Ketorolac (RS37619) hemicalcium is a nonselective COX inhibitor with IC50s of 20 nM and 120 nM for COX-1 and COX-2, respectively. Ketorolac hemicalcium is a non-steroidal anti-inflammatory drug (NSAID) that is used as 0.5% ophthalmic solution for the research of allergic conjunctivitis, cystoid macular edema, intraoperative miosis, and postoperative ocular inflammation and pain. Ketorolac hemicalcium is also a DDX3 inhibitor that can be used in cancer research [1] [4].

Ketorolac (RS37619) salt (0-30 μM, 48 h) effectively kills the oral cancer cells [4]. Ketorolac salt (0-5 μM, 48 h) inhibits the expression of DDX3 protein, and induces apoptosis in H357 cells [4]. Ketorolac salt (0-2.5 μM, 0-16 h) inhibits the proliferation of oral cancer cells [4]. Ketorolac salt (0-50 μM) directly interacts with DDX3 and inhibits the ATPase activity [4]. Cell Viability Assay [4] Cell Line: HOK, SCC4, SCC9 and H357 cells Concentration: 0-30 μM Incubation Time: 48 h Result: Showed inhibition with IC 50 s of 2.6, 7.1 and 8.1 μM against H357, SCC4 and SCC9 cells, respectively. And the normal HOK cell line did not show any cell death effect. Cell Proliferation Assay [4] Cell Line: H357 Concentration: 0.5, 1.0, 1.5, 2.0 and 2.5 μM Incubation Time: 0, 8 and 16 h Result: Inhibited the proliferation. Western Blot Analysis [4] Cell Line: H357 Concentration: 1, 2.5 and 5 μM Incubation Time: 48 h Result: Significantly reduced DDX3 protein expression levels, but not completely ablated as compared to DMSO treated cells. Up regulated the expression of E-cadherin. Apoptosis Analysis [4] Cell Line: H357 Concentration: 2.5 and 5 μM Incubation Time: 48 h Result: Induced apoptosis.

Ketorolac (RS37619) (0.4% ketorolac tromethamine ophthalmic solution) shows powerful ocular anti-inflammatory activities in rabbits [1]. Ketorolac (4 mg/kg/day, p.o.; 2 weeks) has no detrimental effect in the volume fraction of bone trabeculae formed inside the alveolar socket in rats [2]. Ketorolac (60 μg; intrathecal injection; once) attenuates the damage caused by spinal cord ischemia in rats [3]. Ketorolac salt (20 and 30 mg/kg; i.p.; two times in a week for 3 weeks) reduces oral carcinogenesis in mice [4]. Animal Model: New Zealand White rabbits (2.0–2.7 kg), LPS endotoxin-induced ocular inflammation [1] Dosage: 50 μL ketorolac tromethamine ophthalmic solution 0.4% Administration: In eyes, twice, 2 hours and 1 hour before LPS challenge Result: Resulted in a nearly complete inhibition (98.7%) of LPS endotoxin-induced increases in FITC (fluorescein isothiocyanate)-dextran in the anterior chamber, and resulted in a nearly complete inhibition (97.5%) of LPS endotoxin-induced increases in aqueous PGE 2 concentrations in the aqueous humor. Animal Model: Male Wistar rats (400–450 g), spinal cord ischemia model [3] Dosage: 30 and 60 μg Administration: Intrathecal injection, 1 h before the ischemia induction for once Result: Significantly reduced the motor disturbances and improved the survival rate at 60 μg. Animal Model: BALB/c mice, oral carcinogenesis model [4] Dosage: 20 mg/kg and 30 mg/kg Administration: IP injection, two times in a week for 3 weeks Result: Decreased tumor burden, reduced expression of DDX3 and anti-apoptotic proteins (Bcl-2 and Mcl-1).