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58-82-2

中文名稱 BK
英文名稱 BRADYKININ
CAS 58-82-2
分子式 C50H73N15O11
分子量 1060.21
MOL 文件 58-82-2.mol
更新日期 2024/11/03 16:22:37
58-82-2 結(jié)構(gòu)式 58-82-2 結(jié)構(gòu)式

基本信息

中文別名
舒緩激肽
BK 舒緩激肽
緩激肽, >98%
化合物BRADYKININ
BRADYKININ游離態(tài)
亮氨酸腦啡肽 乙酸鹽 水合物
舒緩激肽H-ARG-PRO-PRO-GLY-PHE-SER-PRO-PHE-ARG-OH
[DES-PRO2]-BRADYKININ
ANGIOTENSIN I CONVERTING ENZYME (ACE I) INHIBITOR
英文別名
bk
brs640
prs640
C00306
RPPGFSPFR
BRADYZIDE
Callideic
KallidinⅠ
BRADYKININ
Callidin I
所屬類別
生物化工:多肽

物理化學(xué)性質(zhì)

熔點170°C (rough estimate)
比旋光度D25 -76.5° (c = 1.37 in 1N acetic acid)
沸點811.85°C (rough estimate)
密度1.1171 (rough estimate)
RTECS號EE1530000
折射率1.6930 (estimate)
儲存條件−20°C
儲存條件−20°C
溶解度H2O: >40 mg/mL
溶解度H2O: >40 mg/mL
酸度系數(shù)(pKa)3.34±0.10(Predicted)
形態(tài)白色至灰白色凍干固體
顏色凍干粉
水溶解性Soluble to 1 mg/ml in water.
序列H-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-OH
CAS 數(shù)據(jù)庫58-82-2

安全數(shù)據(jù)

安全說明22-24/25
WGK Germany3
WGK Germany3

常見問題列表

生物活性
Bradykinin是由激肽釋放酶-激肽系統(tǒng)產(chǎn)生的活性肽。 它是炎癥調(diào)節(jié)因子,也被認(rèn)為是幾種血管和腎功能以及神經(jīng)調(diào)節(jié)因子。
靶點

Human Endogenous Metabolite

體外研究

Bradykinin is a potent vasodilator peptide that exerts its vasodilatory action through stimulation of specific endothelial B2 receptors, thereby causing the release of prostacyclin, NO, and EDHF. Bradykinin has been reported to be involved in the progression of many types of cancer. Bradykinin treatment promotes the invasion and migration of colorectal cancer cells. Bradykinin treatment stimulates ERK1/2 activation and IL-6 production. Exogenous bradykinin markedly inhibits TF expression in mRNA and protein level induced by LPS in a dose-dependent manner. The NO synthase antagonist L-NAME and PI3K inhibitor LY294002 dramatically abolish the inhibitory effects of bradykinin on tissue factor expression.

體內(nèi)研究

Application of 1 μM bradykinin to the ovary produces significant decreases in heart rate and mean arterial pressure. In vagotomized animals, application of 1 μM bradykinin to the ovary produces bradycardia and hypotension similar to the responses evoked when vagal innervation is intact. Vascular bradykinin can improve pancreatic microcirculation and hemorheology in rats with severe acute pancreatitis. The pancreatic microcirculatory blood flow volume and velocity in the vascular bradykinin treatment group increases gradually after 48 h. PI3K/Akt signaling pathway activation induced by bradykinin administration reduces the activity of GSK-3β and MAPK, and reduces NF-x03BA;B level in the nucleus, thereby inhibiting TF expression. Consistent with this, intraperitoneal injection of C57/BL6 mice with bradykinin also inhibits the thrombus formation induced by ligation of inferior vena cava.

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