated cleaved-caspase 3 and cleaved-caspase 9.
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Cell Line:HCT-116 (colorectal cancer)
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:48 h
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Result:Dose-dependently arrested cells at S phase and downregulated DNA replication-related proteins (Lig1, FEN1, RPA1, PCNA, MCM4).
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Cell Line:HCT-116 (colorectal cancer))
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:48 h
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Result:Inhibited DNA repair pathways including HR, BER, NER, and MMR at the transcriptional level.
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Cell Line:HCT-116 (colorectal cancer))
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:48 h
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Result:Co-localized with G4-RNA in the cytoplasm, confirming specific targeting of G4-RNA structures. Increased γ-H2A.x, which indicating DNA double-strand breaks.
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Cell Line:HCT-116 (colorectal cancer))
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Concentration:0.5 μM, 1 μM, 2 μM
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Incubation Time:48 h
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Result:Dose-dependently reduced the number of migrated cells.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male BALB/C nude mice (5 weeks old) bearing HCT-116 subcutaneous xenografts[1].
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Dosage:2.5 mg/kg, 5.0 mg/kg, 10.0 mg/kg
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Administration:Intraperitoneal (i.p.) ; once every two days; for 14 days
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Result:All mice survived and remained healthy throughout the 14-day experimental period, with no significant changes in body weight observed among groups, indicating good biocompatibility.
2.5 mg/kg, 5.0 mg/kg and 10.0 mg/kg achieved tumor growth inhibition (TGI) of 29.7%, 56.2% and 78.3 % respectively.
Apoptosis detection showed significantly increased apoptotic cells in the treatment groups via TUNEL and cleaved-caspase3 staining.
Chemical Information
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CAS No. 2563902-57-6
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분자량 495.43
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화학식 C25H23BrN2O2S
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SMILES
CC1(C(/C=C2N(C3=C(S/2)C=CC=C3)C)=[N+](C4=CC=C5C(C=CC=C5)=C41)CC(O)=O)C.[Br-]
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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.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
BYBC-1 Related Classifications
HY-181284 Related Classifications
Powered by Bioz
- BYBC-1
- 2563902-57-6
- BYBC1
- BYBC 1
- G-quadruplex
- DNA/RNA Synthesis
- Ras
- PI3K
- Akt
- ERK
- Caspase
- Apoptosis
- G4-RNA-targeting ligand
- KRAS/NRAS G4-RNA structure
- PI3K/AKT pathways
- MAPK/ERK pathways
- DNA damage response (DDR)
- Cell cycle arrest and apoptosis
- HCT-116 cells
- Colorectal Cance
- HCT-116 xenograft mouse model
- Inhibitor
- inhibitor
- inhibit