产品名称
Ru265, ≥95% (HPLC)
SMILES string
Cl[Ru](N)(N)(N)(N)n[Ru](N)(N)(N)(N)Cl
assay
≥95% (HPLC)
form
powder
color
white to dark beige
solubility
H2O: 2 mg/mL, clear
storage temp.
2-8°C
Quality Level
Biochem/physiol Actions
Ru265 is a non-cytotoxic, aqueous soluble nitrido-bridged dinuclear Ru(IV) complex that acts as a selective mitochondrial calcium uniporter (MCU) inhibitor via a manner distinct from the oxo-bridged Ru360. Ru265 selectively reduces 100 μM histamine-induced mitochondrial [Ca2+] (mCa2+), but not cytosolic [Ca2+] (cCa2+) transient (50 ?M; HeLa) by blocking MCU-mediated mCa2+ uptake at a >10-fold greater potency as Ru360 (IC50 ~2.6 nM vs. 30 nM; HEK293T) without effecting mCa2+ efflux or membrane potential (ΔΨm). Ru265 (50 μM) protects neonatal rat ventricular myocytes from hypoxia/reoxygenation injury by preventing mPTP opening and mCa2+ overload.
Selective mitochondrial calcium uniporter (MCU) inhibitor that blocks mitochondrial Ca2+ uptake at a >10-fold greater potency as Ru360.
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Joshua J Woods et al.
ACS central science, 5(1), 153-166 (2019-01-30)
Mitochondrial Ca2+ (mCa2+) uptake mediated by the mitochondrial calcium uniporter (MCU) plays a critical role in signal transduction, bioenergetics, and cell death, and its dysregulation is linked to several human diseases. In this study, we report a new ruthenium complex
Joshua J Woods et al.
Angewandte Chemie (International ed. in English), 59(16), 6482-6491 (2020-02-11)
The mitochondrial calcium uniporter (MCU) is the ion channel that mediates Ca2+ uptake in mitochondria. Inhibitors of the MCU are valuable as potential therapeutic agents and tools to study mitochondrial Ca2+ . The best-known inhibitor of the MCU is the
Robyn J Novorolsky et al.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 40(6), 1172-1181 (2020-03-05)
The mitochondrial calcium (Ca2+) uniporter (MCU) mediates high-capacity mitochondrial Ca2+ uptake implicated in ischemic/reperfusion cell death. We have recently shown that inducible MCU ablation in Thy1-expressing neurons renders mice resistant to sensorimotor deficits and forebrain neuron loss in a model
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