21593-77-1
21593-77-1 結(jié)構(gòu)式
基本信息
S- 烯丙基-L-半胱氨酸
烯丙基-L-半胱氨酸
DEOXYALLIIN
(L)-3-(ALLYLSULFENYL)-ALANINE
L-DEOXYALLIIN
(R)-ALLYLTHIO-2-AMINOPROPIONIC ACID
S-ALLYL-L-CYSTEINE
s-allylcysteine
Allylcysteine
物理化學(xué)性質(zhì)
制備方法
![L-Cysteine, N-[(1,1-dimethylethoxy)carbonyl]-S-2-propen-1-yl-, methyl ester](/CAS/20210305/GIF/232953-12-7.gif)
232953-12-7
21593-77-1
以BocSacOMe（9.92 g，36.02 mmol）為原料，在250 mL圓底燒瓶中溶解于CH2Cl2（100 mL）。在氬氣保護(hù)下，向溶液中加入TFA（10 mL），室溫攪拌反應(yīng)混合物3小時。通過TLC（展開劑：150% EtOAc的石油醚溶液）監(jiān)測反應(yīng)進(jìn)度，確認(rèn)原料完全消耗（Rf = 0.4）。隨后，通過旋轉(zhuǎn)蒸發(fā)去除溶劑，得到的黃色殘余物在真空下短暫干燥。將粘性殘余物溶解于THF（30 mL）中，冷卻至0℃。向攪拌的溶液中加入LiOH（72 mL，5M水溶液）。移除冰浴，反應(yīng)混合物在室溫下繼續(xù)攪拌1小時。反應(yīng)完成后，用100 mL H2O稀釋，使用DOWEX（R）樹脂中和至pH <7（通過pH試紙檢測）。將所有樹脂轉(zhuǎn)移至空柱中，用500 mL H2O（重力流）洗滌，棄去流出液。產(chǎn)物用5% NH4OH水溶液洗脫，并用50% H2O（洗脫液）洗滌。收集含有(R)-3-(烯丙基硫基)-2-氨基丙酸的級分（Rf = 0.6），通過旋轉(zhuǎn)蒸發(fā)濃縮，得到黃色固體。進(jìn)一步通過柱色譜純化[洗脫劑比例：7:2:1 iPrOH:MeOH:NH4OH（25% 水溶液）]，得到白色晶體Sac（3.29 g，57%）。熔點：212-213℃。1H NMR（400 MHz，D2O）：δH = 2.5-2.70（2H，ABX系統(tǒng)，J = 13.3, 5.3, 6.7 Hz，CH2SAllyl），3.06（2H，d，J = 7.2 Hz，CH2CH=CH2），3.28（1H，dd，J = 6.7, 5.3 Hz，Hα），5.02-5.09（2H，m，HC=CH2），5.71（1H，m，HC=CH2）。
參考文獻(xiàn)：
[1] Journal of the American Chemical Society, 2008, vol. 130, # 30, p. 9642 - 9643
[2] Patent: US2012/178913, 2012, A1. Location in patent: Page/Page column 10-11
| 報價日期 | 產(chǎn)品編號 | 產(chǎn)品名稱 | CAS號 | 包裝 | 價格 |
| 2025/05/22 | HY-W013573 | S-烯丙基-L-半胱氨酸 S-Allyl-L-cysteine | 21593-77-1 | 1 mg | 135元 |
| 2025/05/22 | HY-W013573 | S-烯丙基-L-半胱氨酸 S-Allyl-L-cysteine | 21593-77-1 | 5 mg | 248元 |
| 2025/05/22 | HY-W013573 | S- 烯丙基別半胱氨酸,蒜氨酸 S-Allyl-L-cysteine | 21593-77-1 | 10mg | 400元 |
常見問題列表
It is found that S-Allyl-L-cysteine could protect against amyloid-protein (A)-and tunicamycin-induced cell death in differentiated PC12 cells. Simultaneously applied S-Allyl-L-cysteine (1 μM) suppresses the cell death induced by Aβ 25-35 and Aβ 1-40 in a concentration-dependent manner, and neuronal integrity is almost completely retained. Simultaneously applied S-Allyl-L-cysteine significantly decreases the Aβ-induced level of ROS. The TEAC value of S-Allyl-L-cysteine is lower than that of oxidized GSH, and no antioxidant activity is observed. Intracellular GSH levels remains unaffected by treatment of neurons with S-Allyl-L-cysteine for 24 h. Furthermore, the increase in caspase-12 protein expression is suppressed by simultaneously adding 1 μM S-Allyl-L-cysteine . S-Allyl-L-cysteine up to a concentration 1.0 mM does not exhibit any cytotoxic impact on morphology of myoblast and myotubes in culture observed under bright field microscope. TNF treatment leads to a significant decrease in the intracellular CK activity while S-Allyl-L-cysteine pre-treatment to TNF treated myotubes decreases the release of CK in media. S-Allyl-L-cysteine pre-treatment decreases the level of active form of this enzyme in S-Allyl-L-cysteine+TNF group. Similar observations are recorded at mRNA level for caspase-3. These results illustrate that S-Allyl-L-cysteine regulates apoptotic signals via suppressing the transcription and thus protein expression of caspase-3.