| Identification | Back Directory | [Name]
Aftin-4 | [CAS]
866893-90-5 | [Synonyms]
Aftin-4
Aftin-4 >=98% (HPLC)
AFTIN-4;AFTIN 4;AFTIN4
N6-methyl-(R)-roscovitine
1-Butanol, 2-[[9-(1-methylethyl)-6-[methyl(phenylmethyl)amino]-9H-purin-2-yl]amino]-, (2R)- | [Molecular Formula]
C20H28N6O | [MDL Number]
MFCD30187584 | [MOL File]
866893-90-5.mol | [Molecular Weight]
368.48 |
| Chemical Properties | Back Directory | [storage temp. ]
-20°C | [solubility ]
DMSO: soluble | [form ]
powder | [color ]
white to beige | [InChI]
1S/C20H28N6O/c1-5-16(12-27)22-20-23-18(25(4)11-15-9-7-6-8-10-15)17-19(24-20)26(13-21-17)14(2)3/h6-10,13-14,16,27H,5,11-12H2,1-4H3,(H,22,23,24)/t16-/m1/s1 | [InChIKey]
YPYWONAECUVKHY-MRXNPFEDSA-N | [SMILES]
[n]1(c2nc(nc(c2nc1)N(Cc3ccccc3)C)N[C@@H](CO)CC)C(C)C |
| Hazard Information | Back Directory | [Description]
Aftin-4 is an inducer of amyloid-β (1-42) (Aβ42). It selectively increases extracellular Aβ42 over Aβ40 production in N2a-AβPP695 cells when used at concentrations ranging from 1 to 100 mM. In vivo, aftin-4 (3-20 nmol/animal, i.c.v.) increases hippocampal Aβ42 content, lipid peroxidation, and production of the pro-inflammatory cytokines IL-1β, IL-6, and TNF-α in mice. It also induces spatial working and spatial reference memory deficits in mice, effects that are reversed by co-administration of the γ-secretase inhibitor BMS-299,897. | [Uses]
Aftin 4, is an Amyloid-β42 (Aβ42) inducer, that increases Aβ1-42 levels in vivo in mice and provokes rapidly a sustained toxicity highly reminiscent of Alzheimer’s disease (AD). | [Biochem/physiol Actions]
Aftin-4, an amyloid forty-two inducer, activates γ-secretase, promoting the generation of amyloid-β-1-42 (Aβ1-42) from amyloid-β protein precursor. Aftin-4 increased Aβ-1-42, but not Aβ-1-40 in mouse hipppocampus, accompanied by learning deficits and mitochondrial ultrastructural changes similar to those found in the brains of patients with AD. Aftin-4 can thus be used to induce a rapid, acute Alzheimer′s disease-like toxicity in the rodent brain. | [in vivo]
Aftin-4 increases Aβ1-42 levels in vivo in mice and provokes rapidly a sustained toxicity highly reminiscent of Alzheimer’s disease (AD). Aftin-4 is administered at increasing doses, between 3 and 20 nmol/mouse, into the lateral ventricle and animals are sacrificed at various time points, between 3 to 14 days after injection. The hippocampus is dissected out the contents in Aβ1-40 or Aβ1-42 is determined using a mouse ELISA assay. Aftin-4 dose-dependently and significantly increases Aβ1-42 content, up to +216% at the highest dose tested[1]. | [storage]
+4°C | [References]
[1] ARNAUD HOCHARD. Aftins increase amyloid-β42, lower amyloid-β38, and do not alter amyloid-β40 extracellular production in vitro: toward a chemical model of Alzheimer’s disease?[J]. Journal of Alzheimer’s Disease, 2013, 35 1: 107-120. DOI: 10.3233/jad-121777
[2] JOHANN MEUNIER. Brain toxicity and inflammation induced in vivo in mice by the amyloid-β forty-two inducer aftin-4, a roscovitine derivative.[J]. Journal of Alzheimer’s Disease, 2015, 44 2: 507-524. DOI: 10.3233/jad-140711 |
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