AKT Kinase Inhibitor - CAS 842148-40-7
Not Intended for Therapeutic Use. For research use only.
Category:
Inhibitor
Product Name:
AKT Kinase Inhibitor
Catalog Number:
842148-40-7
Synonyms:
2-Propyn-1-ol, 3-[2-(4-amino-1,2,5-oxadiazol-3-yl)-7-(3-aminopropoxy)-1-ethyl-1H-imidazo[4,5-c]pyridin-4-yl]-
CAS Number:
842148-40-7
Description:
AKT Kinase Inhibitor is a Akt Kinase Inhibitor.
Molecular Weight:
357.37
Molecular Formula:
C16H19N7O3
COA:
Inquire
MSDS:
Inquire
Targets:
Akt
Chemical Structure
CAS 842148-40-7 AKT Kinase Inhibitor

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Reference Reading


1.GDF-15 enhances intracellular Ca2+ by increasing Cav1.3 expression in rat cerebellar granule neurons.
Lu JM1, Wang CY1, Hu C1, Fang YJ1, Mei YA2. Biochem J. 2016 Apr 25. pii: BCJ20160362. [Epub ahead of print]
GDF-15 is a novel member of the transforming growth factor (TGF)-β superfamily that has critical roles in the central and peripheral nervous systems. We previously reported that GDF-15 increased delayed rectifier outward K+ currents and Kv2.1 α subunit expression through the TGF-β receptor (TβR) II to activate Src kinase and Akt/mammalian target of rapamycin (mTOR) signaling in rat cerebellar granule neurons (CGNs). Here, we found that treatment of CGNs with GDF-15 for 24 h increased intracellular Ca2+ concentration [Ca2+]i in response to membrane depolarization, as determined by Ca2+ imaging. Whole cell current recordings indicated that GDF-15 increased the inward Ca2+ current (ICa) without altering steady-state activation of Ca2+ channels. Treatment with nifedipine, an inhibitor of L-type Ca2+ channels, abrogated GDF-15-induced increases in [Ca2+]i and ICa The GDF-15-induced increase in ICa was mediated via upregulation of the Cav1.3 α subunit, which was attenuated by inhibiting Akt/mammalian target of rapamycin and extracellular signal-regulated kinase pathways and by pharmacological inhibition of Src-mediated TβRII phosphorylation.
2.MEK-ERK inhibition potentiates WAY-600-induced anti-cancer efficiency in preclinical hepatocellular carcinoma (HCC) models.
Wang K1, Fan Y2, Chen G3, Wang Z4, Kong D5, Zhang P5. Biochem Biophys Res Commun. 2016 Apr 20. pii: S0006-291X(16)30604-0. doi: 10.1016/j.bbrc.2016.04.099. [Epub ahead of print]
The search for novel anti-hepatocellular carcinoma (HCC) agents is important. Mammalian target of rapamycin (mTOR) hyper-activation plays a pivotal role in promoting HCC tumorigenesis and chemoresistance. The current preclinical study evaluated the potential anti-HCC activity by a potent mTOR kinase inhibitor, WAY-600. We showed that WAY-600 inhibited survival and proliferation of HCC cell lines (HepG2 and Huh7) and primary human HCC cells. Caspase-dependent apoptosis was activated by WAY-600 in above HCC cells. Reversely, caspase inhibitors largely attenuated WAY-600's lethality against HCC cells. At the signaling level, WAY-600 blocked mTOR complex 1/2 (mTORC1/2) assemble and activation, yet activated MEK-ERK pathway in HCC cells. MEK-ERK inhibitors, PD-98059 and MEK-162, or MEK1/2 shRNA significantly potentiated WAY-600's cytotoxicity in HCC cells. Further studies showed that WAY-600 intraperitoneal (i.p.) administration in nude mice inhibited p-AKT Ser-473 and displayed significant anti-cancer activity against HepG2 xenografts.
3.Liraglutide prevents beta-amyloid-induced neurotoxicity in SH-SY5Y cells via a PI3K-dependent signaling pathway.
Liu XY1,2, Wang LX1,2, Chen Z3, Liu LB1,2. Neurol Res. 2016 Apr 23:1-7. [Epub ahead of print]
OBJECTIVES: The aim of the study was to investigate the effects of the GLP-1 analog liraglutide on beta-amyloid (Aβ)-induced neurotoxicity in the human neuroblastoma cell line SH-SY5Y and study the underlying mechanisms.
4.The inhibition of Akt-Pdpk1 interaction efficiently suppresses the growth of murine primary liver tumor cells.
Mäemets-Allas K1, Belitškin D1, Jaks V2. Biochem Biophys Res Commun. 2016 Apr 19. pii: S0006-291X(16)30587-3. doi: 10.1016/j.bbrc.2016.04.082. [Epub ahead of print]
The lack of primary liver tumor cells has hampered testing of potential chemotherapeutic agents in vitro. To overcome this issue we developed a primary mouse liver tumor cell line K07074. The K07074 cells were immortal, exhibited a biliary phenotype, formed colonies in soft agar and displayed an increase in Hedgehog, Notch and Akt signaling. To study the effect of single and combined inhibition of the liver tumor-related pathways on the growth of K07074 cells we treated these with small-molecule antitumor agents. While the inhibition of Akt and Notch pathways strongly inhibited the growth of K07074 cells the inhibition of Wnt and Hedgehog pathways was less efficient in cell growth suppression. Interestingly, the inhibition of Akt pathway at the level of Akt-Pdpk1 interaction was sufficient to suppress the growth of tumor cells and no significant additive effect could be detected when co-treated with the inhibitors of Wnt, Hedgehog or Notch pathways.