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Emixustat hydrochloride

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Emixustat hydrochloride Basic information

Product Name:
Emixustat hydrochloride
Synonyms:
  • (1R)-3-AMino-1-[3-(cyclohexylMethoxyl)phenyl]propan-1-ol hydrochloride
  • (R)-3-Amino-1-(3-(cyclohexylmethoxy)phenyl)propan-1-ol hydrochloride
  • ACU-4429
  • Emixustat hydrochloride
  • Emixustat
  • Benzenemethanol,α-(2-aminoethyl)-3-(cyclohexylmethoxy)-,hydrochloride(1:1),(αR)-
  • Emixustat Hydrochlorde
  • ACU4429;ACU 4429;ACU-4429
CAS:
1141934-97-5
MF:
C16H26ClNO2
MW:
299.83614
Mol File:
1141934-97-5.mol
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Emixustat hydrochloride Chemical Properties

storage temp. 
Store at -20°C
solubility 
DMSO:44.0(Max Conc. mg/mL);146.75(Max Conc. mM)
form 
A crystalline solid
color 
White to off-white
InChI
InChI=1/C16H25NO2.ClH/c17-10-9-16(18)14-7-4-8-15(11-14)19-12-13-5-2-1-3-6-13;/h4,7-8,11,13,16,18H,1-3,5-6,9-10,12,17H2;1H/t16-;/s3
InChIKey
BPZWRYOUJMDQSY-LSQUZMQTNA-N
SMILES
[C@@H](C1=CC=CC(OCC2CCCCC2)=C1)(O)CCN.[H]Cl |&1:0,r|
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Emixustat hydrochloride Usage And Synthesis

Uses

Emixustat (ACU-4429) hydrochloride is an orally active RPE65 inhibitor with an IC50 value of 4.4 nM. Emixustat hydrochloride is also a visual cycle modulator, capable of regulating visual cycle activity by inhibiting retinol isomerization, and holds potential for studying vision disorders such as age-related macular degeneration (AMD)[1][2][3][4].

in vivo

Emixustat (1-10 mg/kg, oral administration, single dose, or twice daily for 6 days; 1 mg/kg, i.p., measurement after 30-60 minutes) reduced cation influx and oxygen consumption in the retinas of brown Norway rats under dark adaptation conditions[3]. Emixustat (0.03-3.0 mg/kg, intravenous injection, once daily for 5 days) inhibits neovascularization and protects the retina in the oxygen-induced retinopathy mouse model[4].

Animal Model:Brown norway rats (200-300 g, 3 months old)[3]
Dosage:1, 5 or 10 mg/kg
Administration:Oral gavage (p.o.), single dose (1, 10 mg/kg), 2 hours followed by 4 hours of dark adaptation, or twice a day for 6 days (5 mg/kg)
Result:Reduced the conductance of the retinal cation channels after dark adaptation.
Animal Model:Brown norway rats (200-300 g, 3 months old)[3]
Dosage:1 mg/kg
Administration:Intravenous injection (i.v.), retinal PO2 was measured 30-60 min later
Result:Reduced the oxygen consumption during dark adaptation.
Animal Model:Oxygen-induced retinopathy (OIR) mice model (BALB/c and 129/Sv / C57BL/6 mixed background)
Dosage:0.03, 0.1, 0.3, 1.0, 3.0 mg/kg
Administration:Intravenous injection (i.v.), once daily for 5 days
Result:Dose-dependently reduced retinal neovascularization.

References

[1] Kiser PD, et al. Catalytic mechanism of a retinoid isomerase essential for vertebrate vision. Nat Chem Biol. 2015 Jun;11(6):409-15. DOI:10.1038/nchembio.1799
[2] Kubota R, et al. Phase 1, dose-ranging study of emixustat hydrochloride (ACU-4429), a novel visual cycle modulator, in healthy volunteers. Retina. 2014 Mar;34(3):603-9. DOI:10.1097/01.iae.0000434565.80060.f8
[3] Kubota R, et al. Emixustat Reduces Metabolic Demand of Dark Activity in the Retina. Invest Ophthalmol Vis Sci. 2019 Nov 1;60(14):4924-4930. DOI:10.1167/iovs.19-28194
[4] Bavik C, et al. Visual Cycle Modulation as an Approach toward Preservation of Retinal Integrity. PLoS One. 2015 May 13;10(5):e0124940. DOI:10.1371/journal.pone.0124940

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