Probably due to transient cell cycle arrest, in which repair machinery is active, what leads to sorting out the DNA damage and giving the time to cell recovery.
To add on the answer given, there is a possibility that your dosage might be too weak to induce apoptosis or inhibition of cell growth. In a study of RITA conducted on head and neck cancer cell lines, a concentration of approximately 5 uM (which is much higher than your tested concentration of 10 nM) induced adequate inhibition on the treated cancer cells (see link below). Given the low concentration of RITA you are using, there might be a chance that inhibitory effects would only start becoming apparent at longer culture periods.
On a side note, some studies have also shown different responses undergone by cell lines which harbor different p53 statuses while others argue that there are p53-independent pathways that RITA might take in inducing cell death.
Article The p53-Reactivating Small Molecule RITA Induces Senescence ...
Article Small molecule RITA binds to p53, blocks p53-HDM-2 interacti...
Article RITA can induce cell death in p53-defective cells independen...