[CAS NO. 5300-03-8]??9-cis-Retinoicacid
PRODUCTS SPECIFICATIONS [5300-03-8]
DESCRIPTION [5300-03-8]
Overview
| MDL | MFCD00270072 |
|---|---|
| Molecular Weight | 300.44 |
| Molecular Formula | C20H28O2 |
| SMILES | CC(/C=C/C(C(C)(CCC1)C)=C1C)=C/C=C/C(C)=C/C(O)=O |
Summary
IC50 & Target
|
Human Endogenous Metabolite |
In Vitro
9-cis-Retinoic acid (1-10 μM; 0-5 days; CA 9-22 and NA cells) treatment significantly decreases proliferation in a dose-dependent manner in CA 9-22 and NA cells
[1]
.
9-cis-Retinoic acid (1 μM; 24 hours) treatment significantly increases PPARγ functional activity by >200% in CA 9-22 and NA aerodigestive cells
[1]
.
9-cis-Retinoic acid treatment results in the formation of a nuclear PPARγ-RXRα heterodimer supershift complex in CA 9-22 cells
[1]
.
9-cis-Retinoic acid inhibits proliferation and induces apoptosis in cutaneous T-cell lymphoma (CTCL) in a dose-dependent and time-dependent manner. 9-cis-Retinoic acid also induces G0/G1 cell cycle arrest by downregulation of cyclin D1. 9-cis-Retinoic acid significantly decreases phosphorylation of JAK1, STAT3, and STAT5 and downregulated Bcl-xL and cyclin D1
[2]
.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Proliferation Assay [1]
| Cell Line: | CA 9-22 and NA cells |
| Concentration: | 1 μM, 10 μM |
| Incubation Time: | 0 day, 1 day, 3 days, 5 days |
| Result: | Significantly decreased proliferation. |
In Vivo
9-cis-Retinoic acid (1 mg/kg; intravenous injection; daily; for 10 days; male C57BL/6J mice) treatment significantly decreases the serum ALT and AST level, alleviates hepatic necrosis of the bile duct ligation (BDL)-mice [3] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
| Animal Model: | Male C57BL/6J mice (6-8 weeks; 19-22 g) treatment with bile duct ligated [3] |
| Dosage: | 1 mg/kg |
| Administration: | Intravenous injection; daily; for 10 days |
| Result: | Significantly decreased the serum ALT and AST level, alleviated hepatic necrosis. |
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date | Phase |
|---|---|---|---|---|
| NCT01891526 | University Hospital, Gentofte, Copenhagen |
Hepatic Insufficiency
|
December 2010 | |
| NCT00001504 | National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) |
Breast Cancer|Breast Neoplasm
|
May 1996 | Phase 1 |
Appearance
Solid
Shipping
Room temperature in continental US; may vary elsewhere.
Storage
-20°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Solvent & Solubility
DMSO : 25 mg/mL ( 83.21 mM ; Need ultrasonic)
Stock Solutions
| Concentration Solvent Mass | 1 mg | 5 mg | 10 mg |
|---|
| 1 mM | 3.3285 mL | 16.6423 mL | 33.2845 mL |
| 5 mM | 0.6657 mL | 3.3285 mL | 6.6569 mL |
| 10 mM | 0.3328 mL | 1.6642 mL | 3.3285 mL |
-
1.
-
2.
Add each solvent one by one: 10% DMSO >> 90% (20% SBE-β-CD in saline)
Solubility: 2.5 mg/mL (8.32 mM); Suspended solution; Need ultrasonic
References
- [1] Raul Rosas, et al. Retinoids Augment Thiazolidinedione PPARγ Activation in Oral Cancer Cells. Anticancer Res. 2020 Jun;40(6):3071-3080.
- [2] Hua Yang, et al. Effects of 9-cis-retinoic Acid on the Proliferation and Apoptosis of Cutaneous T-cell Lymphoma Cells. Anticancer Drugs. 2019 Jan;30(1):56-64.
- [3] Zhiqing Yuan, et al. 9-cis-retinoic Acid Elevates MRP3 Expression by Inhibiting Sumoylation of RXRα to Alleviate Cholestatic Liver Injury. Biochem Biophys Res Commun. 2018 Sep 3;503(1):188-194.
- [4] V M Manzano, et al. Human Renal Mesangial Cells Are a Target for the Anti-Inflammatory Action of 9-cis Retinoic Acid. Br J Pharmacol. 2000 Dec;131(8):1673-83.
- [5] Gro H Mathisen, et al. Delayed Translocation of NGFI-B/RXR in Glutamate Stimulated Neurons Allows Late Protection by 9-cis Retinoic Acid. Biochem Biophys Res Commun. 2011 Oct 14;414(1):90-5.
Synonyms