Exisulind 通过激活蛋白激酶 G (PKG) 诱导细胞凋亡。 Exisulind 在实体瘤和血液癌细胞系中表现出抗肿瘤活性，并且是结肠癌、前列腺癌、膀胱癌、乳腺癌和肺癌啮齿动物模型中肿瘤生长的抑制剂。

Exisulind induces apoptosis through the activation of protein kinase G (PKG). Exisulind exhibits antineoplastic activity in solid tumour and haematological cancer cell lines and is an inhibitor of tumour growth in rodent models of colon, prostate, bladder, mammary and lung cancer.

The topical treatment with NO-Exisulind significantly reduced UVB-induced tumors in SKH-1 hairless mice. The tumors/tumor bearing mouse, the number of tumors/mouse and tumor volume/mouse decreased significantly (P< 0.05) as compared with vehicle-treated and UVB-irradiated positive controls. NO-Exisulind-treated animals showed reduced expression of proliferation markers, such as PCNA and cyclin D1. These mice also manifested increased expression of proapoptotic Bax and decreased expression of antiapoptotic Bcl2 with an increase in the number of TUNEL-positive cells in tumors. NO-Exisulind-treated tumors are less invasive and progress less efficiently from benign to malignant carcinomas[1].

59973-80-7

C20H17FO4S

372.41

Sulindac sulfone;CP248

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years