ChemicalBook CAS DataBase List 2140911-49-3

2140911-49-3

Name	Benzamide, 4-[[[(2-aminoethyl)amino]carbonyl]amino]-N-(1,2,3,4,5,6,7,8-octahydro-1,1,4,4,5,5,8,8-octamethyl-9-anthracenyl)-
CAS	2140911-49-3
Molecular Formula	C32H46N4O2
Molecular Weight	518.73
MOL File	2140911-49-3.mol

Chemical Properties

Boiling point	555.0±50.0 °C(Predicted)
density	1.085±0.06 g/cm3(Predicted)
storage temp.	Store at -20°C
solubility	DMSO : 20 mg/mL (38.56 mM; ultrasonic and warming and adjust pH to 3 with HCl and heat to 60°C)
form	Solid
pka	13.28±0.46(Predicted)
color	White to off-white

Hazard Information

Uses

OAB-14, is a Bexarotene (HY-14171) derivative, improves Alzheimer's disease-related pathologies and cognitive impairments by increasing β-amyloid clearance in APP/PS1 mice. OAB-14 effectively ameliorates the dysfunction of the endosomal-autophagic-lysosomal pathway in APP/PS1 transgenic mice[1][2].

in vivo

OAB-14 significantly alleviates cognitive impairments in amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic mice after administration for 15 days or 3 months. OAB-14 rapidly cleared 71% of Aβ by promoting microglia phagocytosis and increasing IDE and NEP expression. OAB-14 also attenuates the downstream pathological events of Aβ accumulation, such as synaptic degeneration, neuronal loss, tau hyperphosphorylation and neuroinflammation in APP/PS1 mice. OAB-14 has no significant effect on body weight or liver toxicity after acute and chronic treatment^[1].
OAB-14 facilitates receptor-mediated endocytosis and restores autophagy flux via the AMPK/mTOR pathway. OAB-14 enhances the lysosomal activity, and reduced Aβ accumulation in lysosomes is observed in OAB-14-treated AD mice^[2].

storage

Store at -20°C

References

[1] Guo X, et al. OAB-14 Effectively Ameliorates the Dysfunction of the Endosomal-Autophagic-Lysosomal Pathway in APP/PS1 Transgenic Mice. ACS Chem Neurosci. 2021;12(21):3985-3993. DOI:10.1021/acschemneuro.1c00209
[2] Yuan C, et al. OAB-14, a bexarotene derivative, improves Alzheimer's disease-related pathologies and cognitive impairments by increasing β-amyloid clearance in APP/PS1 mice. Biochim Biophys Acta Mol Basis Dis. 2019;1865(1):161-180. DOI:10.1016/j.bbadis.2018.10.028

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