Product Description
Retinoic acid is a natural agonist of RAR nuclear receptors, with IC50s of 14 nM for RARα/β/γ. Retinoic acid also bind to PPARβ/δ, with Kd of 17 nM.
IC50 & Target: IC50: 14 nM (RARα/β/γ)[5]
Kd: 17 nM (PPARβ/δ), 103 nM (PPARα), 178 nM (PPARγ)[2]
In Vitro: Retinoic acid (All-trans-retinoic acid, ATRA) is a highly potent derivative of vitamin A that is required for virtually all essential physiological processes and functions because of its involvement in transcriptional regulation of over 530 different genes. Retinoic acid exerts its actions by serving as an activating ligand of nuclear retinoic acid receptors (RARα-γ), which form heterodimers with retinoid X receptors (RXRα-γ)[1]. Retinoic acid (RA) bound to PPARα and PPARγ with a low affinity demonstrated by Kd values of 100-200 nM. In contrast, Retinoic acid associates with PPARβ/δ with a Kd of 17 nM, revealing both high affinity and isotype selectivity[2]. Undifferentiated P19 cells express the Retinoic acid (RA) receptors RARα, RARβ, RARγ, and PPARβ/δ, as well as the Retinoic acid -binding proteins CRABP-II and FABP5. Induction of differentiation by treatment of cells with Retinoic acid results in transient up-regulation of CRABP-II and down-regulation of FABP5 that are observed at the level of both the respective proteins and mRNAs. Following the initial decrease, the level of both FABP5 protein and mRNA increases to attain a 2-2.5-fold higher level in mature neurons as compared with undifferentiated P19 cells. Induction of differentiation does not markedly affect the levels of either RARα or PPARβ/δ. The level of RARγ mRNA decreases by about 5-fold by day 4 and remained low in mature neurons[3]. Retinoic acid (RA) is a morphogen derived from retinol (vitamin A) that plays important roles in cell growth, differentiation, and organogenesis. The Retinoic acid interacts with retinoic acid receptor (RAR) and retinoic acid X receptor (RXR) which then regulate the target gene expression[4].
Information
CAS No302-79-4
FormulaC20H28O2
Clinical Informationclinicalinformation
PathwayMetabolic Enzyme/Protease
Cell Cycle/DNA Damage
Metabolic Enzyme/Protease
TargetRAR/RXR
PPAR
Endogenous Metabolite
Specifications
FormLight yellow to yellow (Solid)
Purity / Grade>98%
SolubilityH2O : < 0.1 mg/mL (insoluble); DMSO : ≥ 50 mg/mL (166.42 mM)
DMSO : ≥ 50 mg/mL (166.42 mM)
Smilessmiles
Misc Information
Storage Instruction-20°C, sealed storage, away from moisture and light
* In solvent : -80°C, for 6 months
-20°C, 1 month (sealed storage, away from moisture
and light)
Alternative NamesATRA;Tretinoin;Vitamin A acid;all-trans-Retinoic acid
Observed Molecular Weight300.44
NotesInVIVO:
Add each solvent one by one: 10% DMSO >> 40% PEG300 >> 5% Tween-80 >> 45% saline
Solubility: 2.5 mg/mL (8.32 mM); Suspended solution; Need ultrasonic and warming
1. 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
2. Add each solvent one by one: 10% DMSO >> 90% corn oil
Solubility: ≥ 2.5 mg/mL (8.32 mM); Clear solution
3. Add each solvent one by one: 5% DMSO >> 40% PEG300 >> 5% Tween-80 >> 50% saline Solubility: 2.5 mg/mL (8.32 mM); Suspended solution; Need ultrasonic
4. Add each solvent one by one: 5% DMSO >> 95% (20% SBE-β-CD in saline)
Solubility: 2.5 mg/mL (8.32 mM); Suspended solution; Need ultrasonic
InVitro: Retinoic acid (All-trans-retinoic acid, ATRA) is a highly potent derivative of vitamin A that is required for virtually all essential
physiological processes and functions because of its involvement in transcriptional regulation of over 530 different genes.
Retinoic acid exerts its actions by serving as an activating ligand of nuclear retinoic acid receptors (RARα-γ), which form
heterodimers with retinoid X receptors (RXRα-γ)
.
Retinoic acid (RA) bound to PPARα and PPARγ with a low affinity demonstrated by Kd values of 100-200 nM. In contrast,
Retinoic acid associates with PPARβ/δ with a Kd of 17 nM, revealing both high affinity and isotype selectivity
.
Undifferentiated P19 cells express the Retinoic acid (RA) receptors RARα, RARβ, RARγ, and PPARβ/δ, as well as the Retinoic
acid -binding proteins CRABP-II and FABP5. Induction of differentiation by treatment of cells with Retinoic acid results in
transient up-regulation of CRABP-II and down-regulation of FABP5 that are observed at the level of both the respective
proteins and mRNAs. Following the initial decrease, the level of both FABP5 protein and mRNA increases to attain a 2-2.5-
fold higher level in mature neurons as compared with undifferentiated P19 cells. Induction of differentiation does not
markedly affect the levels of either RARα or PPARβ/δ. The level of RARγ mRNA decreases by about 5-fold by day 4 and
remained low in mature neurons
.
Retinoic acid (RA) is a morphogen derived from retinol (vitamin A) that plays important roles in cell growth, differentiation,
and organogenesis. The Retinoic acid interacts with retinoic acid receptor (RAR) and retinoic acid X receptor (RXR) which
then regulate the target gene expression
References1]. Wu L, et al. Retinoid X Receptor Agonists Upregulate Genes Responsible for the Biosynthesis of All-Trans-Retinoic Acid in Human Epidermis. PLoS One. 2016 Apr
14;11(4):e0153556.
[2]. Shaw N, et al. Retinoic acid is a high affinity selective ligand for the peroxisome proliferator-activated receptor beta/delta. J Biol Chem. 2003 Oct 24;278(43):41589-92.
[3]. Yu S, et al. Retinoic acid induces neurogenesis by activating both retinoic acid receptors (RARs) and peroxisomeproliferator-activated receptor β/δ (PPARβ/δ). J Biol
Chem. 2012 Dec 7;287(50):42195-205.
[4]. Kam RK, et al. Retinoic acid synthesis and functions in early embryonic development. Cell Biosci. 2012 Mar 22;2(1):11.
[5]. Apfel C, et al. A retinoic acid receptor alpha antagonist selectively counteracts retinoic acid effects. Proc Natl Acad Sci U S A. 1992 Aug 1;89(15):7129-33.
[6]. Xiu Jun Wang, et al. Identification of retinoic acid as an inhibitor of transcription factor Nrf2 through activation of retinoic acid receptor alpha. Proc Natl Acad Sci U S A.
2007 Dec 4;104(49):19589-94