Chloramphenicol氯霉素,56-75-7

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Chloramphenicol

CAS No. : 56-75-7

MCE 国际站：Chloramphenicol

产品活性：Chloramphenicol 是一种口服有效的广谱抗生素 (antibiotic)。Chloramphenicol 具有抗菌 (antibacterial) 活性。Chloramphenicol 抑制缺氧 A549 和 H1299 细胞中氧不稳定转录因子和缺氧诱导因子-1α (HIF-1α)。Chloramphenicol 可抑制血管内皮生长因子 (VEGF) 和葡萄糖转运蛋白 1 (glucose transporter 1) 的 mRNA 水平，最终降低 VEGF 的释放。Chloramphenicol 可用于厌氧菌感染和肺癌研究。

研究领域：Anti-infection  |  Metabolic Enzyme/Protease  |  Protein Tyrosine Kinase/RTK  |  Autophagy  |  Apoptosis  |  MAPK/ERK Pathway  |  PI3K/Akt/mTOR

作用靶点：Antibiotic  |  Bacterial  |  HIF/HIF Prolyl-Hydroxylase  |  VEGFR  |  Autophagy  |  Apoptosis  |  Beclin1  |  JNK  |  Akt  |  MMP

In Vitro: Chloramphenicol (1-100 μg/mL, 18-24 h) inhibits the HIF-1α pathway in NSCLC cells in a concentration-dependent manner.
Chloramphenicol (100 μg/mL, 0-24 h) induces autophagy in NSCLC cells, substantially increases the levels of autophagic biomarkers (beclin-1, Atg12-Atg5 conjugates, and LC3-II).
Chloramphenicol induces abnormal differentiation and inhibits apoptosis in activated T cells.
Chloramphenicol can inhibit both bacterial and mitochondrial protein synthesis, causing mitochondrial stress and decreased ATP biosynthesis.
chloramphenicol (1-100 μg/mL) can induce matrix metalloproteinase (MMP)-13 expression and increase MMP-13 protein.
chloramphenicol (1-100 μg/mL) can activate c-Jun N-terminal kinases (JNK) and phosphatidylinositol 3-kinase (PI-3K)/Akt signaling, leading to c-Jun protein phosphorylation.
Chloramphenicol acts primarily on the 50S subunit of bacterial 70S rihosomes and inhibits peptide bond formation by suppressing peptidyl transferase activity.

In Vivo: Chloramphenicol (0-3500 mg/kg, Gavage, daily, for 5 days) decreases erythrocytes and erythrocyte precursors and reduces marrow erythroid cells were at day 1 post-dosing, and returns to normal by 14 days post-dosing.

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