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Key Documents

SML3830

Sigma-Aldrich

BAF312

≥98% (HPLC)

Synonym(s):

(E)-1-(4-(1-(((4-cyclohexyl-3-(trifluoromethyl)benzyl)oxy)imino)ethyl)-2-ethylbenzyl)azetidine-3-carboxylic acid, 1-[[4-[(1E)-1-[[[4-Cyclohexyl-3-(trifluoromethyl)phenyl]methoxy]imino]ethyl]-2-ethylphenyl]methyl]-3-azetidinecarboxylic acid, 1-{4-[(1E)-(4-Cyclohexyl-3-trifluoromethyl-benzyloxyimino)-ethyl]-2-ethyl-benzyl}-azetidine-3-carboxylic acid, BAF 312, BAF-312, Siponimod

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About This Item

Empirical Formula (Hill Notation):
C29H35F3N2O3
CAS Number:
Molecular Weight:
516.60
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

-10 to -25°C

Biochem/physiol Actions

BAF312 (Siponimod) is an orally active, potent and subtype-selective sphingosine-1-phosphate (S1P) receptor agonist (GTPγ binding EC50 = 0.39 nM/S1P1, 0.98 nM/S1P5, 750 nM/S1P4, >1 µM/S1P3, >10 µM/S1P2). BAF312 oral administration causes a dose-dependent decrease in peripheral lymphocyte counts (by 88% 8h post 1 mg/kg, by 50% 6h post 0.14 mg/kg).

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Discovery of BAF312 (Siponimod), a Potent and Selective S1P Receptor Modulator
ACS Medicinal Chemistry Letters, 4(3), 333-337 (2013)
P Gergely et al.
British journal of pharmacology, 167(5), 1035-1047 (2012-06-01)
BAF312 is a next-generation sphingosine 1-phosphate (S1P) receptor modulator, selective for S1P(1) and S1P(5 ) receptors. S1P(1) receptors are essential for lymphocyte egress from lymph nodes and a drug target in immune-mediated diseases. Here, we have characterized the immunomodulatory potential
Samuel J Jackson et al.
Journal of neuroinflammation, 8, 76-76 (2011-07-07)
Microglial activation in multiple sclerosis has been postulated to contribute to long-term neurodegeneration during disease. Fingolimod has been shown to impact on the relapsing remitting phase of disease by modulating autoreactive T-cell egress from lymph organs. In addition, it is

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