2. Apoptosis Cell Cycle/DNA Damage Immunology/Inflammation NF-κB Metabolic Enzyme/Protease
  3. Ferroptosis DNA Alkylator/Crosslinker DNA/RNA Synthesis Apoptosis Reactive Oxygen Species (ROS)
  4. HJ03

HJ03 是一种可透过血脑屏障的、口服有效的 DNA 损伤和铁死亡 (ferroptosis) 诱导剂。HJ03 通过增加细胞内 ROS、Fe2+ 蓄积和脂质过氧化作用触发铁死亡。HJ03 可诱导 DNA 加合物和链间交联，阻断 DNA 复制与转录，使细胞停滞于 G2/M 期并诱导细胞凋亡 (apoptosis)。HJ03 可用于多形性胶质母细胞瘤和结直肠癌的研究。

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HJ03

HJ03 Chemical Structure

CAS No. : 3028123-48-7

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HJ03 相关抗体

Top Publications Citing Use of Products

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

HJ03 is a blood-brain barrier-permeable, orally active DNA damage and ferroptosis inducer. HJ03 triggers ferroptosis by increasing intracellular ROS, Fe2+ accumulation and lipid peroxidation. HJ03 induces DNA adducts and interstrand crosslinks, blocks DNA replication and transcription, arrests cells at the G2/M phase and induces apoptosis. HJ03 can be used in the research of glioblastoma multiforme and colorectal cancer[1].

体外研究
(In Vitro)

HJ03 (24-72 h) 可强效抑制 U251、U87、T98G、HCT116、MSH6 缺失型 U251 及 MSH6 缺失型 T98G 细胞的活力，在 24、48、72 h 孵育条件下的 IC50 值范围为 0.8914 μM 至 61.65 μM，且其活性与 MGMT 和 MSH6 状态无关[1]。
HJ03 (0.25-8 μM; 14 days) 呈剂量依赖性抑制 U251、U87 和 T98G 细胞的集落形成[1]。
HJ03 (4-16 μM; 72 h) 可抑制 U87 球状体活力并诱导细胞死亡，其中 16 μM 可导致球状体近乎完全死亡[1]。
HJ03 (1-5 μM; 48-72 h) 诱导 U251 和 U87 细胞发生 G2/M 期阻滞，并可调节 U251、U87 及 T98G 细胞中细胞周期相关蛋白 (p21、p-CDK1、CDK1、cyclin B1)[1]。
HJ03 (1-40 μM; 48-72 h) 可通过切割 caspase-3/7/9 和 PARP，以剂量依赖的方式诱导 U251、U87 和 T98G 细胞发生细胞凋亡[1]。
HJ03 (1-80 μM; 48-72 h) 诱导 U251、U87 和 T98G 细胞发生铁死亡，其机制为上调 ROS、Fe2+ 和 MDA 水平，下调 SLC7A11，并上调 p53 或 ATF3[1]。
HJ03 (0.4-50 μM; 15-72 h) 诱导 U251、U87 及 T98G 细胞发生 DNA 损伤，其机制为激活 ATM-Chk2 DNA 损伤应答通路；同时诱导纯化的线性化 pBR322 DNA 发生剂量依赖性的 DNA 交联与烷基化[1]。

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

HJ03 相关抗体:

Cell Proliferation Assay[1]

Cell Line: U251, U87, T98G
Concentration: 0.25, 0.5 andn 1 μM (U251); 1, 2 and 4 μM (U87); 2, 4 and 8 μM (T98G)
Incubation Time: 14 days
Result: Reduced colony formation significantly in U251 cells treated with 0.25, 0.5, or 1 μM compared to control.
Almost completely inhibited U87 cell colony formation at concentrations >2 μM.
Induced comparable colony formation inhibition in T98G cells treated with 2 μM to that of 50 μM TMZ.

