SML3656
PAPTP trifluoroacetate
≥98% (HPLC)
别名:
(3-(4-(4-((7-Oxo-7H-furo[3,2-g]benzopyran-4-yl)oxy)butoxy)phenyl)propyl)triphenyl phosphonium trifluoroacetate, (3-(4-(4-(7-Oxo-7H-furo[3,2-g]chromen-4-yloxy)butoxy)phenyl)propyl)triphenylphosphonium trifluoroacetate
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选择尺寸
关于此项目
经验公式（希尔记法）:
C42H38O5P · xC2HF3O2
分子量:
653.72 (free base basis)
UNSPSC Code:
12352200
NACRES:
NA.21
InChI
1S/C42H38O5P/c43-41-25-24-37-40(47-41)31-39-38(26-29-45-39)42(37)46-28-11-10-27-44-33-22-20-32(21-23-33)13-12-30-48(34-14-4-1-5-15-34,35-16-6-2-7-17-35)36-18-8-3-9-19-36/h1-9,14-26,29,31H,10-13,27-28,30H2/q+1
InChI key
MHIFCBNYOHOSHK-UHFFFAOYSA-N
SMILES string
O=C1C=CC2=C(C3=C(C=C2O1)OC=C3)OCCCCOC4=CC=C(C=C4)CCC[P+](C5=CC=CC=C5)(C6=CC=CC=C6)C7=CC=CC=C7
assay
≥98% (HPLC)
form
powder
storage condition
desiccated
color
white to beige
storage temp.
-10 to -25°C
Quality Level
Biochem/physiol Actions
Kv1.3-selective, mitochondria-targeting Kv1.3 blocker that induces ROS-mediated cancer-selective killing both in vitro and in vivo. More effective than PAP-1.
PAPTP is a PAP-1-derivatized Kv1.3-selective potassium channel blocker with a positively charged lipophilic propyl-triphenylphosphonium (TP) moiety that allows mitochondria-targeted PAPTP delivery. Mitochondria Kv1.3 inhibition induces oxygen species (ROS)-mediated cancer-selective killing both in cultures (by 28%/69%/95% post 24-hr 0/1/10 µM PAPTP treatment of primary B-CLL; 20%/24% normal B-cell death with 0/20 µM PAPTP) and in murine orthotopic models of melanoma and pancreatic ductal adenocarcinoma in vivo (5 µmol/kg q.o.d. via i.p.). PAPTP exhibits higher anti-cancer efficacy than PAP-1 both in vitro and in vivo, and and is less affected by ultidrug resistance (MDR).
Disclaimer
Hygroscopic
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Sofia Parrasia et al.
Pharmaceuticals (Basel, Switzerland), 14(2) (2021-02-11)
A developing family of chemotherapeutics-derived from 5-(4-phenoxybutoxy)psoralen (PAP-1)-target mitochondrial potassium channel mtKv1.3 to selectively induce oxidative stress and death of diseased cells. The key to their effectiveness is the presence of a positively charged triphenylphosphonium group which drives their accumulation
Elisa Venturini et al.
Neuro-Signals, 25(1), 26-38 (2017-09-05)
Glioblastoma (GBM) is one of the most aggressive cancers, counting for a high number of the newly diagnosed patients with central nervous system (CNS) cancers in the United States and Europe. Major features of GBM include aggressive and invasive growth
Roberta Peruzzo et al.
Frontiers in oncology, 7, 239-239 (2017-10-17)
Previous results link the mitochondrial potassium channel Kv1.3 (mitoKv1.3) to the regulation of apoptosis. By synthesizing new, mitochondria-targeted derivatives (PAPTP and PCARBTP) of PAP-1, a specific membrane-permeant Kv1.3 inhibitor, we have recently provided evidence that both drugs acting on mitoKv1.3
Luigi Leanza et al.
Cancer cell, 31(4), 516-531 (2017-04-12)
The potassium channel Kv1.3 is highly expressed in the mitochondria of various cancerous cells. Here we show that direct inhibition of Kv1.3 using two mitochondria-targeted inhibitors alters mitochondrial function and leads to reactive oxygen species (ROS)-mediated death of even chemoresistant
Faye L Styles et al.
Cell death & disease, 12(4), 372-372 (2021-04-09)
Cellular energy metabolism is fundamental for all biological functions. Cellular proliferation requires extensive metabolic reprogramming and has a high energy demand. The Kv1.3 voltage-gated potassium channel drives cellular proliferation. Kv1.3 channels localise to mitochondria. Using high-resolution respirometry, we show Kv1.3
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