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product name BTB06584


Description: BTB06584 is an IF1-dependent, selective inhibitor of the mitochondrial F1 Fo-ATPase. BTB06584 inhibited F1 Fo-ATPase activity with no effect on ΔΨm or O2 consumption. BTB06584 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. 

References: Br J Pharmacol. 2014 Sep;171(18):4193-206.



Molecular Weight (MW)

417.82
Formula

C19H12ClNO6S
CAS No.

219793-45-0
Storage

-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)

DMSO: 84 mg/mL (201.0 mM)
Water: <1 mg/mL 
Ethanol: <1 mg/mL 
Solubility (In vivo)

 
Synonyms

 

other peoduct :References PubMed ID::http://www.ncbi.nlm.nih.gov/pubmed/19399708

In Vitro

In vitro activity: BTB06584 IF1-dependently inhibits F1 Fo-ATPase activity with no effect on without compromising ATP synthesis, and also limits ischemia-induced injury caused by reversal of the mitochondrial F1 Fo-ATP synthase.


Kinase Assay


Cell Assay: BTB inhibited F1Fo-ATPase activity with no effect on the mitochondrial membrane potential (ΔΨm) or O2 consumption. ATP consumption decreased via inhibition of respiration, and ischaemic cell death was reduced. BTB efficiency increased by IF1 overexpression and reduced by silencing this protein. In addition, BTB rescued defective haemoglobin synthesis in zebrafish pinotage (pnt) mutants in which expression of the Atpif1a gene is lost.

In Vivo BTB06584 rescues the defective haemoglobin synthesis in zebrafish pinotage (pnt) mutants without causing significant toxicity. 
Animal model  
Formulation & Dosage  
References Br J Pharmacol. 2014 Sep;171(18):4193-206.

IKK 16

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Author: Sodium channel

Share this post on:

product name BTB06584


Description: BTB06584 is an IF1-dependent, selective inhibitor of the mitochondrial F1 Fo-ATPase. BTB06584 inhibited F1 Fo-ATPase activity with no effect on ΔΨm or O2 consumption. BTB06584 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. 

References: Br J Pharmacol. 2014 Sep;171(18):4193-206.



Molecular Weight (MW)

417.82
Formula

C19H12ClNO6S
CAS No.

219793-45-0
Storage

-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)

DMSO: 84 mg/mL (201.0 mM)
Water: <1 mg/mL 
Ethanol: <1 mg/mL 
Solubility (In vivo)

 
Synonyms

 

other peoduct :References PubMed ID::http://www.ncbi.nlm.nih.gov/pubmed/19399708

In Vitro

In vitro activity: BTB06584 IF1-dependently inhibits F1 Fo-ATPase activity with no effect on without compromising ATP synthesis, and also limits ischemia-induced injury caused by reversal of the mitochondrial F1 Fo-ATP synthase.


Kinase Assay


Cell Assay: BTB inhibited F1Fo-ATPase activity with no effect on the mitochondrial membrane potential (ΔΨm) or O2 consumption. ATP consumption decreased via inhibition of respiration, and ischaemic cell death was reduced. BTB efficiency increased by IF1 overexpression and reduced by silencing this protein. In addition, BTB rescued defective haemoglobin synthesis in zebrafish pinotage (pnt) mutants in which expression of the Atpif1a gene is lost.

In Vivo BTB06584 rescues the defective haemoglobin synthesis in zebrafish pinotage (pnt) mutants without causing significant toxicity. 
Animal model  
Formulation & Dosage  
References Br J Pharmacol. 2014 Sep;171(18):4193-206.

IKK 16

Share this post on:

Author: Sodium channel