CAS NO: | 4759-48-2 |
包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
100mg | 电议 |
Storage | Store at -20°C |
M.Wt | 300.44 |
Cas No. | 4759-48-2 |
Formula | C20H28O2 |
Solubility | insoluble in H2O; ≥13.8 mg/mL in DMSO; ≥24.3 mg/mL in EtOH with gentle warming and ultrasonic |
Chemical Name | (2Z,4E,6E,8E)-3,7-dimethyl-9-(2,6,6-trimethylcyclohexen-1-yl)nona-2,4,6,8-tetraenoic acid |
Canonical SMILES | CC1=C(C(CCC1)(C)C)C=CC(=CC=CC(=CC(=O)O)C)C |
运输条件 | 蓝冰运输或根据您的需求运输。 |
一般建议 | 为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。 |
Cell experiment:[1] | |
Cell lines | Primary human sebocytes |
Reaction Conditions | 7 ~ 14 d incubation |
Applications | Isotretinoin decreased sebocyte proliferation in a dose- and time-dependent manner, with IC50 values being 10 μM after a 7-d incubation and 1 μM after a 14-d incubation, respectively. Isotretinoin (8 d) also inhibited the synthesis of triglycerides, wax/stearyl esters and free fatty acids, and modulated keratin expression in primary human sebocytes at a concentration of 0.1 μM. |
Animal experiment:[2] | |
Animal models | Male inbred Lewis (LEW, RT11) and Fisher (F344, RT11v1) rats, 200 ~ 220 g |
Dosage form | 2 mg/kg/day Administered orally for 8 weeks |
Applications | Isotretinoin reduced chronic rejection damage and decreased mRNA expression of IFN-γ and IL-10 in allografts in chronic Fisher344?Lewis transplant mice, an allograft nephropathy model. Thus, isotretinoin could serve as a potent immunosuppressive and anti-fibrotic agent able to prevent and inhibit progression of chronic allograft nephropathy. |
Note | The technical data provided above is for reference only. |
References: 1. Zouboulis CC, Korge B, Akamatsu H, et al. Effects of 13-cis-retinoic acid, all-trans-retinoic acid, and acitretin on the proliferation, lipid synthesis and keratin expression of cultured human sebocytes in vitro. Journal of Investigative Dermatology, 1991, 96(5): 792-797. 2. Adams J, Kiss E, Arroyo AB, et al. 13-cis retinoic acid inhibits development and progression of chronic allograft nephropathy. The American Journal of Pathology, 2005, 167(1): 285-298. |