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557440

Sigma-Aldrich

Ru360

≥97%, solid, Ca2+ uptake blocker in mitrochondria, Calbiochem®

Synonym(s):

Ru360, (μ)[(HCO₂)(NH₃)₄Ru]₂OCl₃

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About This Item

Empirical Formula (Hill Notation):
C2H26Cl3N8O5Ru2
Molecular Weight:
550.78
UNSPSC Code:
12352200
NACRES:
NA.77

product name

Ru360, Ru360, is a cell-permeable oxygen-bridged dinuclear ruthenium amine complex. Binds to mitochondria with high affinity (Kd = 340 pM) and blocks Ca2+ uptake into mitochondria in vitro (IC₅₀ = 184 pM).

Quality Level

100

Assay

≥97%

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
desiccated (hygroscopic)
protect from light

color

green

solubility

deoxygenated water: 0.5 mg/mL

shipped in

ambient

storage temp.

−20°C

General description

A cell-permeable oxygen bridged dinuclear ruthenium amine complex that has been shown to bind to mitochondria with high affinity (Kd = 0.34 nM) and specifically blocks Ca2+ uptake into mitochondria in vitro (IC50 = 184 pM) and in situ in intact myocytes (for complete block after incubation with ~10 µM of Ru360 for 30 min. Does not affect other cellular Ca2+ transport processes involved in cardiac muscle contraction even at micromolar levels.
A cell-permeable oxygen-bridged dinuclear ruthenium amine complex that has been shown to bind to mitochondria with high affinity (Kd = 340 pM). Specifically blocks Ca2+ uptake into mitochondria in vitro (IC50 = 184 pM) and in situ in intact myocytes (complete block after incubation with ~10 µM of Ru360 for 30 min). Does not affect other cellular Ca2+ transport processes involved in cardiac muscle contraction, even at micromolar levels.
Note: 1 set = 10 x 100 µg.

Biochem/physiol Actions

Cell permeable: yes
Primary Target
Ca2+ uptake into mitochondria in vitro
Product does not compete with ATP.
Reversible: no
Target IC50: 184 pM blocking Ca2+ uptake into mitochondria in vitro; and in situ in intact myocytes; Kd = 340 pM for binding mitochondria

Packaging

Packaged under inert gas

Warning

Toxicity: Standard Handling (A)

Reconstitution

Unstable in solution; reconstitute just prior to use.

Other Notes

Sanchez, J.A., et al. 2001. J. Physiol. 536, 387.
Bassani, R.A., et al. 1998. Cell Calcium23, 433.
Matlib, M.A., et al. 1998. J. Biol. Chem.273, 10223.
Zhou, Z., et al. 1998. J. Physiol.507 (pt 2), 379.
Emerson, J., et al. 1993. J. Am. Chem. Soc.115, 11799.
Ying, W.-L., et al. 1991. Biochemistry30, 4949.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

11 - Combustible Solids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Listings

Regulatory Listings are mainly provided for chemical products. Only limited information can be provided here for non-chemical products. No entry means none of the components are listed. It is the user’s obligation to ensure the safe and legal use of the product.

JAN Code

557440-MG:
557440-500UG:
557440-100UG:
557440-1SET:

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Madison X Rodriguez et al.
STAR protocols, 2(4), 100979-100979 (2021-12-09)
The mitochondrial calcium uniporter, which mediates mitochondrial Ca2+ uptake, regulates key cellular functions, including intracellular Ca2+ signaling, cell-fate determination, and mitochondrial bioenergetics. Here, we describe two complementary strategies to quantify the uniporter's transport activity. First, we detail a mitochondrial Ca2+
Rachel L Doser et al.
eLife, 13 (2024-03-14)
Our understanding of mitochondrial signaling in the nervous system has been limited by the technical challenge of analyzing mitochondrial function in vivo. In the transparent genetic model Caenorhabditis elegans, we were able to manipulate and measure mitochondrial reactive oxygen species
Michael J Bround et al.
Scientific reports, 14(1), 6751-6751 (2024-03-22)
Mitochondrial Ca2+ overload can mediate mitochondria-dependent cell death, a major contributor to several human diseases. Indeed, Duchenne muscular dystrophy (MD) is driven by dysfunctional Ca2+ influx across the sarcolemma that causes mitochondrial Ca2+ overload, organelle rupture, and muscle necrosis. The
MCU Upregulation Overactivates Mitophagy by Promoting VDAC1 Dimerization and Ubiquitination in the Hepatotoxicity of Cadmium.
Liu, et al.
Advanced science (Weinheim, Baden-Wurttemberg, Germany), 10, e2203869-e2203869 (2023)
Peu Santra et al.
Disease models & mechanisms, 14(7) (2021-07-24)
The vacuolar-type H+-ATPase (V-ATPase) is a multi-subunit proton pump that regulates cellular pH. V-ATPase activity modulates several cellular processes, but cell-type-specific functions remain poorly understood. Patients with mutations in specific V-ATPase subunits can develop sensorineural deafness, but the underlying mechanisms
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