DNA damage response (DDR) pathway is one of the fundamental cellular processes that maintain the
integrity of our genome. It encompasses cellular networks that involve DNA repair and cell cycle
checkpoints1
. DDR pathway proteins are also responsible for limiting the effectiveness associated
with various modes of the genotoxic agent2
. Due to proficient DNA repair mechanisms, cancer cells
overturn the induced damage resulting in Chemo and radio-resistance. Thus, making DDR proteins an
appealing target.
Ataxia-telangiectasia and Rad3 related (ATR) kinase is one of the major sensor protein in the DNA
damage repair (DDR) pathway. ATR recognizes DNA strand breaks and activated downstream
protein involved in cell cycle arrest and DNA repair3
. Cancer cell deficient in ataxia-telangiectasia
mutated (ATM) or P53 protein shows selective sensitization to ATR Inhibition, thus making ATR an
important drug target4
. Despite having this understanding for more than a decade, there are no
clinically approved ATR inhibitors. This study shows that SPK98, an in-house synthesized ATR
inhibitor showing differential specificity towards ATM or P53 deficient cells. Microscopic studies
also revealed that combinatorial treatment of SPK98 and UV results in mitotic defect due to
incompetent DNA repair5
. All these preliminary cellular studies suggest that SPK98 has the potential
to be explored further in preclinical settings as a potential anticancer agent.

Employing SPK98 for selective sensitization of ATM or P53 deficient cancer cell

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27th CRSI National Symposium in Chemistry

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