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Signaling Pathway




DAPT Chemical Structure

DAPT is inhibitor of γ-secretase. DAPT causes a reduction in Aβ40 and Aβ42 levels in human primary neuronal cultures (IC50 values are 115 and 200 nM for total Aβ and Aβ42 respectively) and in brain extract, cerebrospinal fluid and plasma in vivo. Does not

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DAPT Data Sheet

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Purity: 99.83%

Cell Cycle/DNA Damage

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Biological Activity of DAPT

DAPT is inhibitor of γ-secretase. DAPT causes a reduction in Aβ40 and Aβ42 levels in human primary neuronal cultures (IC50 values are 115 and 200 nM for total Aβ and Aβ42 respectively) and in brain extract, cerebrospinal fluid and plasma in vivo. Does not effect APPα and APPβ levels. DAPT blocks Notch signaling in hybrid human-mouse fetal thymus organ culture (FTOC). Activity causes neural cells to commit to neuronal differentiation.

Clinical Information


References on DAPT

1 . Oikawa N, Goto M, Ikeda K, Taguchi R, Yanagisawa K.The γ-secretase inhibitor DAPT increases the levels of gangliosides at neuritic terminals of differentiating PC12 cells.Neurosci Lett. 2012 Sep 6;525(1):49-53. Epub 2012 Jul 31.
Mutations in presenilins are the major cause of early onset familial Alzheimer disease. It has recently been argued that clinical presenilin mutations work as loss-of-function but not toxic gain-of-function. To investigate whether presenilins are involved in the regulation of the distribution of neuronal membrane lipids, we treated neuronally differentiated PC12 cells with DAPT, an inhibitor of presenilin-dependent γ-secretase, and performed lipid analyses of neuritic terminals, which is an initial site of Aβ deposition in brains, using liquid chromatography/electrospray ionization tandem mass spectrometry (LC/ESI-MS/MS) in combination with multiple reaction monitoring (MRM). With DAPT treatment, levels of sphingomyelin, phosphatidylcholine, and cholesterol remained unchanged. However, DAPT treatment increased the ganglioside levels in PC12 neuritic terminals. Together with a previous finding that accumulation of gangliosides at neuritic terminals facilitates Aβ assembly and deposition, the present data suggest that the loss-of-function of presenilins, i.e., a decrease in γ-secretase activity, has an impact on neuronal membrane architecture in a way that eventually exacerbates Alzheimer pathology.

2 . Yuan YY, Zeng ZY, Chen JM.[Effect of DAPT on Proliferation and Apoptosis of Human Multiple Myeloma Cell Line RPMI8226].Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2012 Jul;20(4):922-5.
The aim of this study was to explore the effect of DAPT (N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycinet-butyl ester) on proliferation in vitro of human multiple myeloma cell line RPMI8226 and its underlying mechanism. The proliferation of RPMI8226 cells was detected by CCK-8 method; flow cytometry was employed to assay the cell apoptosis rate;the expressions of Notch1 and Hes1 proteins were detected by Western blot. The results indicated that the proliferation of human RPMI8226 cells significantly decreased after treatment with DAPT 0.5 - 5.0 μmol/L for 24 - 72 h (P < 0.05) in a concentration- and time-dependent manner. DAPT significantly induced apoptosis of RPMI8226 cells (P < 0.05). The expressions of Notch1 and Hes1 proteins were gradually downregulated with the increase of DAPT concentration. It is concluded that the DAPT can inhibit the proliferation of RPMI8226 cells, which may be related with the down-regulation of the protein expression of Notchl and Hes1.

3 . Zhou JX, Han JB, Chen SM, Xu Y, Kong YG, Xiao BK, Tao ZZ.γ-secretase inhibition combined with cisplatin enhances apoptosis of nasopharyngeal carcinoma cells.Exp Ther Med. 2012 Feb;3(2):357-361. Epub 2011 Dec 6.
The Notch signaling pathway plays an important role in the proliferation and differentiation of cells. Although recent studies have shown that Notch plays a role in the mechanisms of cisplatin resistance, the mechanism by which Notch plays roles in intrinsic or acquired cisplatin resistance remains unclear. In the present study, poorly differentiated nasopharyngeal carcinoma cells were treated with a γ-secretase inhibitor (DAPT), which led to a decrease in the Notch intracellular domain and inhibition of Notch signaling. Treatment was not sufficient to induce pronounced apoptosis of CNE-2 cells, but did result in the down-regulation of the P-glycoprotein and ERCC1 protein. In contrast, the combined treatment of DAPT and cisplatin induced substantial cell apoptosis compared to cisplatin treatment alone.

4 . Munnamalai V, Hayashi T, Bermingham-McDonogh O.Notch prosensory effects in the Mammalian cochlea are partially mediated by fgf20.J Neurosci. 2012 Sep 12;32(37):12876-84.
Hearing loss is becoming an increasingly prevalent problem affecting more than 250 million people worldwide. During development, fibroblast growth factors (FGFs) are required for inner ear development as well as hair cell formation in the mammalian cochlea and thus make attractive therapeutic candidates for the regeneration of sensory cells. Previous findings showed that Fgfr1 conditional knock out mice exhibited hair cell and support cell formation defects. Immunoblocking with Fgf20 antibody in vitro produced a similar phenotype. While hair cell differentiation in mice starts at embryonic day (E)14.5, beginning with the inner hair cells, Fgf20 expression precedes hair cell differentiation at E13.5 in the cochlea. This suggests a potential role for Fgf20 in priming the sensory epithelium for hair cell formation. Treatment of explants with a gamma-secretase inhibitor, DAPT, decreased Fgf20 mRNA, suggesting that Notch is upstream of Fgf20. Notch signaling also plays an early role in prosensory formation during cochlear development. In this report we show that during development, Notch-mediated regulation of prosensory formation in the cochlea occurs via Fgf20. Addition of exogenous FGF20 compensated for the block in Notch signaling and rescued Sox2, a prosensory marker, and Gfi1, an early hair cell marker in explant cultures. We hypothesized that Fgf20 plays a role in specification, amplification, or maintenance of Sox2 expression in prosensory progenitors of the developing mammalian cochlea.

5 . El Mouedden et al (2006) Reduction in Abeta levels in Sprague Dawley rat after oral administration of the functional gamma-secretase inhibitor, DAPT: a novel non-transgenic model for Abeta production inhibitors. Curr.Pharmaceut.Des. 12 671.
Considerable effort has been made to develop drugs that delay or prevent neurodegeneration. These include inhibitors of Abeta-generating proteases for the treatment of Alzheimer's disease. Testing the amyloid hypothesis in vivo requires molecules that are capable of entering the CNS and that produce a substantial reduction in brain Abeta levels. Plaque-developing APP transgenic mice are currently widely used as an in vivo model of choice as these animals produce readily measurable amounts of human Abeta. They are very useful in the testing of a variety of amyloid-lowering approaches but their use for compound screening is often limited by their cost. Transgenic animals also require extensive, time-consuming breeding programs and can show high inter-animal differences in the expression level of the transgene. ...

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