2. Metabolic Enzyme/Protease Cell Cycle/DNA Damage Immunology/Inflammation NF-κB Apoptosis Autophagy
  3. Mitochondrial Metabolism DNA/RNA Synthesis Reactive Oxygen Species (ROS) Apoptosis Autophagy Caspase Bcl-2 Family Atg8/LC3
  4. XAN-5

XAN-5 是一种线粒体 DNA G-四链体 (mtG4) 配体，其 Kd 值为 3.8 μM。XAN-5 可选择性结合并稳定 mtG4 结构，从而破坏线粒体基因转录与 DNA 复制。XAN-5 可诱导线粒体功能障碍、活性氧 (ROS) 过量产生、G0 期阻滞及半胱天冬酶依赖性细胞凋亡 (apoptosis)。XAN-5 可抑制自噬 (autophagy) 并诱导免疫原性细胞死亡。XAN-5 可抑制小鼠肝癌模型中的肿瘤生长，同时增强肿瘤浸润性 CD4+ 和 CD8+ T 细胞。XAN-5 可同时靶向两种肿瘤耐药机制。XAN-5 可用于肝癌的相关研究。

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XAN-5

XAN-5 Chemical Structure

CAS No. : 3062796-70-4

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XAN-5 相关抗体

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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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Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

XAN-5 is a mitochondrial DNA G-quadruplex (mtG4) ligand with a Kd of 3.8 μM. XAN-5 selectively binds and stabilizes mtG4 structures, disrupting mitochondrial gene transcription and DNA replication. XAN-5 triggers mitochondrial dysfunction, ROS overproduction, G0 phase arrest and caspase-dependent apoptosis. XAN-5 inhibits autophagy and induces immunogenic cell death. XAN-5 inhibits tumor growth in a mouse liver cancer model while enhancing tumor-infiltrating CD4+ and CD8+ T cells. XAN-5 targets two cancer resistance mechanisms simultaneously. XAN-5 can be used for the research of liver cancer[1].

IC50 & Target[1]

Caspase-8

 

Caspase-9

 

Caspase-3

 

Bax

 

Bcl-2

 

bad

 

体外研究
(In Vitro)

XAN-5 (10 μM; 2 h) 可稳定 mtG4 模型 mt6363，其 ΔTm 为 10 °C[1]。
XAN-5 (5 μM; 30 min) 可选择性地在 HepG2 细胞的线粒体中富集[1]。
XAN-5 (0.25-4 μM; 24 h) 可强效抑制肝癌 HepG2 细胞的增殖 (IC50 = 1.8 μM)，同时对正常肝脏及乳腺上皮细胞的毒性较低[1]。
XAN-5 (1-4 μM; 24 h) 可显著降低 HepG2 细胞中 OXPHOS 基因 ATP6、CYTB 和 COX-1 的转录水平[1]。
XAN-5 (1-4 μM; 24 h) 可在体外以剂量依赖方式抑制 HepG2 细胞中的 mtDNA 复制，在 4 μM 浓度下可使 D-Loop 拷贝数降低 80%[1]。
XAN-5 (1-4 μM; 24 h) 可在 HepG2 细胞中诱导浓度依赖性的活性氧过量生成，线粒体膜电位耗散并降低 ATP 水平[1]。
XAN-5 (1-4 μM; 24 h) 于 1 μM 浓度时可诱导 HepG2 细胞发生 G0/G1 期阻滞，而 2 μM 和 4 μM 浓度则可使亚 G0 期凋亡细胞群分别逐步增加[1]。
XAN-5 (1-4 μM; 24 h) 可在 HepG2 细胞中诱导剂量依赖性细胞凋亡，4 μM 浓度下膜联蛋白 V 阳性细胞占比为 30%[1]。
XAN-5 (1-4 μM; 24 h) 可在体外以剂量依赖方式抑制 HepG2 细胞的自噬，其证据包括 LC3B-II 转化减少、p62 蓄积、ATG 基因表达受抑以及 DAPGreen 荧光强度降低，该效应由活性氧介导[1]。
XAN-5 (1-4 μM; 24 h) 可诱导 HepG2 细胞发生免疫原性细胞死亡，其特征为钙网蛋白表达上调、细胞表面钙网蛋白水平升高以及细胞外 ATP 水平上升[1]。
XAN-5 (0.25-4 μM; 0-7 days) 以浓度依赖性方式显著抑制 HepG2 细胞的迁移、集落形成以及 3D 肿瘤球体的生长[1]。

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

XAN-5 相关抗体:

Real Time qPCR[1]

Cell Line: HepG2 cells
Concentration: 1, 2, 4 μM
Incubation Time: 24 h
Result: Reduced ATP synthase subunit 6 (ATP6), Cytochrome b (CYTB), and cytochrome c oxidase subunit 1 (COX-1) expression.

Cell Cycle Analysis[1]

Cell Line: HepG2 cells
Concentration: 1, 2, 4 μM
Incubation Time: 24 h
Result: Induced G0/G1 phase arrest at 1 μM, increasing the proportion of cells in this phase from 57.9% to 60.9% while decreasing the G2/M phase population from 17.1% to 14.2%.
At 2 and 4 μM, progressively increased the sub-G0 phase (indicative of apoptotic cell death) from 8.9% to 12.2% and finally 30%, respectively.

Western Blot Analysis[1]

Cell Line: HepG2 cells
Concentration: 1, 2, 4 μM
Incubation Time: 24 h
Result: Led to cytochrome c release from mitochondria, cleavage of caspase-9, caspase-3, and PARP, activation of caspase-8, and cleavage of BID into truncated BID (tBID), confirming activation of both intrinsic (mitochondrial) and extrinsic (death receptor) apoptotic pathways.
Reduced Bcl-2 and Bad levels and increased Bax levels.

Cell Autophagy Assay[1]

Cell Line: HepG2 cells
Concentration: 1, 2, 4 μM
Incubation Time: 24 h
Result: Effectively downregulated the LC3B-II/LC3B-I ratio, caused accumulation of p62/SQSTM1, decreased expression of autophagy-related genes (ATG3, ATG5, ATG7, and ATG12), and reduced DAPGreen fluorescence intensity in a dose-dependent manner, indicating impaired autophagosome formation and autophagic flux inhibition.
Reversed by the ROS scavenger N-acetylcysteine, confirming ROS mediation.
体内研究
(In Vivo)

XAN-5 (10 mg/kg；每 48 小时一次，持续 6 天) 在 BALB/c 小鼠 H22 肝癌模型中可诱导肿瘤体积缩小 59%，抑制肿瘤细胞增殖，提高肿瘤浸润及脾脏中 CD4+ 和 CD8+ T 细胞的频率，且在测试剂量下未观察到明显的全身毒性[1]。

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

570.05

Formula

C29H28ClNO7S
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

XAN-5 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 *
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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:

XAN-53062796-70-4XAN5XAN 5Mitochondrial MetabolismDNA/RNA SynthesisReactive Oxygen Species (ROS)ApoptosisAutophagyCaspaseBcl-2 FamilyAtg8/LC3Autophagy-related 8| HepG2 cellsmitochondrial dysfunctionmouse liver cancer modelmtG4CD4+ T cellsreactive oxygen speciesmitochondrial DNA G-quadruplexautophagic fluxCD8+ T cellscaspase-dependent apoptosisInhibitorinhibitorinhibit

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