| 包装 | 价格(元) |
| 50mg | 电议 |
| 10mg | 电议 |
KML 29 is reported to display IC50 values of 43, 15, and 5.9 nM toward rat, mouse, and human monoacylglycerol lipase (MAGL), respectively.
Cell lines | A431, H1975, B16-F10, OVCAR-3, HT-29, HCC827, Hela, A549 |
Preparation Method | cells (~1,000 per well) in 100 µl of culture medium were plated in a 96-well plate for 24 h and 100 µl of medium with KML29 was added to each well for 48 h. Then 10 µl of CCK8 solution was added and incubated at 37!栦or 2 h. |
Reaction Conditions | 20 µM KML29 for 48 h |
Applications | The selective MAGL inhibitor KML29 showed antiproliferative activity against B16-F10 and HT-29 cells. |
Animal models | MCAO rats |
Preparation Method | 1 mg/kg KML 29, a potent covalent inhibitor of MAGL, was administered intravenously for three days. |
Dosage form | intravenous injection, 1 mg/kg/d for 3 days |
Applications | Treatment with KML 29 reduced the area showing lower radioactivity in the ipsilateral region. In the ipsilateral side of the ischemia rat with no medication, the AUC ratios in the cortex and striatum were 0.49 ± 0.04 and 0.73 ± 0.02, respectively. The corresponding ratios were improved 0.72 ± 0.07 in the cortex and 0.88 ± 0.04 in the striatum by KML 29 treatment, respectively. |
| 产品描述 | KML 29 is reported to display IC50 values of 43, 15, and 5.9 nM toward rat, mouse, and human monoacylglycerol lipase (MAGL), respectively[1]. KML29 potently and selectively inhibited MAGL in vitro and in vivo with minimal cross-reactivity toward other central and peripheral serine hydrolases, including no detectable activity against FAAH[1]. KML 29 acted as a selective MAGL inhibitor showed antiproliferative activity against B16-F10 and HT-29 cells, while showed no significant effect on A431, H1975, OVCAR-3, HCC827, Hela and A549 cell lines[2]. KML 29 delays onset, progression and survival in the low-copy SOD1G93A Amyotrophic lateral sclerosis (ALS) mouse. oral administration of KML 29 is therapeutic by delaying onset, improving symptoms and extending lifespan, which was associated with increasing tissue levels of neurotrophic factors and decreasing pro-inflammatory cytokines[3]. Acute administration of KML 29 mostly increased 2-AG levels in fat, brain and spinal cord without any effect on AEA levels. KML 29 also reduced arachidonic acid levels in the CNS and peripheral organs[4]. References: |
m.cnreagent.com