5,5,8,8-Tetramethyl-5,6,7,8-tetrahydronaphthalen-2-ylamine (BAT-008826)
* For research use only

Catalog number
CAS number
Molecular Formula
Molecular Weight
5,5,8,8-Tetramethyl-5,6,7,8-tetrahydronaphthalen-2-ylamine; 5,6,7,8-Tetrahydro-5,5,8,8-tetramethyl-2-naphthylamine
Melting Point
Boiling Point
310.189ºC at 760 mmHg
1.Experimental effect of retinoic acids on apoptosis during the development of diabetic retinopathy.
Nishikiori N1, Osanai M, Chiba H, Kojima T, Inatomi S, Ohguro H, Sawada N. Clin Ophthalmol. 2008 Mar;2(1):233-5.
PURPOSE: This study was conducted to investigate whether retinoic acids (RAs) had any effect on apoptosis during the development of diabetic retinopathy.
2.Reversal by RARα agonist Am580 of c-Myc-induced imbalance in RARα/RARγ expression during MMTV-Myc tumorigenesis.
Bosch A, Bertran SP, Lu Y, Garcia A, Jones AM, Dawson MI, Farias EF. Breast Cancer Res. 2012 Aug 24;14(4):R121. doi: 10.1186/bcr3247.
INTRODUCTION: Retinoic acid signaling plays key roles in embryonic development and in maintaining the differentiated status of adult tissues. Recently, the nuclear retinoic acid receptor (RAR) isotypes α, β and γ were found to play specific functions in the expansion and differentiation of the stem compartments of various tissues. For instance, RARγ appears to be involved in stem cell compartment expansion, while RARα and RARβ are implicated in the subsequent cell differentiation. We found that over-expressing c-Myc in normal mouse mammary epithelium and in a c-Myc-driven transgenic model of mammary cancer, disrupts the balance between RARγ and RARα/β in favor of RARγ.
3.The effect of Am-80, a synthetic retinoid, on spinal cord injury-induced motor dysfunction in rats.
Takenaga M1, Ohta Y, Tokura Y, Hamaguchi A, Shudo K, Okano H, Igarashi R. Biol Pharm Bull. 2009 Feb;32(2):225-31.
The present study investigated the effect of 4[(5,6,7,8-tetrahydro-5,5,8,8,-tetramethyl-2-naphthalenyl)carbamoyl] benzoic acid (Am-80), a synthetic retinoid, on spinal cord injury (SCI) in rats. Treatment with Am-80 (orally and subcutaneously) significantly promoted recovery from SCI-induced motor dysfunction. On day 28 after injury, the lesion cavity was markedly reduced, while the expression of myelin basic protein (MBP; myelin), betaIIItubulin (neuron), and glial fibrillary acidic protein (GFAP; astrocyte) was increased, in comparison with SCI controls. Interestingly, expression of neurotrophin receptor, tyrosine kinase B (TrkB) was over 3-fold higher after Am-80 treatment than in SCI controls. A lot of TrkB-positive cells as well as brain-derived neurotrophic factor (BDNF)-positive ones were observed around the injured site. Am-80 (10 microM) combined with BDNF (100 ng/ml) promoted extensive neurite outgrowth and TrkB gene expression by cultured SH-SY5Y cells, as did all-trans retinoic acid (ATRA).
4.Gene regulation of CYP4F11 in human keratinocyte HaCaT cells.
Wang Y1, Bell JC, Keeney DS, Strobel HW. Drug Metab Dispos. 2010 Jan;38(1):100-7. doi: 10.1124/dmd.109.029025.
Mechanisms regulating CYP4F genes remain under investigation, although characterization of CYP4F regulatory modalities would facilitate the discovery of new drug targets. This present study shows that all-trans- and 9-cis-retinoic acids can inhibit CYP4F11 expression in human keratinocyte-derived HaCaT cells. Transrepression of many genes by retinoic acids is mediated by interactions between retinoid receptors and the activator protein 1 (AP-1) complex. Proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta, which can activate the AP-1 complex, induce CYP4F11 transcription in HaCaT cells. The c-Jun N-terminal kinase (JNK)-specific inhibitor 1,9-pyrazoloanthrone (SP600125) blocked the induction of CYP4F11 by both cytokines, indicating involvement of the JNK pathway. Furthermore, TNF-alpha failed to induce CYP4F11 transcription when HaCaT cells were preincubated with retinoic acids. Retinoic acids are ligands for the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs).
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