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

BYBC-1 是高选择性 RNA G-四链体 (G4) 靶向配体，对 KRAS、NRAS 的 G4-RNAs 具有高亲和力 (Kd=0.05-0.28 μM) 。BYBC-1通过稳定 KRAS、NRAS 的 G4-RNA 结构，阻断 PI3K/AKT、MAPK/ERK 通路，激活 DNA 损伤应答 (DDR) ，抑制能量代谢，诱导 S 期阻滞与凋亡 (apoptosis)。BYBC-1 对非恶性成纤维细胞具有较高的特异性，体内可显著抑制 HCT-116 移植瘤的生长。BYBC-1 可用于结直肠癌相关研究。

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BYBC-1

BYBC-1 Chemical Structure

CAS No. : 2563902-57-6

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BYBC-1 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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].

体外研究
(In Vitro)

BYBC-1 展现出强效的抗癌细胞增殖活性 (48 h)，其 IC50值如下：HCT-116 (1.09 μM)、SW480 (2.88 μM)、PANC-1 (1.38 μM)、A549 (2.19 μM)、MDA-MB-231 (2.88 μM)、SK-MEL-2 (4.74 μM)、HepG2 (4.13 μM) 及 HeLa (3.56 μM) 细胞，同时对非恶性成纤维细胞 (HFF1 和 BJ 细胞，IC50>20 μM) 相比具有 > 20 倍的选择性[1]。
BYBC-1 (0.5-2 μM；48 h) 可下调 HCT-116 细胞中 KRAS 及 NRAS 蛋白表达[1]。
BYBC-1 (0.5-2 μM；48 h) 可抑制 HCT-116 细胞中 PI3K/AKT 及 MAPK/ERK 通路[1]。
BYBC-1 (0.5-2 μM；48 h) 可激活 HCT-116 细胞的 DNA 损伤应答，抑制 HR、BER、NER 及 MMR 修复通路，升高 CHK1、CHK2 磷酸化水平，并诱导 S 期阻滞 [1]。
BYBC-1 (0.5-2 μM；3 h) 可抑制 HCT-116 细胞的线粒体呼吸和糖酵解[1]。
BYBC-1 (0.5-2 μM；48 h) 可抑制 HCT-116 细胞迁移和细胞凋亡 [1]。
BYBC-1 (0.5-2 μM；8 days) 可抑制 HCT-116 多细胞肿瘤球生长[1]。

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

BYBC-1 相关抗体:

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.
体内研究
(In Vivo)

BYBC-1 (2.5-10.0 mg/kg；腹腔注射；每两天一次；连续 14 天) 可抑制 HCT-116 异种移植小鼠的肿瘤生长，且具有良好的生物相容性[1]。

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.
分子量

495.43

Formula

C25H23BrN2O2S
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

BYBC-1 相关分类

  • 摩尔计算器

  • 稀释计算器

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
× = ×
C1   V1   C2   V2
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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