Table 6. Early clinical trials of PI3K pathway inhibitors in association with another targeted therapy in OC.
| Trial phase and/or population feature | Treatment | No. of OC patients | Efficacy | Reference |
| Phase II | Temsirolimus + bevacizumab | 31 | RR = 12% | Morgan et al.[64] |
| Randomized II | Bevacizumab +/- everolimus | 150 | Improved RR with the combination (19% vs. 9%) No impact on PFS or OS |
Tew et al.[67] |
| Phase I | Everolimus + bevacizumab + panitumumab (an EGFR antibody) | 4 | 3 cases of SD for 11 to >40 months | Vlahovic et al.[56] |
| Phase Ib, OC expansion cohort with biomarker selected (low-RAS signature) | IGF-1R antibody, dalo tuzumab + ridaforolimus or MK2206 (Akt inhibitor) | 12 | 3 cases of SD | Brana et al. [59] |
| Phase Ib, KRAS-mutated OC expansion cohort | BYL719 (PI3K inhibitor) + MEK162 (MEK inhibitor) | 4 | 3 cases of confirmed PR | Juric et al. [61] |
| RAS-mutated OC | PI3K inhibitor + MEK inhibitor (NOS) | 13 | 6 cases of PR | Spreafico et al. [62] |
| ER + and/or PgR + OC | Everolimus + letrozole | 10 | 2 demonstrated minimal response or SD >6 months | Wheler et al. [70] |
PI3K, phosphatidylinositol 3 kinase; ER, estrogen receptor; PgR, progesterone receptor; EGFR, epidermal growth factor receptor; IGR-1R, insulin growth factor 1 receptor; RR, response rate; PFS, progression-free survival; OS, overall survival; SD, stable disease; PR, partial response; NOS, not otherwise specified.