Tetramethylrhodamine, Ethyl Ester, Perchlorate (TMRE)
Tetramethylrhodamine, Ethyl Ester, Perchlorate (TMRE)
Invitrogen™

Tetramethylrhodamine, Ethyl Ester, Perchlorate (TMRE)

Tetramethylrhodamine, ethyl ester (TMRE) is a cell-permeant, cationic, red-orange fluorescent dye that is readily sequestered by active mitochondria.Dissolve the dyeRead more
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Catalog NumberQuantity
T669Promo Image25 mg
Catalog number T669
Price (CNY)
2,559.00
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Ends: 31-Dec-2025
3,467.00
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25 mg
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Quantity:
25 mg
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Price (CNY)
2,559.00
Online Exclusive
Ends: 31-Dec-2025
3,467.00
Save 908.00 (26%)
25 mg
Add to cart
Ask our AI about this Product

Tetramethylrhodamine, ethyl ester (TMRE) is a cell-permeant, cationic, red-orange fluorescent dye that is readily sequestered by active mitochondria.

Dissolve the dye in high-quality anhydrous DMSO or ethanol to prepare stock concentration at 1 to 10 mM.



Visualize staining your cell without wasting your reagents, antibodies, or time with our new Stain-iT Cell Staining Simulator.

For Research Use Only. Not for use in diagnostic procedures.
Specifications
Detection MethodFluorescence
Excitation/Emission549/574 nm
Molecular Weight (g/mol)514.96
Quantity25 mg
Shipping ConditionRoom Temperature
Sub Cellular LocalizationMitochondria
ColorRed-Orange
For Use With (Equipment)Fluorescence Microscope
Product TypeTMRE
Unit Size25 mg
Contents & Storage
Store in freezer (-5°C to -30°C) and protect from light.
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Frequently asked questions (FAQs)

I am seeing high background outside of my neuronal cells when using membrane potential indicators. What can I do to reduce background?

If you use our FluoVolt Membrane Potential Kit (Cat. No. F10488), the kit provides a background suppressor to reduce this problem. For other indicators, consider the use of BackDrop Background Suppressor (Cat no. R37603, B10511, and B10512).

Find additional tips, troubleshooting help, and resources within our Cell Analysis Support Center.

What is the difference between fast and slow-response membrane potential probes?

Molecules that change their structure in response to the surrounding electric field can function as fast-response probes for the detection of transient (millisecond) potential changes. Slow-response dyes function by entering depolarized cells and binding to proteins or membranes. Increased depolarization results in additional dye influx and an increase in fluorescence, while hyperpolarization is indicated by a decrease in fluorescence. Fast-response probes are commonly used to image electrical activity from intact heart tissues or measure membrane potential changes in response to pharmacological stimuli. Slow-responding probes are often used to explore mitochondrial function and cell viability.

Find additional tips, troubleshooting help, and resources within our Cell Analysis Support Center.

What type of membrane potential indicators do you offer and how should I choose one for my experiment?

A membrane potential indicator selection guide can be found here (https://www.thermofisher.com/us/en/home/life-science/cell-analysis/cell-viability-and-regulation/ion-indicators/membrane-potential-indicators.html).

Find additional tips, troubleshooting help, and resources within our Cell Analysis Support Center.

Figures

Fluorescence spectra

Fluorescence spectra

Documents & Downloads

Certificates

Lot #Certificate TypeDateCatalog Number(s)
3135775Certificate of AnalysisApr 14, 2025T669
2978503Certificate of AnalysisSep 30, 2024T669
2897784Certificate of AnalysisApr 23, 2024T669
2765694Certificate of AnalysisOct 19, 2023T669
2685408Certificate of AnalysisJun 20, 2023T669
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Safety Data Sheets

Citations & References (159)

Citations & References
Abstract
A hyperfused mitochondrial state achieved at G1-S regulates cyclin E buildup and entry into S phase.
Authors:Mitra K, Wunder C, Roysam B, Lin G, Lippincott-Schwartz J,
Journal:Proc Natl Acad Sci U S A
PubMed ID:19617534
Mitochondria undergo fission-fusion events that render these organelles highly dynamic in cells. We report a relationship between mitochondrial form and cell cycle control at the G(1)-S boundary. Mitochondria convert from isolated, fragmented elements into a hyperfused, giant network at G(1)-S transition. The network is electrically continuous and has greater ATP ... More
Antiapoptotic effect of nicorandil mediated by mitochondrial atp-sensitive potassium channels in cultured cardiac myocytes.
Authors:Akao M, Teshima Y, Marbán E
Journal:J Am Coll Cardiol
PubMed ID:12204514
OBJECTIVES: We examined whether nicorandil, a clinically useful drug for the treatment of ischemic syndromes, inhibits myocardial apoptosis. BACKGROUND: Nicorandil has been reported to have a cardioprotective action through activation of mitochondrial ATP-sensitive potassium (mitoK(ATP)) channels. Based on our recent observation that mitoK(ATP) channel activation has a remarkable antiapoptotic effect ... More
Synaptic mitochondria are more susceptible to Ca2+overload than nonsynaptic mitochondria.
Authors:Brown MR, Sullivan PG, Geddes JW
Journal:J Biol Chem
PubMed ID:16517608
'Mitochondria in nerve terminals are subjected to extensive Ca2+ fluxes and high energy demands, but the extent to which the synaptic mitochondria buffer Ca2+ is unclear. In this study, we identified a difference in the Ca2+ clearance ability of nonsynaptic versus synaptic mitochondrial populations enriched from rat cerebral cortex. Mitochondria ... More
Age-related macular degeneration. The lipofusion component N-retinyl-N-retinylidene ethanolamine detaches proapoptotic proteins from mitochondria and induces apoptosis in mammalian retinal pigment epithelial cells.
Authors:Suter M, Remé C, Grimm C, Wenzel A, Jäättela M, Esser P, Kociok N, Leist M, Richter C
Journal:J Biol Chem
PubMed ID:11006290
'10-20% of individuals over the age of 65 suffer from age-related macular degeneration (AMD), the leading cause of severe visual impairment in humans living in developed countries. The pathogenesis of this complex disease is poorly understood, and no efficient therapy or prevention exists to date. A precondition for AMD appears ... More
VDAC-dependent permeabilization of the outer mitochondrial membrane by superoxide induces rapid and massive cytochrome c release.
Authors:Madesh M, Hajnóczky G
Journal:J Cell Biol
PubMed ID:11739410
'Enhanced formation of reactive oxygen species (ROS), superoxide (O2*-), and hydrogen peroxide (H2O2) may result in either apoptosis or other forms of cell death. Here, we studied the mechanisms underlying activation of the apoptotic machinery by ROS. Exposure of permeabilized HepG2 cells to O2*- elicited rapid and massive cytochrome c ... More
159 total citations

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