Cell Viability Assay[1]

Cell Line: U87
Concentration: 4, 8 and 16 μM
Incubation Time: 72 h
Result: Induced U87 spheroid shrinkage and cell death at 4 μM.
Caused almost complete spheroid death at 16 μM.

Cell Cycle Analysis[1]

Cell Line: U251, U87, T98G
Concentration: 1, 2 and 4 μM (U251); 5 μM (U87)
Incubation Time: 48 h, 72 h
Result: Arrested 21.8%, 33%, and 70.3% of U251 cells in G2/M phase after 48 h treatment with 1, 2, 4 μM, respectively.
Increased G2/M arrest in U251 cells to 24.1%, 50.5%, and 67.8% after 72 h treatment with 1, 2, 4 μM, respectively.
Increased U87 cell G2/M arrest by >35% after 48 and 72 h treatment with 5 μM.
Increased p21 and p-CDK1, and decreased CDK1 and cyclin B1 in U251, U87, and T98G cells in a concentration-dependent manner.

Apoptosis Analysis[1]

Cell Line: U251, U87, T98G
Concentration: 1, 2 and 4 μM (U251); 5, 10 and 20 μM (U87); 10, 20 and 40 μM (T98G)
Incubation Time: 48 h, 72 h
Result: Induced significant apoptosis in U251 cells after 48 h incubation with 1, 2, 4 μM.
Triggered significant apoptosis in U87 cells after 48 h incubation with 5, 10, 20 μM.
Induced significant apoptosis in T98G cells after 48 h incubation with 20, 40 μM.
药代动力学
(Parmacokinetics)
Species Dose Route Cmax Tmax (Plasma) T1/2 Tmax (Brain)
Mice[1] 66 mg/kg p.o. 649.5 nM 0.25 h 0.4 h 0.5 h
体内研究
(In Vivo)

HJ03 (2-20 mg/kg；口服；每周连续给药 5 天；共 4 周) 可显著延长原位胶质母细胞瘤荷瘤小鼠的生存期[1]。
HJ03 (2-132 mg/kg；口服；每日一次；连续 7 天) 在最高 66 mg/kg 的剂量下对健康小鼠具有良好的耐受性，未观察到显著体重下降或血液学毒性，而 132 mg/kg 剂量会引发轻度血液学毒性[1]。

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

Animal Model: C57BL/6 (male, 8 weeks old, intracranial stereotactic injection of 2×105 firefly luciferase-expressing CT2A cells)[1]
Dosage: 2 mg/kg; 20 mg/kg
Administration: p.o.; 5 consecutive days per week; 4 weeks
Result: Significantly prolonged mouse survival at 20 mg/kg compared to vehicle control and TMZ (HY-17364) groups.
Showed 20 mg/kg dose was significantly more effective than 2 mg/kg dose at prolonging survival.
Made treated mice regain lost body weight more quickly than TMZ-treated mice following treatment cessation.
Animal Model: C57BL/6 (male, 6-8 weeks old, 20±2 g)[1]
Dosage: 2 mg/kg; 20 mg/kg; 66 mg/kg; 132 mg/kg
Administration: p.o.; daily; 7 days
Result: Caused no significant weight loss in any HJ03 dose group over 7-day treatment period.
Maintained white blood cell and lymphocyte counts within normal physiological ranges in 2, 20, and 66 mg/kg dose groups; induced significant decrease in white blood cell and lymphocyte counts below normal ranges only in 132 mg/kg dose group.
Kept red blood cell counts within normal ranges across all HJ03 dose groups.
分子量

482.75

Formula

C16H22Cl3N7O4
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

HJ03 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:

HJ033028123-48-7HJ 03HJ-03FerroptosisDNA Alkylator/CrosslinkerDNA/RNA SynthesisApoptosisReactive Oxygen Species (ROS)ferroptosiscolorectal cancerU87U251p53blood-brain barrierglioblastomaATF3SLC7A11DNA damageInhibitorinhibitorinhibit

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HY-181982
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