产品名称
MitoPQ, ≥90% (HPLC)
InChI
1S/C39H46N2P.3HI/c1-40-30-25-35(26-31-40)36-27-32-41(33-28-36)29-17-6-4-2-3-5-7-18-34-42(37-19-11-8-12-20-37,38-21-13-9-14-22-38)39-23-15-10-16-24-39;;;/h8-16,19-28,30-33H,2-7,17-18,29,34H2,1H3;3*1H/q+3;;;/p-3
InChI key
AOZZGHKENAZYTD-UHFFFAOYSA-K
SMILES string
C[N+]1=CC=C(C=C1)C2=CC=[N+](C=C2)CCCCCCCCCC[P+](C3=CC=CC=C3)(C4=CC=CC=C4)C5=CC=CC=C5.[I-].[I-].[I-]
assay
≥90% (HPLC)
form
powder
storage condition
desiccated
color
brown to brown-red
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
Quality Level
Application
MitoPQ has been used to enhance mitochondrial reactive oxygen species (mitoROS) production in T-cell culture and investigate its influence over T-cell differentiation.
General description
MitoPQ (MitoParaquat) is a mitochondria-targeted redox cycler composed of the lipophilic triphenylphosphonium (TP) cation-conjugated paraquat that induces mitochondria superoxide production via redox cycling at the complex I flavin site. MitoPQ increases mitochondria superoxide production at a ~1000-fold higher efficacy than untargeted paraquat using either live cells (fold of change of MitoSox fluorescence = 1.4/1 μM & 3.2/5 μM MitoPQ vs 1.2/5 mM PQ; C2C12 myoblasts) or isolated mitochondria (fold of increase of H2O2 efflux = 4.6/1 μM MitoPQ vs 2.6/1 mM PQ; rat heart mitochondria). MitoPQ is a valuable tool for conducting cellular and in vivo investigations into the role of mitochondrial superoxide generation in redox biology. Additionally, it can be utilized as a catalyst or co-stressor to replicate metabolic and neurodegenerative disease traits in experimental models.
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Bile acid metabolites control TH17 and Treg cell differentiation
Hang S, et al.
Nature, 143?148-143?148 (2019)
Ellen L Robb et al.
Free radical biology & medicine, 89, 883-894 (2015-10-11)
Superoxide is the proximal reactive oxygen species (ROS) produced by the mitochondrial respiratory chain and plays a major role in pathological oxidative stress and redox signaling. While there are tools to detect or decrease mitochondrial superoxide, none can rapidly and
Daniel J Fazakerley et al.
The Journal of biological chemistry, 293(19), 7315-7328 (2018-03-31)
Mitochondrial oxidative stress, mitochondrial dysfunction, or both have been implicated in insulin resistance. However, disentangling the individual roles of these processes in insulin resistance has been difficult because they often occur in tandem, and tools that selectively increase oxidant production
Eva Sidlauskaite et al.
Redox biology, 16, 344-351 (2018-03-28)
Developmental synapse pruning refines burgeoning connectomes. The basic mechanisms of mitochondrial reactive oxygen species (ROS) production suggest they select inactive synapses for pruning: whether they do so is unknown. To begin to unravel whether mitochondrial ROS regulate pruning, we made
Brígida R Pinho et al.
Free radical biology & medicine, 130, 318-327 (2018-11-06)
Superoxide generation by mitochondria respiratory complexes is a major source of reactive oxygen species (ROS) which are capable of initiating redox signaling and oxidative damage. Current understanding of the role of mitochondrial ROS in health and disease has been limited
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