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Benzamide PARP inhibitor

Cat.No.S4715

Benzamide, a derivative of benzoic acid, is an inhibitor of poly(ADP-ribose) polymerase with an IC50 of 3.3 μM.
Benzamide PARP inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 121.14

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Quality Control

Batch: S471501 DMSO]24 mg/mL]false]Ethanol]24 mg/mL]false]Water]Insoluble]false Purity: 98.79%
98.79

Solubility

In vitro
Batch:

DMSO : 24 mg/mL (198.11 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Ethanol : 24 mg/mL

Water : Insoluble

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In vivo
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

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.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
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Chemical Information, Storage & Stability

Molecular Weight 121.14 Formula

C7H7NO

 Storage (From the date of receipt)
CAS No. 55-21-0 Download SDF Storage of Stock Solutions

Mechanism of Action

Targets/IC50/Ki
PARP
(Cell-free assay)
3.3 μM
In vitro
Benzamide, an inhibitor of PARP is protective against excitatory amino acid-induced cell death in primary cultures of neurons derived from neonatal rat brain. In addition, this compound has more recently been shown to partially prevent the loss of dopaminergic cells and the increase in reactive gliosis caused by METH in vitro in fetal rat mesencephalic cells in culture. It prevents transformation in a cell cycle-specific manner, maximal prevention coinciding with early S phase, also characteristic of maximal susceptibility to transformation.
In vivo
PARP inhibitor benzamide is neuroprotective in C57Bl/6N mice against different types of neurotoxicities and without affecting body temperature. This compound treatment significantly decreases the iNOS expression and number of apoptotic neurons and thereby improves the neuronal survival and memory during GCI. Its administration (160 mg/kg i.p.) does not induce hypothermia and reaches the CNS in 30 min in the concentration range of 0.09-0.64 mM, at which, it shows neuroprotection.
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/2538435/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01161836 Completed
Advanced Solid Tumors
Sanofi
 July 2010 Phase 1

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