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1-BOC-4-ETHOXYCARBONYL PIPERAZINE - CAS 219509-82-7

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Category
Main Product
Product Name
1-BOC-4-ETHOXYCARBONYL PIPERAZINE
Catalog Number
219509-82-7
Synonyms
1-BOC-4-ETHOXYCARBONYL PIPERAZINE
CAS Number
219509-82-7
Molecular Weight
258.31
Molecular Formula
C12H22N2O4
COA
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MSDS
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Canonical SMILES
CCOC(=O)N1CCN(CC1)C(=O)OC(C)(C)C
InChI
InChI=1S/C12H22N2O4/c1-5-17-10(15)13-6-8-14(9-7-13)11(16)18-12(2,3)4/h5-9H2,1-4H3
InChIKey
QKOGYJOCBHEODH-UHFFFAOYSA-N
Structure
CAS 219509-82-7 1-BOC-4-ETHOXYCARBONYL PIPERAZINE
Specification
Purity
95%
Reference Reading
1.Novel piperazine core compound induces death in human liver cancer cells: possible pharmacological properties.
Samie N1, Muniandy S2, Kanthimathi MS2,3, Haerian BS1, Raja Azudin RE4. Sci Rep. 2016 Apr 13;6:24172. doi: 10.1038/srep24172.
The current study evaluates the cytotoxic mechanism of a novel piperazine derivate designated as PCC against human liver cancer cells. In this context, human liver cancer cell lines, SNU-475 and 243, human monocyte/macrophage cell line, CRL-9855, and human B lymphocyte cell line, CCL-156, were used to determine the IC50 of PCC using the standard MTT assay. PCC displayed a strong suppressive effect on SNU-475 and SNU-423 cells with an IC50 value of 6.98 ± 0.11 μg/ml and 7.76 ± 0.45 μg/ml respectively, after 24 h of treatment. Significant dipping in the mitochondrial membrane potential and elevation in the released of cytochrome c from the mitochondria indicated the induction of the intrinsic apoptosis pathway by PCC. Activation of this pathway was further evidenced by significant activation of caspase 3/7 and 9. PCC was also shown to activate the extrinsic pathways of apoptosis via activation of caspase-8 which is linked to the suppression of NF-ƙB translocation to the nucleus.
2.Synthesis and characterization of a disubstituted piperazine derivative with T-type channel blocking action and analgesic properties.
Pudukulatham Z1, Zhang FX2, Gadotti VM2, M'Dahoma S2, Swami P1, Tamboli Y1, Zamponi GW3. Mol Pain. 2016 Apr 6;12. pii: 1744806916641678. doi: 10.1177/1744806916641678. Print 2016.
BACKGROUND: T-type calcium channels are important contributors to signaling in the primary afferent pain pathway and are thus important targets for the development of analgesics. It has been previously reported that certain piperazine-based compounds such as flunarizine are able to inhibit T-type calcium channels. Thus, we hypothesized that novel piperazine compounds could potentially act as analgesics.
3.A novel inhibitor of p75-neurotrophin receptor improves functional outcomes in two models of traumatic brain injury.
Delbary-Gossart S1, Lee S2, Baroni M3, Lamarche I4, Arnone M4, Canolle B4, Lin A2, Sacramento J2, Salegio EA2, Castel MN4, Delesque-Touchard N4, Alam A4, Laboudie P4, Ferzaz B4, Savi P4, Herbert JM4, Manley GT2, Ferguson AR2, Bresnahan JC2, Bono F5, Beattie MS6. Brain. 2016 Apr 15. pii: aww074. [Epub ahead of print]
The p75 neurotrophin receptor is important in multiple physiological actions including neuronal survival and neurite outgrowth during development, and after central nervous system injury. We have discovered a novel piperazine-derived compound, EVT901, which interferes with p75 neurotrophin receptor oligomerization through direct interaction with the first cysteine-rich domain of the extracellular region. Using ligand binding assays with cysteine-rich domains-fused p75 neurotrophin receptor, we confirmed that EVT901 interferes with oligomerization of full-length p75 neurotrophin receptor in a dose-dependent manner. Here we report that EVT901 reduces binding of pro-nerve growth factor to p75 neurotrophin receptor, blocks pro-nerve growth factor induced apoptosis in cells expressing p75 neurotrophin receptor, and enhances neurite outgrowthin vitro Furthermore, we demonstrate that EVT901 abrogates p75 neurotrophin receptor signalling by other ligands, such as prion peptide and amyloid-β.
4.Piperazine-based Alpha-1 AR Blocker, Naftopidil, Selectively Suppresses Malignant Human Bladder Cells via Induction of Apoptosis.
Nakagawa YU1, Nagaya H2, Miyata T2, Wada Y2, Oyama T2, Gotoh A3. Anticancer Res. 2016 Apr;36(4):1563-70.
A retrospective observational cohort study has shown that exposure to alpha-1 adrenergic receptor (AR) blocker reduces the risk of bladder cancer (BCa). We investigated the antitumor activity of alpha-1 blockers, that are administered long-term therapeutically, in BCa. The antitumor activity of alpha-1 blockers was evaluated in terms of cell viability, cell cycle, competition, and apoptotic signaling in BCa cells. Our cell viability studies showed that naftopidil was one of the strongest alpha-1 AR blockers, regarding its antitumor action in BCa cells, independent of the grade of malignancy, but with no similar action on normal human bladder cells. Oral administration of naftopidil reduced tumor volume in a xenograft model. Our own competitive analysis using an alpha-1 AR agonist and other alpha-1 AR blockers showed that naftopidil activated cell death signaling without inhibitory action on alpha-1 ARs. We conclude that naftopidil has potential as an antitumor drug against BCa in vitro and in vivo.
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