| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
Cell lines | BJ-TERT/LT/ST/RASV12 and DRD cells |
Preparation method | Soluble in DMSO. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
Reacting condition | 5 μg/ml, 2 days |
Applications | RSL3 displayed synthetic lethality with oncogenic RAS in both BJ-TERT/LT/ST/RASV12 and DRD cells. RSL3 inhibited the growth of BJ-TERT/LT/ST/RASV12 and DRD cells as low as 10 ng/ml and started to kill sensitive cells as early as 8 hr after treatment. Longer treatment with RSL3 had little effect on the viability of cells lacking oncogenic RAS. RSL3 induced rapid and nonapoptotic cell death in oncogenic ras containing tumorigenic cells. |
Animal models | Athymic nude mice xenografted with BJeLR cells |
Dosage form | Subcutaneous injection (s.c.), 100 mg/kg, twice each week for 2 weeks. |
Application | RSL3 prevented tumor growth in a xenograft model. (1S, 3R)-RSL3 significantly prevented tumor growth. (1S, 3R)-RSL3 significantly reduced tumor volume via the induction of ferroptosis. Intraperitoneal injection of (1S, 3R)-RSL3 showed no toxicity up to 400 mg/kg dose, which suggested that (1S, 3R)-RSL3 was well tolerated. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| 文献引用 | |
| 产品描述 | RSL3 is identified as a potent ferroptosis-triggering agent, which is dependent on the activity of GPX4. RSL3 behaved as an inhibitor of GPX4, reducing the expression of GPX4 and inducing ferroptotic death of head and neck cancer cell[1] In vitro study demonstrated that RSL3 have a degree of synthetic lethality with oncogenic RAS. RSL3 showed rapid and potent ability to induce synthetic lethality with oncogenic RAS. RSL3 inhibited the growth of BJ-TERT/LT/ST/RASV12 and DRD cells as low as 10 ng/ml and started to kill sensitive cells as early as 8 h after treatment. The growth inhibitory effect and the selectivity of RSL3 were confirmed by trypan blue exclusion assay, which demonstrated the potency and selectivity of RSL3. Moreover, longer treatment with RSL3 had little effect on the viability of cells lacking oncogenic RAS, confirming the qualitative nature of RSL3’s selectivity.[2] In vivo study determined that RSL3-induced ferroptosis could be enhanced by cetuximab with the mechanism of suppressing the Nrf2/HO-1 axis. A DLD-1 xenograft nude mouse model was established to further explored whether cetuximab promotes RSL3-induced ferroptosis in vivo. All the mice survived well after cell implantation or were treated with vehicle, RSL3, cetuximab, or RSL3 in combination with cetuximab. However, administration of RSL3 alone and treatment with both RSL3 and cetuximab led to a decrease in tumour size and tumour volume. Meanwhile, the relative levels of Nrf2 and HO-1 were decreased and that keap1 expressed was relatively increased after co-treatment with RSL3 and cetuximab.[3] References: |
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