BTB06584 - CAS 219793-45-0
Catalog number: 219793-45-0
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
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BTB06584 is an IF1-dependent, selective inhibitor of the mitochondrial F1 Fo-ATPase. It may represent a valuable tool to selectively inhibit mitochondrial F1 Fo-ATPase activity without compromising ATP synthesis and to limit ischaemia-induced injury caused by reversal of the mitochondrial F1 Fo-ATPsynthase.
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1.Controlled and Impaired Mitochondrial Quality in Neurons: Molecular Physiology and Prospective Pharmacology.
Matic I1, Strobbe D1, Frison M2, Campanella M3. Pharmacol Res. 2015 Sep;99:410-24. doi: 10.1016/j.phrs.2015.03.021. Epub 2015 Apr 23.
Tuned mitochondrial physiology is fundamental for qualitative cellular function. This is particularly relevant for neurons, whose pathology is frequently associated with mitochondrial deficiencies. Defects in mitochondria are indeed key features in most neurodegenerative diseases such as Alzheimer's Disease (AD), Parkinson's Disease (PD), Huntington's Disease (HD) and Amyotrophic Lateral Sclerosis (ALS). When mitochondrial coupling impairs, so does cell metabolism, trafficking and the signaling depending on the homeostasis of the mitochondrial network. Moreover, the quality control of mitochondria - via the process of mitochondrial autophagy - results biased in neurodegeneration stemming major interest on the molecular determinants of this process among neuroscientists. In this review, we highlight the most notable and acknowledged deficiencies of mitochondrial function and their relationship with diseases occurring in neurons and their transmission.
2.The compound BTB06584 is an IF1 -dependent selective inhibitor of the mitochondrial F1 Fo-ATPase.
Ivanes F1, Faccenda D, Gatliff J, Ahmed AA, Cocco S, Cheng CH, Allan E, Russell C, Duchen MR, Campanella M. Br J Pharmacol. 2014 Sep;171(18):4193-206. doi: 10.1111/bph.12638. Epub 2014 Jul 1.
BACKGROUND AND PURPOSE: Ischaemia compromises mitochondrial respiration. Consequently, the mitochondrial F1 Fo-ATPsynthase reverses and acts as a proton-pumping ATPase, so maintaining the mitochondrial membrane potential (ΔΨm ), while accelerating ATP depletion and cell death. Here we have looked for a molecule that can selectively inhibit this activity without affecting ATP synthesis, preserve ATP and delay ischaemic cell death.
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CAS 219793-45-0 BTB06584

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