 COA |
MSDS |
 HPLC |
NMR |
| CAS No: | 312636-16-1 |
| Molecular formula(MF) | C15H11ClN2Os |
| Molecular Weight(MW): | 302.78 |
| Alias |
| In vitro | DMSO | 61 mg/mL (201.46 mM) |
|---|---|---|
| Ethanol | 61 mg/mL (201.46 mM) | |
| Water | <1 mg/mL | |
| In vivo | 30% PEG400+0.5% Tween80+5% propylene glycol | 20 mg/mL |
| Description | SKI II is a highly selective and non ATP-competitive sphingosine kinase (SphK) inhibitor with IC50 of 0.5 μM, while exhibiting no inhibitory action on other kinases including PI3K, PKCα and ERK2. | ||
|---|---|---|---|
| Targets |
|
||
| In vitro |
SKI II potently inhibits endogenous SK activities in the breast cancer cell line MDA-MB-231. SKI II demonstrates significantly antiproliferative effects in human cancer cell lines including T-24, MCF-7, MCF-7/VP, NCI/ADR with IC50 of 4.6 μM , 1.2 μM, 0.9 μM and 1.3 μM, respectively. SKI II also induces apoptosis of T24 cells consistent with the hypothesized consequence of reducing S1P levels. [1] As demonstrated previously in MDA-MB-231 cells, SKI II decreases S1P formation in JC cells in a concentration-dependent manner, with IC50 of 12 μM. [2] In addition, SKI-II can reverse drug resistance of SGC7901/DDP to cisplatin by down-regulating expression of P-gp and up-regulating apoptosis through down-regulation of SphK1. [3] |
||
| In vivo | SKI II (50 mg/kg) after intraperitoneal or oral administration significantly decreases tumor growth a syngeneic Balb/c mouse solid tumor model that uses JC mammary adenocarcinoma cells relative to control groups with no overt toxicity or weight loss.[2] SKI-II (50 mg/kg ip) ameliorates antigen-induced bronchial smooth muscle hyperresponsiveness in mice by endogenously inhibiting generation of S1P. [4] |