|S3021||Rimonabant||<1 mg/mL||25 mg/mL||2 mg/mL|
|S1544||AM1241||<1 mg/mL||101 mg/mL||<1 mg/mL|
|S2819||AM251||<1 mg/mL||40 mg/mL||<1 mg/mL|
|S8012||Otenabant (CP-945598) HCl||<1 mg/mL||5 mg/mL||<1 mg/mL|
|S2854||BML-190||<1 mg/mL||22 mg/mL||<1 mg/mL|
|S2778||GW842166X||<1 mg/mL||20 mg/mL||<1 mg/mL|
|S1534||Org 27569||<1 mg/mL||82 mg/mL||<1 mg/mL|
- Cannabinoid Receptor抑制剂（7）
Rimonabant是一个大脑中心大麻素受体（CB1）特异性口服拮抗剂。在hCB1转染HEK293细胞中IC50浓度为13.6 nM，EC50浓度为17.3 nM。
AM1241是一种选择性的cannabinoid CB2 receptor激动剂，Ki为3.4 nM，比作用于CB1受体选择性高82倍。
AM1241 increased ki67+ positive cells and decreased cardiac fibrosis after MI. A, Masson's trichrome-stained myocardial sections from a sub- group of animals at POD 28. B, Comparison of fibrosis areas in all groups. *, P<0.05 vs. MI group; #, P<0.05 vs. MI+AM group. C, Immunohistochemistry of Ki67 (green), and DAPI (blue) staining in adjacent infarction areas. D, Comparison of ki67 positive cells in all groups. *, P<0.05 vs. MI group; #, P<0.05 vs. MI+AM group. Scale bar, 20 μm.
Inhibition of CB1 suppresses the proliferation and migration and induces apoptosis of RCC cells. a Western blot analysis of CB1 protein in RCC cell lines (786-O, CAKI-1, CAKI-2, 769-P, A498, and ACHN) and normal cell line HK-2, and β-actin was used as a loading control for western blot assays. b RCC cell lines were treated at the indicated concentrations for different time points, and the cell viability was analyzed by MTT assay. AM251-induced cell death in 769-P cells in a dose- and time-dependent manner. c AM251-induced cell death in 786-O cells in a dose- and timedependent manner. d AM251 reduced migration in 786-O and 769-P cell lines at 20 and 30 μM concentrations. e The transmembrane cell number of 786-O and 769-P cells after treatment with different concentrations of AM251 significantly decreased compared with untreated control.
Otenabant (CP-945598) HCl是一种有效的，选择性cannabinoid receptor CB1拮抗剂，Ki为0.7 nM，比作用于人类CB2受体选择性高10，000倍。Phase 1。
BML-190是一种选择性的cannabinoid CB2 receptor逆向激动剂，Ki为435 nM，比作用于CB1受体选择性高50倍。
The effect of BML-190 on DSS-treated Rassf1a +/- mice. DSS-treated Rassf1a+/- mice were given 3% DSS in drinking water for 7 days followed by fresh water for recovery for another 7 days. BML-190 was administrated orally (100µg/g body weight) on days 2, 4, 5and 7. BML-190 did not protect DSS-treated Rassf1a+/- from inflammation induced injury. n=6-10 for all.
GW842166X是一种有效的，高选择性cannabinoid receptor CB2受体激动剂，EC50为63 nM，对CB1受体没有显著的活性。Phase 2。
Org 27569是cannabinoid CB1 receptor变构调节剂，通过增强激动剂亲和力而诱导CB1受体状态改变，且降低逆向激动剂的亲和力。