Ketoprofen (RP-19583) is a propionic acid derivate and nonsteroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic and antipyretic effects. Ketoprofen inhibits the activity of the enzymes cyclo-oxygenase I and II, resulting in a decreased formation of precursors of prostaglandins and thromboxanes. The resulting decrease in prostaglandin synthesis, by prostaglandin synthase, is responsible for the therapeutic effects of ibuprofen. Ketoprofen also causes a decrease in the formation of thromboxane A2 synthesis, by thromboxane synthase, thereby inhibiting platelet aggregation.

COX-1:2 nM, COX-2:26 nM

Ketoprofen联合UVB照射在浓度依赖的方式内对HaCaT细胞产生细胞毒性作用并抑制DNA合成，抑制细胞增长。Ketoprofen通过调节cdc2、cyclin B1、Chk1、Tyr15磷酸化的cdc2和p21的水平，诱导G2/M细胞周期阻滞。Ketoprofen和UVB的联合照射还促使cyclin B1-cdc2-p21复合物显著积累，同时伴随着Tyr15磷酸化cdc2和p21蛋白水平的升高。Ketoprofen联合UVB照射，通过DAPI染色增强HaCaT细胞对UVB辐射的凋亡反应。[1]

Ketoprofen以1%浓度于适宜的局部应用载体中，可有效抑制猕猴牙周炎模型中的GCF-LTB4与GCF-PGE2，改变齿槽骨活性。[2] Ketoprofen（3.63 mg/kg ）在减轻蹄痛和跛行方面，效果超过2.2 mg/kg Ketoprofen和phenylbutazone。[3] Ketoprofen比局部麻醉（LA）或尾部硬膜外麻醉（EPI）更能有效降低皮质酮水平，并部分逆转去势后平均日增重（ADG）的下降。[4] Ketoprofen以40和80 mg/kg饮食剂量，可将饮食小鼠的尿路移行细胞癌发生率降低70%以上。[5]