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185413-30-3

中文名稱 AC-PHE-GLU-TRP-THR-PRO-GLY-TRP-TYR-GLN-L-AZETIDINE-2-CARBONYL-TYR-ALA-LEU-PRO-LEU-NH2
英文名稱 AF12198
CAS 185413-30-3
分子式 C96H123N19O22
分子量 1895.12
MOL 文件 185413-30-3.mol
更新日期 2025/02/14 09:06:36
185413-30-3 結(jié)構(gòu)式 185413-30-3 結(jié)構(gòu)式

基本信息

英文別名
AF12198
AC-PHE-GLU-TRP-THR-PRO-GLY-TRP-TYR-GLN-AZE-TYR-ALA-LEU-PRO-LEU-NH2
AC-PHE-GLU-TRP-THR-PRO-GLY-TRP-TYR-GLN-L-AZETIDINE-2-CARBONYL-TYR-ALA-LEU-PRO-LEU-NH2
AC-PHE-GLU-TRP-THR-PRO-GLY-TRP-TYR-GLN-L-AZETIDINE-2-CARBOXYLIC ACID-TYR-ALA-LEU-PRO-LEU-NH2

物理化學(xué)性質(zhì)

熔點>179°C (dec.)
儲存條件−20°C
儲存條件−20°C
溶解度DMSO(微溶)、甲醇(微溶)、水(微溶)
形態(tài)solid
顏色白色至灰白色

安全數(shù)據(jù)

WGK Germany3
WGK Germany3
AC-PHE-GLU-TRP-THR-PRO-GLY-TRP-TYR-GLN-L-AZETIDINE-2-CARBONYL-TYR-ALA-LEU-PRO-LEU-NH2價格(試劑級)
報價日期產(chǎn)品編號產(chǎn)品名稱CAS號包裝價格
2025/02/08HY-P1110AC-PHE-GLU-TRP-THR-PRO-GLY-TRP-TYR-GLN-L-AZETIDINE-2-CARBONYL-TYR-ALA-LEU-PRO-LEU-NH2
AF12198
185413-30-31mg1200元
2025/02/08HY-P1110AC-PHE-GLU-TRP-THR-PRO-GLY-TRP-TYR-GLN-L-AZETIDINE-2-CARBONYL-TYR-ALA-LEU-PRO-LEU-NH2
AF12198
185413-30-35mg3500元
2025/02/08HY-P1110AF12198185413-30-310 mg5425元

常見問題列表

生物活性
AF12198 是針對人類I型白介素-1 受體 (IL1R1) (IC50=8 nM) 的有效,選擇性和特異性肽拮抗劑,但不是針對人類 II 型受體 (IC50=6.7 μM) 或鼠 I 型受體 (IC50>200 μM)。AF12198 抑制 IL-1 誘導(dǎo)的 IL-8 產(chǎn)生 (IC50=25 nM) 和 IL-1誘導(dǎo)的細(xì)胞間粘附分子 1 (ICAM-1) 表達(dá) (IC50=9 nM)。AF12198 具有抗炎活性,并在體內(nèi)阻斷了對 IL-1 的反應(yīng)。
靶點

IL1R1

8 mM (IC 50 )

體外研究

AF12198 competes for binding of 125 I-IL-1α with an IC 50 of 8.0 nM, nearly equal to that of IL-1ra, IC 50 of 4.0 nM for the type I receptor.AF12198 (0-5 ng; 8 hours) inhibits IL-6 induction with an IC 50 of 15 μM whereas IL-1ra inhibits with an IC 50 of 2 nM?in heparinized human?primate blood. Meanwhile, With blood from cynomolgus monkeys, the IC 50 values are 17 μM for AF12198 and 30 nM for IL-1ra. Additionally, AF12198 or IL-1RA alone does not induce IL-6 in blood from either humans or cynomolgus monkeys.

體內(nèi)研究

AF12198 (intravenous infusion; 16?mg/kg; 30?min before LPS intravenous injection) significantly attenuates the increase in lung MPO activity induced by LPS in acute lung inflammation and it reduces the lung microvascular leakage from rats inflamed with LPS at the 4?h (32.6%), 12?h (50.1%) and 24?h (65.3%) after LPS.

Animal Model: Male Wistar rats
Dosage: 16?mg/kg
Administration: Intravenous infusion; 30?min before LPS intravenous injection
Result: Decreased pulmonary microvascular leakage in rats.
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