| Name | Retinoic acid |
| Description | Retinoic acid (Tretinoin), a metabolite of vitamin A, is a natural agonist of the retinoic acid receptor RAR and inhibits RARα/β/γ (IC50=14 nM). Retinoic acid induces cellular differentiation, reduces cellular proliferation, and inhibits tumorigenesis. |
| Cell Research | Retinoic acid is dissolved in DMSO and stored, and then diluted with appropriate medium before use[3]. P19 cell are induced to undergo neuronal differentiation according to established procedures. Briefly, cells are cultured on 1% agarose-coated 10 cm dishes at 3×10 5 cells/mL in α-minimal essential medium supplemented with 10% FBS. Differentiation is induced by addition of Retinoic acid (1 μM) and medium containing Retinoic acid replaced 2 days later. On day 4, cell aggregates are collected by centrifugation, separated to single cells by trypsin/EDTA treatment, replated onto poly-L-lysine-coated plates, and cultured in α-minimal essential medium supplemented with 10% FBS. On day 6, medium is replaced with neurobasal medium containing B27 supplement and 2 mM GlutaMAX. Medium is replaced every 2 days for an additional week[3]. |
| In vitro | Tretinoin prevents skin atrophy induced by corticosteroids in hairless mice. When co-administered with miquimod in guinea pigs, tretinoin induces tattoo fading and moderate pigment clearance histopathologically. Applications of tretinoin on incisions in the skin of 45 CD-1 mice increase fibroblast differentiation and reduce collagen production. In aged male Fischer 344 rats treated with tretinoin, renal cortex protein content is 30% lower compared to controls, potentially due to suppressed expression of tumor necrosis factor-β1 and osteopontin. |
| In vivo | In studies evaluating the impact on glutathione levels and catalase activity, Tretinoin increased both metrics in a time- and dose-dependent manner, offering protective and mitigating effects against H2O2 cytotoxicity in human renal mesangial cells. Treatment with Tretinoin resulted in elevated mRNA levels of catalase and γ-glutamylcysteine synthetase (the catalytic subunit responsible for the rate-limiting step in reduced glutathione synthesis) in cultured mesangial cells. Additionally, Tretinoin upregulated matrix metalloproteinase-8/13 in human keloid-derived fibroblasts. |
| Storage | keep away from direct sunlight,store at low temperature | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| Solubility Information | DMSO : 45 mg/mL (149.78 mM)
10% DMSO+40% PEG300+5% Tween 80+45% Saline : 5.6 mg/mL (18.64 mM), Suspension. Please add co-solvents sequentially, clarifying the solution as much as possible before adding the next one. Dissolve by heating and/or sonication if necessary. Working solution is recommended to be prepared and used immediately.
Ethanol : 6 mg/mL (19.97 mM)
H2O : < 1 mg/mL (insoluble or slightly soluble)
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| Keywords | PPAR | inhibit | Endogenous Metabolite | RAR/RXR | Inhibitor | Retinoic acid | Retinoic acid receptors | Retinoid X receptors | Peroxisome proliferator-activated receptors | Autophagy |
| Inhibitors Related | Sucrose | Hydroxychloroquine | Daidzein | Guanidine hydrochloride | Ferulic Acid | Paeonol | Glycerol | Thymidine |
| Related Compound Libraries | Anti-Tumor Natural Product Library | Terpene Natural Product Library | Anti-Cancer Clinical Compound Library | Natural Product Library | FDA-Approved Drug Library | Natural Product Library for HTS | Anti-Aging Compound Library | Bioactive Compounds Library Max | Anti-Cancer Active Compound Library | Anti-Cancer Drug Library |
United States
