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- 详细信息
- 文献和实验
- 技术资料
- 保存条件:
Store at -20℃ for one year(Powder);Store at 2-4℃ for two weeks;Store at -20℃ for six months after dissolution.
- 库存:
99
- 供应商:
爱必信(上海)生物科技有限公司
- CAS号:
83730-53-4
- 规格:
1g/500mg/200mg/50mg
| 规格: | 1g | 产品价格: | ¥5821.0 |
|---|---|---|---|
| 规格: | 500mg | 产品价格: | ¥2613.0 |
| 规格: | 200mg | 产品价格: | ¥1676.0 |
| 规格: | 50mg | 产品价格: | ¥728.0 |
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抑制剂描述: 产品名称:L-Buthionine-(S,R)-Sulfoximine 产品别名:见爱必信官网 英文别名:L-Buthionine-(S,R)-Sulfoximine 靶点:Others CAS:83730-53-4 纯度:≥97% 外观:见爱必信官网 保存方法:Store at -20℃ for one year(Powder);Store at 2-4℃ for two weeks;Store at -20℃ for six months after dissolution. 描述: L-Buthionine-(S,R)-Sulfoximine is an irreversible inhibitor of γ-glutamylcysteine synthetase (Ki <100 μM), the rate-limiting enzyme for L-glutathione (GSH) synthesis, that induces oxidative stress in cells by depleting GSH. Administration of L-Buthionine-(S,R)-Sulfoximine leads to decreased GSH levels in virtually all tissues and is associated with tissue damage and apoptosis. Whereas elevated glutathione levels are associated with tumor cell resistance, L-Buthionine-(S,R)-Sulfoximine has been shown to enhance the toxicity of various chemotherapeutic agents in drug-resistant tumors. 溶解性:H2O : 41.67 mg/mL (187.44 mM; Need ultrasonic) 体外研究: L-Buthionine-(S,R)-sulfoximine (BSO: 50 μM) treatment for 48 hr results in a 95% decrease in ZAZ and M14 melanoma cell line GSH levels, and a 60% decrease in GST enzyme activity. GST-π protein and mRNA levels are significantly reduced in both cell lines. L-Buthionine-(S,R)-sulfoximine (BSO) induces oxidative stress in a cell by irreversibly inhibiting g-glutamylcysteine synthetase, an essential enzyme for the synthesis of glutathione (GSH). 体内研究:The average number of eye-spots (mean±SEM) is 5.36±0.29 (n=46), 7.79±0.45 (n=34) and 8.78±0.61 (n=32) in untreated controls, 2 mM L-Buthionine-(S,R)-sulfoximine (BSO) and 20 mM BSO treated mice, respectively. The 2 mM BSO treatment results in ~30% more eye-spots, and the 20 mM treatment results in 40% more eye-spots compared with untreated mice. It is showed that BSO causes an elevated frequency of DNA deletions during mouse development. BSO treatment reduced GSH concentration in mouse fetuses by 55% and 70% at 2 mM and 20 mM BSO doses, respectively, compared to untreated mice. Co-treatment with 2 mM BSO and 20 mM NAC depleted GSH to a similar extent as 2 mM BSO, consistent with the function of BSO to inhibit the g-GCS enzyme indispensable for GSH synthesis. Like GSH, cysteine levels dropped following BSO treatment.
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S-Adenosyl-L-Homocysteine Hydrolase
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