2. Cell Cycle/DNA Damage MAPK/ERK Pathway GPCR/G Protein PI3K/Akt/mTOR Stem Cell/Wnt Apoptosis
  3. G-quadruplex DNA/RNA Synthesis Ras PI3K Akt ERK Caspase Apoptosis
  4. 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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BYBC-1

BYBC-1 Chemical Structure

CAS No. : 2563902-57-6

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BYBC-1 Related Antibodies

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RNASE L DNA Polymerases RNA Polymerases Helicases DNA Ligase

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K-Ras H-Ras N-Ras Ras

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PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

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Akt Akt1 Akt2 Akt3

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ERK ERK1 ERK2 ERK5 ERK8

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Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

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Description

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[1].

In Vitro

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]
. BYBC-1 (0.5-2 μM; 48 h) downregulates KRAS and NRAS protein expression in HCT-116 cells[1]
. BYBC-1 (0.5-2 μM; 48 h) inhibits PI3K/AKT and MAPK/ERK pathways in HCT-116 cells[1]
. 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]
. BYBC-1 (0.5-2 μM; 3 h) suppresses mitochondrial respiration and glycolysis in HCT-116 cells[1]
. BYBC-1 (0.5-2 μM; 48 h) inhibits migration and induces apoptosis in HCT‑116 cells[1]
. BYBC-1 (0.5-2 μM; 8 days) inhibits growth of HCT-116 multicellular tumor spheroids[1]
.

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

BYBC-1 Related Antibodies

Cell Viability Assay[1]

Cell Line: HCT-116 (colorectal cancer), PANC-1 (pancreatic cancer), MDA-MB-231 (breast cancer), HFF1 (human fibroblast), BJ (human fibroblast)
Concentration: 0.5 μM, 1 μM, 2 μM
Incubation Time: 48 h
Result: Exhibited potent antiproliferative activity with > 20-fold selectivity over nonmalignant fibroblast cells.

Cell Proliferation Assay[1]

Cell Line: HCT-116 (colorectal cancer))
Concentration: 0.5 μM, 1 μM, 2 μM
Incubation Time: 48 h
Result: Dose-dependently reduced colony formation and cell proliferation.

Western Blot Analysis[1]

Cell Line: HCT-116 (colorectal cancer)
Concentration: 0.5 μM, 1 μM, 2 μM
Incubation Time: 48 h
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.

Cell Cytotoxicity Assay[1]

Cell Line: HCT-116 (colorectal cancer), HFF1 (human fibroblast), BJ (human fibroblast)
Concentration: 0.5 μM, 1 μM, 2 μM, >20 μM
Incubation Time: 48 h
Result: Showed low cytotoxicity to nonmalignant fibroblast cells (IC50 > 20 μM) while exerting potent cytotoxicity to colorectal cancer cells.

Apoptosis Analysis[1]

Cell Line: HCT-116 (colorectal cancer)
Concentration: 0.5 μM, 1 μM, 2 μM
Incubation Time: 48 h
Result: Dose-dependently increased apoptotic rate. Upregulated cleaved-caspase 3 and cleaved-caspase 9.

Cell Cycle Analysis[1]

Cell Line: HCT-116 (colorectal cancer)
Concentration: 0.5 μM, 1 μM, 2 μM
Incubation Time: 48 h
Result: Dose-dependently arrested cells at S phase and downregulated DNA replication-related proteins (Lig1, FEN1, RPA1, PCNA, MCM4).

RT-PCR[1]

Cell Line: HCT-116 (colorectal cancer))
Concentration: 0.5 μM, 1 μM, 2 μM
Incubation Time: 48 h
Result: Inhibited DNA repair pathways including HR, BER, NER, and MMR at the transcriptional level.

Immunofluorescence[1]

Cell Line: HCT-116 (colorectal cancer))
Concentration: 0.5 μM, 1 μM, 2 μM
Incubation Time: 48 h
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.

Cell Migration Assay [1]

Cell Line: HCT-116 (colorectal cancer))
Concentration: 0.5 μM, 1 μM, 2 μM
Incubation Time: 48 h
Result: Dose-dependently reduced the number of migrated cells.
In Vivo

BYBC-1 (2.5-10.0 mg/kg; i.p.; once every two days; for 14 days) inhibits tumor growth and exhibits good biocompatibility in HCT-116 xenograft mice[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Male BALB/C nude mice (5 weeks old) bearing HCT-116 subcutaneous xenografts[1].
Dosage: 2.5 mg/kg, 5.0 mg/kg, 10.0 mg/kg
Administration: Intraperitoneal (i.p.) ; once every two days; for 14 days
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.
Molecular Weight

495.43

Formula

C25H23BrN2O2S
CAS No.
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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Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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BYBC-1 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

BYBC-12563902-57-6BYBC1BYBC 1G-quadruplexDNA/RNA SynthesisRasPI3KAktERKCaspaseApoptosisPhosphoinositide 3-kinasePKBProtein kinase BExtracellular signal regulated kinasesG4-RNA-targeting ligandKRAS/NRAS G4-RNA structurePI3K/AKT pathwaysMAPK/ERK pathwaysDNA damage response (DDR)Cell cycle arrest and apoptosisHCT-116 cellsColorectal CanceHCT-116 xenograft mouse modelInhibitorinhibitorinhibit

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