product name KC7F2
Description: KC7F2 is a potent HIF-1 pathway inhibitor with potential anticancer activity. KC7F2 is cytotoxic to a variety of cancer cell lines with an IC50 value of 15-25 µM. KC7F2 markedly inhibited HIF-mediated transcription in cells derived from different tumor types, including glioma, breast, and prostate cancers, and exhibited enhanced cytotoxicity under hypoxia. KC7F2 prevented the activation of HIF-target genes such as carbonic anhydrase IX, matrix metalloproteinase 2, endothelin 1, and enolase 1.
References: Clin Cancer Res. 2009 Oct 1;15(19):6128-36; Neuropharmacology. 2014 Feb;77:428-40; Synapse. 2014 Sep;68(9):402-9.
570.38
Formula
C16H16Cl4N2O4S4
CAS No.
927822-86-4
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (175.3 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19426689
| In Vitro |
In vitro activity: KC7F2 inhibits HRE-driven transcription and decreases HIF-1α protein levels in LN229-HRE-AP cells. KC7F2 shows a dose-response cytotoxicity with IC50 of approximately 15 to 25 μM in cancer cells MCF7, LNZ308, A549, U251MG, and LN229. In D54MG glioma cells, KC7F2 inhibits colony formation, especially under hypoxia. In hypoxic microglial cultures, KC7F2 downregulates the expression of TfR and DMT, and reduces the HIF-1α mediated iron accumulation. Kinase Assay: Cells are incubated at 37°C in a humidified atmosphere containing 5% CO2 and 21% O2 (normoxia) or 1% O2 (hypoxia) in a hypoxia workstation. The LN229-HRE-AP reporter cell line for HIF transcriptional activity is created by stably transfecting LN229 cells with the pACN188 plasmid, which contains an alkaline phosphatase gene driven by six HREs derived from the VEGF gene. Cell Assay: Cells (Human dermal microvascular endothelial cells and mouse neurons; MCF7, LNZ308, A549, U251MG, and LN229 cell lines) are seeded onto 96-well plates (4 × 103/well) and cultured under normoxic (21% O2) and hypoxic (1% O2) conditions with different concentrations of KC7F2 for 72 h or treated for various times with 20 μM KC7F2. For proliferation analysis, cells are fixed with 50% trichloroacetic acid for 1 h at 4°C, followed by staining with 0.4% sulforhodamine B dissolved in 1% acetic acid for 30 min at room temperature. Plates are washed five times with 1% acetic acid to remove unbound dye. Bound dye is dissolved by adding 10 mM unbuffered Tris base. Cell proliferation is calculated by measuring OD values at 564 nm using a spectrophotometer. |
|---|---|
| In Vivo | KC7F2 significantly reduces the latent period in the pentylenetetrazole kindling rat model and increases the rate of spontaneous recurrent seizures during the chronic stage in the lithium-pilocarpine rat model. |
| Animal model | In a rat epilepsy model, KC7F2 significantly shortened the latent period in the PTZ kindling model and increased the rate of spontaneous recurrent seizures during the chronic stage in the lithium-pilocarpine model |
| Formulation & Dosage | |
| References | Clin Cancer Res. 2009 Oct 1;15(19):6128-36; Neuropharmacology. 2014 Feb;77:428-40; Synapse. 2014 Sep;68(9):402-9. |
