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Merck

557440

Ru360

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

Synonyme(s) :

Ru360, (μ)[(HCO2)(NH3)4Ru]2OCl3

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500 μG

306,00 €

1 SET

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306,00 €

Disponible dès aujourd'huiDétails

A propos de cet article

Formule empirique (notation de Hill) :
C2H26Cl3N8O5Ru2
Poids moléculaire :
550.78
UNSPSC Code:
12352200
NACRES:
NA.77

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Nom du produit

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).

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

Quality Level

100

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Cet article
124014124013420130
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).

Sigma-Aldrich

557440

Ru360

Akt Inhibitor VII, TAT-Akt-in The Akt Inhibitor VII, TAT-Akt-in controls the biological activity of Akt. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

Sigma-Aldrich

124014

Akt Inhibitor VII, TAT-Akt-in

Akt Inhibitor VI, Akt-in The Akt Inhibitor VI, Akt-in controls the biological activity of Akt. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

Sigma-Aldrich

124013

Akt Inhibitor VI, Akt-in

JNK Inhibitor III, Cell-Permeable The JNK Inhibitor III, Cell-Permeable controls the biological activity of JNK. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

Millipore

420130

JNK Inhibitor III, Cell-Permeable

form

solid

form

solid

form

lyophilized solid

form

lyophilized solid

assay

≥97%

assay

≥95% (HPLC)

assay

≥95% (HPLC)

assay

≥95% (HPLC)

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

manufacturer/tradename

Calbiochem®

Quality Level

100

Quality Level

100

Quality Level

100

Quality Level

100

storage temp.

−20°C

storage temp.

2-8°C

storage temp.

2-8°C

storage temp.

−20°C

solubility

deoxygenated water: 0.5 mg/mL

solubility

water: 1 mg/mL

solubility

water: 1 mg/mL

solubility

DMSO: 100 mg/mL, acetic acid: 100 mg/mL

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

Disclaimer

Toxicity: Standard Handling (A)

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.

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.

Packaging

Packaged under inert gas

Preparation Note

Unstable in solution; reconstitute just prior to use.

Legal Information

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

Classe de stockage

11 - Combustible Solids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificats d'analyse (COA)

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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
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+
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
Lianne Pope et al.
Cell chemical biology, 27(5), 511-524 (2020-02-16)
The trinuclear ruthenium amine ruthenium red (RuR) inhibits diverse ion channels, including K2P potassium channels, TRPs, the calcium uniporter, CALHMs, ryanodine receptors, and Piezos. Despite this extraordinary array, there is limited information for how RuR engages targets. Here, using X-ray
Wenbo Zhu et al.
Frontiers in microbiology, 13, 861734-861734 (2022-04-02)
Human cytomegalovirus (HCMV) infection can induce apoptosis of vascular endothelial cells, which may be the most important element of development and progression of reported atherosclerosis caused by HCMV. As there are no specific drugs to clear HCMV infection, exploration of
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