Replaces Prod. #: BML-PI154
Cell permeable inhibitor of γ-secretase (IC50=115nM for total β-amyloid, IC50=200nM for β-amyloid 1-42). It reduces Aβ levels in vivo in plasma and cerebrospinal fluid in young and aged Tg2576 mice. It blocks the proteolytic processing of neurotrophin receptor alike death domain protein (NRADD)Does not inhibit presenilinase. Antagonizes Notch signaling through inhibition of Notch processing. DAPT treatment can influence hematopoietic cell fate decisions and enhances neuronal differentiation in embryonic stem cell-derived embryoid bodies independent of sonic hedgehog (shh) signaling.
Product Specification
| Alternative Name: | N-[N-(3,5-Difluorophenacetyl-L-alanyl)]-S-phenylglycine t-butyl ester, γ-Secretase inhibitor IX |
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| Formula: | C23H26F2N2O4 |
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| MW: | 432.5 |
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| Purity: | ≥98% (NMR) |
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| Appearance: | White to off-white solid. |
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| CAS: | 208255-80-5 |
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| Solubility: | Soluble in 100% ethanol, DMSO (20mg/ml) or dichloromethane. |
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| Long Term Storage: | -20°C |
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| Use/Stability: | Stock solutions are stable for up to 3 months when stored at -20°C. |
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| Handling: | After reconstitution, prepare aliquots and store at -20°C. Packaged under inert gas. Protect from light. |
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Product Literature References
DLL1-mediated Notch activation regulates endothelial identity in mouse fetal arteries: I. Sorensen, et al.; Blood
113, 5680 (2009),
Abstract;
Release of a membrane-bound death domain by gamma-secretase processing of the p75NTR homolog NRADD: J. Cell. Sci.
117, 4099 (2004),
Abstract;
Presenilin endoproteolysis mediated by an aspartyl protease activity pharmacologically distinct from gamma-secretase: W.A. Campbell, et al.; J. Neurochem.
85, 1563 (2003),
Abstract;
The gamma-secretase inhibitor N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester reduces A beta levels in vivo in plasma and cerebrospinal fluid in young (plaque-free) and aged (plaque-bearing) Tg2576 mice: T.A. Lanz et al.; J. Pharmacol. Exp. Ther.
305, 864 (2003),
Abstract;
A gamma-secretase inhibitor blocks Notch signaling in vivo and causes a severe neurogenic phenotype in zebrafish: A. Geling et al.; EMBO Rep.
3, 688 (2002),
Abstract;
Functional gamma-secretase inhibitors reduce beta-amyloid peptide levels in brain: H.F. Dovey, et al.; J. Neurochem.
76, 173 (2001),
Abstract;