Key result
EODB (12 uM) significantly protected H9C2 and primary rat cardiomyocytes against doxorubicin-induced apoptotic and necrotic death (p<0.05) and inhibited JNK activation without reducing antitumor efficacy.
Why the study?
Does 3-[2-(4-ethylphenyl)-2-oxoethyl]-1,2-dimethyl-1H-3,1-benzimidazol-3-ium bromide (EODB) prevent doxorubicin-induced cardiomyocyte death without compromising the antitumor activity of doxorubicin in cultured rat cardiomyocytes and human tumor cell lines?
Does 3-[2-(4-ethylphenyl)-2-oxoethyl]-1,2-dimethyl-1H-3,1-benzimidazol-3-ium bromide (EODB) prevent doxorubicin-induced cardiomyocyte death without compromising the antitumor activity of doxorubicin in cultured rat cardiomyocytes and human tumor cell lines?
High-throughput screening identified a novel benzimidazole derivative (EODB) that protects primary rat cardiomyocytes from doxorubicin-induced apoptotic and necrotic death via JNK pathway inhibition without impairing doxorubicin's anticancer efficacy.
Answers are grounded in this paper and cite their sources.
EODB may protect cardiomyocytes from doxorubicin toxicity in vitro; leaves open clinical translation and in vivo testing.
Antracyclines are effective antitumor agents. One of the most commonly used antracyclines is doxorubicin, which can be successfully used to treat a diverse spectrum of tumors. Application of these drugs is limited by their cardiotoxic effect, which is determined by a lifetime cumulative dose. We set out to identify by high throughput screening cardioprotective compounds protecting cardiomyocytes from doxorubicin-induced injury. Ten thousand compounds of ChemBridge's DIVERSet compound library were screened to identify compounds that can protect H9C2 rat cardiomyocytes against doxorubicin-induced cell death. The most effective compound proved protective in doxorubicin-treated primary rat cardiomyocytes and was further characterized to demonstrate that it significantly decreased doxorubicin-induced apoptotic and necrotic cell death and inhibited doxorubicin-induced activation of JNK MAP kinase without having considerable radical scavenging effect or interfering with the antitumor effect of doxorubicin. In fact the compound identified as 3-[2-(4-ethylphenyl)-2-oxoethyl]-1,2-dimethyl-1H-3,1-benzimidazol-3-ium bromide was toxic to all tumor cell lines tested even without doxorubicine treatment. This benzimidazole compound may lead, through further optimalization, to the development of a drug candidate protecting the heart from doxorubicin-induced injury.
No takes yet. Share an insight, caveat, or question.
Gergely et al. (2015) studied Doxorubicin-induced cardiomyocyte injury / cardiotoxicity. 3-[2-(4-ethylphenyl)-2-oxoethyl]-1,2-dimethyl-1H-3,1-benzimidazol-3-ium bromide (EODB) vs. Vehicle control (DMSO) with doxorubicin (300 ng/mL or 300 nM) was evaluated on Cardiomyocyte viability and cell death (assessed by MTT assay, Coomassie cell-covered surface area, calcein-AM hydrolysis, caspase-3 activity, and LDH release) at 24 hours (p=<0.05). EODB (12 uM) significantly protected H9C2 and primary rat cardiomyocytes against doxorubicin-induced apoptotic and necrotic death (p<0.05) and inhibited JNK activation without reducing antitumor efficacy.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: