VBIT-4 VDAC inhibitor

Cat.No.S3544

VBIT-4 is a voltage-dependent anion channel (VDAC) oligomerization inhibitor that decreases mitochondrial DNA (mtDNA) release, type I interferon (IFN) signaling, neutrophil extracellular traps, and disease severity in a mouse model of systemic lupus erythematosus.
VBIT-4 VDAC inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 457.87

Quality Control

Products Often Used Together with VBIT-4

VBIT-12

It and VBIT-12 prevent mitochondrial dysfunction and apoptosis in T2D and lupus models by inhibiting VDAC1 oligomerization and correcting protein misdirection to the plasma membrane.

BAI1

It rescues the decreased inner mitochondrial membrane (IMM) protein levels after endolysosomal damage in human iPSC-derived macrophages (iPSDM) better than BAI1.

IFN alpha-IFNAR-IN-1 hydrochloride

It and IFN α-IFNAR-IN-1 with MnCl2 decrease the release of mitochondrial DNA and reduce lipid peroxidation and ROS levels in MC38 cells.

Z-VAD-FMK

It and ZVAD treatment demonstrate a robust response to anti-CD3 + anti-CD28 stimulation in COVID-A T cells.

Chemical Information, Storage & Stability

Molecular Weight 457.87 Formula

C21H23ClF3N3O3

Storage (From the date of receipt) 3 years -20°C powder
CAS No. 2086257-77-2 -- Storage of Stock Solutions

Synonyms N/A Smiles OCC(CC(=O)NC1=CC=C(Cl)C=C1)N2CCN(CC2)C3=CC=C(OC(F)(F)F)C=C3

Solubility

In vitro
Batch:

DMSO : 92 mg/mL (200.93 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 92 mg/mL

Water : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Mechanism of Action

Targets/IC50/Ki
VDAC [1]
mtDNA [1]
IFN [1]
In vitro

VBIT-4 rapidly inhibits the loss of ATP, which is a consequence of its translocation to the plasma membrane caused by VDAC1 overexpression, in plVdac1-expressing INS-1 cells.[2]

In vivo

VBIT-4 prevents increases in water consumption and polyuria in the db/db mice, also counteracts VDAC1 overexpression, preventing mistargeting to the β cell surface under glucotoxic conditions. Through the prevention of VDAC1 gene expression, this compound may have disease-modifying actions.[2]

References

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