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Merck

B7688

PiB

≥98% (HPLC)

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About This Item

Empirical Formula (Hill Notation):
C22H18N2O8
CAS Number:
Molecular Weight:
438.39
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352200
MDL number:
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Product Name

PiB, ≥98% (HPLC)

InChI key

WNKQGFNIIHNGQM-UHFFFAOYSA-N

SMILES string

O=C(C1=C2C(C3=CC=C24)=C(C(N(CC(OCC)=O)C3=O)=O)C=C1)N(CC(OCC)=O)C4=O

InChI

1S/C22H18N2O8/c1-3-31-15(25)9-23-19(27)11-5-7-13-18-14(8-6-12(17(11)18)20(23)28)22(30)24(21(13)29)10-16(26)32-4-2/h5-8H,3-4,9-10H2,1-2H3

assay

≥98% (HPLC)

form

powder

color

white to light brown

solubility

DMSO: 1-2 mg/mL (warmed)

storage temp.

2-8°C

Quality Level

Biochem/physiol Actions

PiB is a Pin-1 inhibitor.
PiB is an inhibitor of the peptidylprolyl isomerase Pin-1. Inhibition of Pin-1 leads to destabilization of the transcription factor Nanog, which is required for maintenance of embryonic stem cell cultures.

Storage Class

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


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Sven H C Askes et al.
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Light upconversion is a very powerful tool in bioimaging as it can eliminate autofluorescence, increase imaging contrast, reduce irradiation damage, and increase excitation penetration depth in vivo. In particular, triplet-triplet annihilation upconverting (TTA-UC) nanoparticles and liposomes offer high upconversion efficiency
Lisa Vermunt et al.
Neurology, 92(23), e2699-e2705 (2019-05-10)
To identify potential predictors for outcome in individuals with mild cognitive impairment (MCI) who have reverted to normal cognition (NC). We selected individuals with MCI, who reverted at follow-up to NC, with follow-up after reversion from Alzheimer's Disease Neuroimaging Initiative.
Takamasa Yokoi et al.
Frontiers in aging neuroscience, 10, 304-304 (2018-10-23)
Background: Imaging studies in Alzheimer's disease (AD) have yet to answer the underlying questions concerning the relationship among tau retention, neuroinflammation, network disruption and cognitive decline. We compared the spatial retention patterns of 18F-THK5351 and resting state network (RSN) disruption
Christopher M Lee et al.
Journal of Alzheimer's disease : JAD, 62(4), 1691-1702 (2018-04-05)
On target 18F-Flortaucipir (FTP) binding of Alzheimer's disease tau aggregates and off-target binding of melanocytes have been demonstrated with autoradiography. We aimed to investigate the hypothesis that if binding in choroid plexus (CP) is due to melanocytes, the signal would
Inge M W Verberk et al.
Alzheimer's research & therapy, 12(1), 118-118 (2020-09-30)
Blood-based biomarkers for Alzheimer's disease (AD) might facilitate identification of participants for clinical trials targeting amyloid beta (Abeta) accumulation, and aid in AD diagnostics. We examined the potential of plasma markers Abeta(1-42/1-40), glial fibrillary acidic protein (GFAP) and neurofilament light

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