(±)-CPSI-1306 is an orally active MIF antagonist[1].
(±)-CPSI-1306 细胞实验
Cell Line
Concentration
Treated Time
Description
References
MVT-1
0.5 and 2 μM
48 h
CPSI-1306 significantly reduced the viability of TNBC cells and induced intrinsic apoptosis by altering mitochondrial membrane potential, cytochrome c release, and activation of different caspases.
Cell Death Dis. 2020 Sep 17;11(9):774
(±)-CPSI-1306 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
NSG mice
MDA-MB-231 mammary fat pad xenograft model
Oral
10 or 20 mg/kg
Three times a week for 4 weeks
CPSI-1306 treatment significantly reduced tumor volume and weight and inhibited lung metastasis. Histological analysis revealed a higher number of apoptotic cells in CPSI-1306-treated tumors compared to vehicle controls.
Cell Death Dis. 2020 Sep 17;11(9):774
Skh-1 hairless mice
UVB-induced squamous cell carcinoma model
Oral
20 mg/kg
5 consecutive days before UVB exposure; or 10 weeks UVB exposure followed by 8 weeks CPSI-1306 treatment
CPSI-1306 significantly reduced UVB-induced skin inflammation and squamous cell carcinoma development, decreased skin thickness and MPO activity, increased keratinocyte apoptosis and p53 expression, and reduced proliferation and DNA damage.
Mol Cancer Res. 2014 Sep;12(9):1292-302
(±)-CPSI-1306 动物研究
Animal study
Treatment with CPSI-1306 leads to a significant decrease in blood glucose levels in mice, which is associated with a reduction in serum levels of inflammatory cytokines[1].CPSI-1306-induced keratinocyte apoptosis can be detected as early as 30 minutes after a single UV irradiation. At 6, 24 and 48 hours after UV irradiation, CPSI-1306-treated mice showed a significant increase in cleaved caspase-3 expression compared to control mice. CPSI-1306 reduces acute UVB-induced keratinocyte DNA damage and UVB-induced acute inflammation[2].
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