2. Autophagy Apoptosis Protein Tyrosine Kinase/RTK
  3. Autophagy Ferroptosis ROS Kinase
  4. DHODH-IN-33

DHODH-IN-33 是一种选择性 DHODH 抑制剂，对 A549 细胞 (IC50 = 5.22 μM) 和 5637 细胞 (IC50 = 3.03 μM) 具有强效活性。DHODH-IN-33 可诱导自噬 (autophagy) 依赖性铁死亡 (ferroptosis) (表现为线粒体功能障碍、脂质过氧化和 ROS 积累) ，且在体内无显著毒性。DHODH-IN-33 抗癌作用是通过促进二氢乳清酸脱氢酶的自噬依赖性降解实现的。DHODH-IN-33 可用于非小细胞肺癌和膀胱癌研究。

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DHODH-IN-33

DHODH-IN-33 Chemical Structure

CAS No. : 3026839-88-0

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DHODH-IN-33 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

DHODH-IN-33 is a selective dihydroorotate dehydrogenase (DHODH) inhibitor with potent activity against A549 (IC50 = 5.22 μM) and 5637 (IC50 = 3.03 μM). DHODH-IN-33 induces autophagy-dependent ferroptosis (mitochondrial dysfunction, lipid peroxidation, and ROS accumulation) with no notable toxicity in vivo. DHODH-IN-33 exerts anti-cancer effect by promoting the autophagy-dependent degradation of DHODH. DHODH-IN-33 can be used for non-small cell lung cancer and bladder cancer[1].

体外研究
(In Vitro)

DHODH-IN-33 (compound 3af) (48 小时) 对 A549 细胞 (IC50 = 5.22 μM) 和 5637 细胞 (IC50 = 3.03 μM) 表现出强效活性[1]。
DHODH-IN-33 (5 和 10 μM, 48 小时) 不通过凋亡机制诱导 A549 细胞死亡[1]。
DHODH-IN-33 (5 和 10 μM, 24 小时) 在 A549 细胞中将铁死亡的诱导与自噬激活联系起来，主要通过协同降解氧化还原稳定酶实现[1]。
DHODH-IN-33 (5 和 10 μM, 48 小时) 通过启动自噬、抑制 DHODH 和脂质过氧化来诱导自噬依赖性铁死亡，作为 A549 细胞的主要死亡途径，这两者共同作为上游开关来驱动下游的脂质过氧化执行事件[1]。

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

DHODH-IN-33 相关抗体:

Apoptosis Analysis[1]

Cell Line: A549 cells
Concentration: 5, 10 μM
Incubation Time: 48 h
Result: Exhibited 10.95% and 21.24% apoptosis at concentration of 5 μM and 10 μM, respectively.

Western Blot Analysis[1]

Cell Line: A549 cells
Concentration: 5, 10 μM
Incubation Time: 24 h
Result: Downregulated the expression of DHODH, but had little effect on the level of GPX4.
Increased the Beclin-1 and LC3 II (lipidated form) levels.

Cell Viability Assay[1]

Cell Line: A549 cells
Concentration: 5, 10 μM
Incubation Time: 48 h
Result: Inhibited the cell viability of the A549 cells at various concentrations, particularly at a concentration of 10 μM.
Caused cytotoxicity can be reversed by 3-MA, Lip-1 and MitoQH2 with efficacy in the order of 3-MA > Lip-1 > MitoQH2.

Western Blot Analysis[1]

Cell Line: A549 cells
Concentration: 5, 10 μM
Incubation Time: 24 h
Result: Caused an upregulation of LC3 II and a downregulation of DHODH that were not significantly reversed by the addition of either the lipid peroxidation inhibitor Lip-1 or the DHODH enzyme substitute MitoQH2.
体内研究
(In Vivo)

DHODH-IN-33 (compound 3af) (10 和 20 mg/kg，腹腔注射，每 48 小时一次，持续 14 天) 在小鼠皮下 A549 异种移植瘤模型中通过自噬依赖性铁死亡通路发挥抗肿瘤作用其中铁死亡是主要机制、自噬激活是关键前提，同时在 BALB/c 裸鼠中保持了良好的耐受性[1]。

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

Animal Model: BALB/c nude mice (8 week-old)[1]
Dosage: 10 or 20 mg/kg
Administration: i.p., once every 48 h for 14 days
Result: Achieved tumor growth inhibition rates of 19.37% and 58.33% on day 14 at the corresponding doses of 10 mg/kg and 20 mg/kg, respectively.
Upregulated the expression level of LC3 II at administration of 20 mg/kg.
Increased ACSL4 protein.
分子量

407.48

Formula

C23H21NO4S
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

DHODH-IN-33 相关分类

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Keywords:

DHODH-IN-333026839-88-0AutophagyFerroptosisROS KinaseDHODHferroptosisdihydroorotate dehydrogenaselung cancerInhibitorinhibitorinhibit

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