Phosphodiesterase 3 (PDE3) is one member of the PDE family and has two subtypes, PDE3A and PDE3B. PDE3A mainly expresses in heart, platelet, vascular smooth muscle, and oocytes and is involved in oocyte maturation and platelet aggregation. PDE3B mostly expresses in white and brown adipose cells, hepatocytes, renal collecting duct epithelium, and developing spermatocytes and is important for the regulation of glucose and lipid metabolism. In particular, PDE3 acts as a potential therapeutic target in GIST cell lines and xenograft models. Especially, PDE3 plays an important role in the growth of human submandibular gland intercalated ductal cells. PDE3 inhibitors suppress meiosis in oocytes by decreasing the level of cAMP and blocking the extrusion of the first polar body.

PDE3A and PDE3B highly express in gastrointestinal stromal tumors compared to many other types of human cancer, which may open an opportunity for efficient targeted therapy. DNMDP potently and selectively inhibits PDE3A and PDE3B and kills cancer cells by inducing PDE3A/B interactions with SFLN12. BRD9500 is a DNMDP analog. Particularly, BRD9500 is active in an SK-MEL-3 xenograft model of cancer. Furthermore, BRD9500 inhibits PDE3A and PDE3B with IC50s of 10 and 27 nM, respectively. BRD9500 shows high plasma levels in mice after i.v. (1 mg/kg) as well as po (2 mg/kg) dosing over eight hours making it a valuable candidate for in vivo xenograft testing.

BRD9500 induces PDE3A/SLFN12 binding in HeLa cells and is active with oral dosing in a mouse xenograft model of melanoma. In addition, PDE3A and SLFN12 expression levels together serve as a predictive biomarker for BRD9500 sensitivity.

To summarise, BRD9500 is a PDE3A modulator for SLFN12-dependent cancer cell killing. Moreover, BRD9500 increases PDE3A/B biochemical inhibition 10-fold.

Reference:
Timothy A Lewis,et al. Optimization of PDE3A Modulators for SLFN12-Dependent Cancer Cell Killing. ACS Med Chem Lett. 2019 Oct 18;10(11):1537-1542.