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Merck
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Documenti fondamentali

SML2916

Sigma-Aldrich

AAL-R

≥98% (HPLC)

Sinonimo/i:

(R)-2-Amino-2-methyl-4-[4-(heptyloxy)phenyl]butan-1-ol, (R)-2-Amino-4-(4-(heptyloxy)phenyl)-2-methylbutan-1-ol, (R)-2-Amino-4-(4-heptyloxyphenyl)-2-methylbutanol, AAL(R)

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About This Item

Formula empirica (notazione di Hill):
C18H31NO2
Numero CAS:
Peso molecolare:
293.44
Codice UNSPSC:
41106300
Codice UNSPSC:
12352200
NACRES:
NA.77

Livello qualitativo

Saggio

≥98% (HPLC)

Stato

powder

Colore

white to beige

Solubilità

DMSO: 2 mg/mL, clear

Temperatura di conservazione

2-8°C

Stringa SMILE

C[C@](N)(CO)CCC1=CC=C(C=C1)OCCCCCCC

InChI

1S/C18H31NO2/c1-3-4-5-6-7-14-21-17-10-8-16(9-11-17)12-13-18(2,19)15-20/h8-11,20H,3-7,12-15,19H2,1-2H3/t18-/m1/s1
ITJCKQTXCLGXHE-GOSISDBHSA-N

Azioni biochim/fisiol

AAL-R [AAL(R)] is a FTY720 (fingolimod) analog and a much more rapidly activated sphingosine 1-phosphate receptor (S1P) agonist by sphingosine kinase 2 (SphK2)-mediated phosphorylation in vitro and in vivo. AAL-R triggers lymphocytes apoptosis in a SphK2-dependent manner (34%/84% remaining parental/SphK2-deficient Jurkat; 24 h 5 μM) with a significantly higher efficacy than its S-enantiomer AAL-S or FTY720 (%PI- mouse splenocytes = 27/ALL-R vs 56/FTY720 or ALL-S; 24 h 4 μM). AAL-R (0.1-0.3 mg/kg intratracheally), but not ALL-S, inhibits T-cell response to influenza infection and reduces pulmonary inflammation during Bordetella pertussis infection in mice (0.5 mg/kg intranasally).
More phosphorylatable FTY720 (fingolimod) analog with greater SphK2-dependent sphingosine 1-phosphate receptor (S1P) agonist efficacy in vitro and in vivo.

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


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Certificati d'analisi (COA)

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Jeremy Ardanuy et al.
Journal of immunology (Baltimore, Md. : 1950), 204(8), 2192-2202 (2020-03-11)
Type I and III IFNs play diverse roles in bacterial infections, being protective for some but deleterious for others. Using RNA-sequencing transcriptomics we investigated lung gene expression responses to Bordetella pertussis infection in adult mice, revealing that type I and
Ciaran Skerry et al.
The Journal of infectious diseases, 215(2), 278-286 (2016-11-07)
Recent data have demonstrated the potential of sphingosine 1-phosphate (S1P) receptor (S1PR) agonism in the treatment of infectious diseases. A previous study used a murine model of Bordetella pertussis infection to demonstrate that treatment with the S1PR agonist AAL-R reduces

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