65391-42-6
65391-42-6 結(jié)構(gòu)式
基本信息
[(2S,3R)-3-AMINO-2-HYDROXY-4-PHENYLBUTANOYL]-L-LEUCINE HYDROCHLORIDE
(AMINO-2-HYDROXY-4-PHENYLBUTYRYL)-L-LEUCINE HYDROCHLORIDE
BESTATIN
BESTATIN HCL
BESTATIN HYDROCHLORIDE
N-[(2S,3R)-3-AMINO-2-HYDROXY-4-PHENYLBUTYRYL]-L-LEUCINE HYDROCHLORIDE
N-(3R-AMINO-2S-HYDROXY-1-OXO-4-PHENYLBUTYL)-L-LEUCINE, MONOHYDROCHLORIDE
N-(2S,3R-3-AMINO-2-HYDROXY-4-PHENYLBUTY- RYL)-L-LEUCINE HCL
Bestatin.HCI
物理化學(xué)性質(zhì)
安全數(shù)據(jù)
應(yīng)用領(lǐng)域
常見問題列表
根據(jù)最易反應(yīng)的底物不同可分為亮氨酸氨肽酶、纈氨酸氨肽酶、苯丙氨酸氨肽酶、脯氨酸氨肽酶等。
有關(guān)氨肽酶的概述、分類、制備方法、藥理作用等是由Chemicalbook的丁紅編輯整理。（2015-12-02）
用于脫除蛋白水解液的苦味
氨肽酶最顯著的作用在于脫除蛋白水解液的苦味，如大豆蛋白水解液，多肽的苦味與其N端疏水性氨基酸的量成正比，外肽酶可以有效的切除這些疏水性氨基酸。
蛋白質(zhì)的深度水解
與蛋白酶復(fù)合使用，可以大幅度提高蛋白質(zhì)的水解度。在醬油釀造、干酪生產(chǎn)及其它蛋白水解產(chǎn)品的制備過程中，可以提高蛋白質(zhì)的利用率，節(jié)省成本。如崔春、趙謀明等利用風(fēng)味蛋白酶（蛋白酶和氨肽酶的復(fù)合體）深度酶解藍(lán)園魚參蛋白，酶解 6h 后蛋白質(zhì)的利用率即達(dá)到 83.3%，21h 時水解度達(dá)到59.7%。
生物活性多肽的制備
生物活性多肽大部分是細(xì)胞生長因子，它們在體內(nèi)含量極低，但生物活性極高，對多種細(xì)胞生理功能和代謝活動發(fā)揮著生物調(diào)節(jié)作用。具有保健和美容的功能。通過控制蛋白質(zhì)的酶解來得到特定的活性肽是制備活性多肽的一種安全且高效的途徑。劉通訊等先用蛋白酶對大豆分離蛋白進(jìn)行水解，然后再用氨肽酶進(jìn)行水解，研究發(fā)現(xiàn)，產(chǎn)品中的多肽含量相對單一用蛋白酶水解約能提高 12%左右。
Bestatin enhances ATRA-induced differentiation and inhibits ATRA-driven phosphorylation of p38 MAPK in ATRA-sensitive APL NB4 cells. Bestatin can not reverse the differentiation block in ATRA-resistant APL MR2 cells. CD13 ligation with anti-CD13 antibody WM-15 results in phosphorylation of p38 MAPK, reduces the inhibition of Bestatin on the phosphorylation of p38 MAPK, and completely abolishes the enhancement of Bestatin on ATRA-inducing differentiation in NB4 cells. Bestatin (600 μM)-treated cells progress slower through the cell cycle due to decreased rate of cell growth and the frequency of cell division. Bestatin inhibits the frequency of mitosis and the inherent multinuclearity in D. discoideum, and is not cytotoxic to D. discoideum cells at 0-600 μM. Bestatin inhibits aminopeptidase activity in lysates of PsaA-GFP- and GFP-expressing cells by 69.39% ± 10.5% and 39.93% ± 18.7% of control, respectively.
Bestatin (20 μM) significantly reduces CD13 expression in diabetic mice and results a significant inhibition of MMP-9 specific gelationolytic band densities compared to diabetic vehicle-treated mice. Bestatin treatment significantly inhibits the expression of VEGF and heparanase in diabetic mice. Intravitreal bestatin treatment significantly downregulates the expression of both HIF-1α and VEGF in diabetic mice retinas. Furthermore, the upregulated expression of heparanase in diabetic mice retinas is significantly inhibited by intravitreal bestatin treatment. Bestatin (10, 1, and 0.1mg/kg, i.p.) treatment before the antigen-potentiated humoral response to SRBC results in an increased number of splenocytes producing hemolytic anti-SRBC antibodies (PFC) and the 2-ME-resistant serum hemagglutinin titer (at a dose of 0.1 mg/kg). Bestatin (1 and 0.1 mg/kg) administered to mice five times on alternate days after cyclophosphamide injection does not change the suppressive effect of the drug regarding the number of PFC, and even causes the further decrease of the total anti-SRBC hemagglutinins at dose of 1 mg/kg on day 7 after antigen stimulation.