There will be a HazMat fee per item when shipping a dangerous goods. The HazMat fee will be charged to your UPS/DHL/FedEx collect account or added to the invoice unless the package is shipped via Ground service. Ship by air in Excepted Quantity (each bottle), which is up to 1g/1mL for class 6.1 packing group I or II, and up to 25g/25ml for all other HazMat items.
Type
HazMat fee for 500 gram (Estimated)
Excepted Quantity
USD 0.00
Limited Quantity
USD 15-60
Inaccessible (Haz class 6.1), Domestic
USD 80+
Inaccessible (Haz class 6.1), International
USD 150+
Accessible (Haz class 3, 4, 5 or 8), Domestic
USD 100+
Accessible (Haz class 3, 4, 5 or 8), International
MitoPQ acts as a mitochondria-focused redox cycler, generating superoxide through redox cycling at complex I's flavin site, thus selectively boosting superoxide levels within mitochondria. It is applicable in studies of antioxidants[1].
体外研究
MitoPQ (5 μM, 0.5 s-20 min) enhances MitoSOX fluorescence in a dose- and time-dependent fashion in C2C12 myoblasts[1].
MitoPQ (1-10 μM, 6 h) elevates MnSOD expression at doses of 1-5 μM and reduces MnSOD expression at a dose of 10 μM in C2C12 myoblasts[1].
MitoPQ (1-10 μM, 24 h) led to an increase in HCT-116 cell mortality[1].
MitoPQ 细胞实验
Cell Line
Concentration
Treated Time
Description
References
U2OS cells
30 µM
24 hours
To investigate the effect of MitoPQ on huntingtin aggregation in a Huntington's disease cell model. Results showed that MitoPQ increased mutant huntingtin aggregation without increasing cell death.
Free Radic Biol Med. 2019 Jan;130:318-327
Hepa1c1c7 mouse hepatoma cells
5 μM
48 hours
To evaluate Nrf2 pathway activation via NQO1 activity assay. Results showed no induction of NQO1 activity by MitoPQ treatment.
J Biol Chem. 2021 Jan-Jun;296:100169
C2C12 mouse myoblasts
5 μM
1 and 4 hours
To assess the effect of mitochondrial-specific superoxide production on Nrf2 activation. Results showed that MitoPQ selectively increased mitochondrial superoxide production but did not activate the Nrf2 pathway (no increase in Nrf2 protein levels or nuclear translocation).
J Biol Chem. 2021 Jan-Jun;296:100169
L6 myotubes
0.5-1 μM
30 minutes to 2 hours
MitoPQ rapidly induced mitochondrial oxidative stress and impaired insulin-stimulated GLUT4 translocation in muscle cells.
J Biol Chem. 2018 May 11;293(19):7315-7328
3T3-L1 adipocytes
<10 μM
2 hours
MitoPQ selectively increased mitochondrial oxidants in adipocytes without impairing respiration, recapitulating features of insulin resistance.
J Biol Chem. 2018 May 11;293(19):7315-7328
HeLa cells
20 μM
24 hours
To investigate the effects of MitoPQ on mitochondrial protein oxidation and Ct infection. Results showed MitoPQ increased mitochondrial protein sulfenylation and significantly reduced the number and size of Ct inclusions.
Protein Sci. 2019 Jan;28(1):216-227
MitoPQ 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice
Myocardial infarction model
Intraperitoneal injection
0.1 µg/kg body weight
Once daily for 8 days
MitoPQ treatment increased cardiac fibroblast proliferation and total numbers post-myocardial infarction.
Cell Stem Cell. 2022 Feb 3;29(2):281-297. e12
Zebrafish
Zebrafish larvae
Water exposure
1-10 µM
48 hours
To investigate the effect of MitoPQ in inducing a parkinsonian phenotype in zebrafish. Results showed that MitoPQ decreased sensorimotor reflexes, spontaneous movement and brain tyrosine hydroxylase levels, with partial rescue of phenotypes by antioxidant or monoaminergic potentiation strategies.
Free Radic Biol Med. 2019 Jan;130:318-327
Xenopus laevis tadpoles
NMJ synaptic inactivity model
Immersion treatment
5 µM
Single treatment, 60 min duration
Selectively induced mitochondrial ROS to recapitulate synaptic inactivity-induced motor deficits; MnTnBuOE-2-PyP5+ significantly mitigated MitoPQ-induced motor deficits by blocking mitochondrial ROS.
Redox Biol. 2018 Jun;16:344-351
Mice
HFHSD-induced insulin resistance model
Ex vivo tissue incubation
25-50 μM
Single dose, 1-2 hours duration
MitoPQ induced mitochondrial-specific oxidative stress and impaired insulin action in adipose tissue explants.
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