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Erastin

CAS No. : 571203-78-6

MCE 国际站：Erastin

产品活性：Erastin 是一种铁死亡 (ferroptosis) 诱导剂。Erastin 可选择性杀伤细胞，靶向表达 RAS 致癌突变体的细胞。Erastin 的铁死亡诱导机制与 ROS 和铁依赖性信号传导有关。Erastin 能够抑制电压依赖性阴离子通道 (VDAC2/VDAC3)，加速氧化，导致内源活性氧积累。Erastin 还破坏线粒体通透性过渡孔 (mPTP)，表现出抗肿瘤活性。

研究领域：Apoptosis  |  Membrane Transporter/Ion Channel

作用靶点：Ferroptosis  |  VDAC

In Vitro: Erastin (10 μM; 24 h) triggers ferroptosis in ectopic endometrial stromal cells (EESCs), and increases the total ROS level at 9 h.
Erastin shorts mitochondria and increases membrane density in EESCs.
Erastin (10 μM; 9 h) decreases the mRNA expression levels of iron-related proteins, such FPN (iron exporter) in EESCs. However, FPN overexpression significantly inhibits erastin-induced ferroptosis in EESCs.
Erastin (10 μM; 24 h) induces mitochondrial permeability transition pore (mPTP) opening in HT-29 colorectal cancer cells.
Erastin (30 μM; 72 h) significantly inhibits the growth of HT-29 colorectal cancer cells.
The molecular mechanism by which Erastin induces ferroptosis is related to genes regulating iron or mitochondrial fatty acid metabolism. Includes ribosomal protein L8, iron response element binding protein 2 (IREB2), ATP synthase F0 complex subunit C3, citrate synthase, tetrapeptide repeat domain 35, and acyl-CoA synthetase family member 2 (ACSF2).

In Vivo: Erastin can be used in animal modeling to construct ferroptosis induction model.

Erastin (40 mg/kg; i.p.; once every 3 days for 2 weeks) suppresses endometriotic implants in the mouse endometriosis model, indicating Erastin regresses ectopic lesions by trigging ferroptosis.
Erastin (10 mg/kg, 30 mg/kg; i.p.; once daily for 4 weeks) suppresses HT-29 xenograft growth in SCID mice, with more potent efficacy under 30 mg/kg treatment.

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