1188-38-1
1188-38-1 结构式
基本信息
卡哥鲁酸
氨甲酰谷氨酸
N-氨甲酰基谷氨酸
N-氨基甲酰谷氨酸
N-氨甲酰-L-谷氨酸
N-氨基甲酰-L-谷氨酸
N-氨基甲酰基-L-谷氨酸
N-氨基甲酰谷氨酸(NCG)
N-氨基甲酰-L-谷氨酸(N-氨甲酰-L-谷氨酸)
Carbaglu
N-Cbm-Glu-OH
carglumicaci
CargluMic Acid
ureidoglutaricacid
n-carbamylglutamate
carbamylglutamicacid
N-Carbamyl-L-glutamic
N-Carbamyl-L-glutamate
物理化学性质
安全数据
常见问题列表
CPS1
Carglumic acid suppresses cell viability in the pancreatic ductal adenocarcinoma cell lines, triple-negative breast cancer cell lines, hepatoma cell lines, and human non-small cell lung carcinoma cell lines in a dose-dependent manner. The 50% inhibitory concentration (IC 50 ) of Carglumic acid against those cell lines is between 5 and 7.5 mM. The results show that Carglumic acid does not induce complete cell cycle arrest. Instead, there are more sub-G1 cells among Carglumic acid-treated AsPC1 and MDA-MB-231 cells than among untreated cells. In AsPC1 and HPDE-E6E7 cells, the IC 50 s of Carglumic acid are 5 mM and over 10 mM, respectively . In MDA-MB-231 and MCF-12A cells, the IC 50 s of Carglumic acid are 5 mM and 6 mM, respectively.
The results show that Carglumic acid, but not the vehicle control, markedly inhibits tumor growth. In the orthotopic pancreatic cancer model, tumor growth inhibition by Carglumic acid on day 21 is 80% (P<0.01). In the orthotopic triple-negative breast cancer model, tumor growth inhibition by Carglumic acid on day 20 is 82% (P<0.01). These results indicate that Carglumic acid suppresses tumor growth in pancreatic cancer and triple-negative breast cancer. On day 20, mean tumor growth inhibition in orally and intravenously treated mice is 55% and 93%, respectively, relative to untreated mice (P<0.01).