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Table 6. Early clinical trials of PI3K pathway inhibitors in association with another targeted therapy in OC

From: The PI3K/Akt/mTOR pathway in ovarian cancer: therapeutic opportunities and challenges

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%) Tew et al.[67]
No impact on PFS or OS
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 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]
  1. 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.