Loss of proliferation in ATL-derived cell lines by the Pim-kinase inhibitor AZD1208 (D). Cell counts were repeated at least twice. Results represent the percentage of cells alive after 5 days of Pim inhibitor treatment, compared with 5 days treated with DMSO. For AZD1208, cells were treated with 0, 5, or 10 μM AZD1208. Normal PBMCs (n = 2) were used as a control. Western blots indicate loss of Pim1 targets, p-4EBP1 (Thr37/46), p-p70S6K (Thr389), and loss of pBad (Ser20) (negligible for Smi-4a) after 24 hours with 0, 5, or 10 μM AZD1208; or DMSO control.
Dutasteride, however, is a so-called dual inhibitor with both 5α-R1 and 5α-R2 inhibition. IC50 for 5α-R1 is 7 nM but 6 nM for 5α-R2. As mentioned above, it reduces DHT > 90% overall, or precisely % and for intraprostatic DHT the reduction is 97-99%. Dutasteride has also been found to inhibit 5α-R3, in vitro, with IC50= nM.  The 2,5-difluorophenyl side chain on the D-ring of the compound shows significant lipophilic features and as increased lipophilicity enhances the potency of the compounds binding at pocket site, its potency is much greater than of finasteride. 
The insulin-like growth factors play a major role in regulating cell proliferation and inhibiting apoptosis. The IGFs are expressed ubiquitously and act in an autocrine/paracrine manner through binding to the IGF-1 receptor (IGF-1R). The bioavailability of IGF in tissues is determined by both local and systemic factors. The local factors include the levels of receptors that are expressed, various IGF binding proteins (IGFBPs), and IGFBP proteases. The systemic factors involved are mainly those that regulate the circulating levels of IGFs, such as growth hormone (GH) and various nutritional factors. Studies in cultured cells have demonstrated that the IGF-1R is frequently overexpressed in cancer cell lines.