Table 2.

Therapy exposure

	AKT1 mutant, n=153, N (%)	AKT1 wildtype, n=302 N (%)	All, n=455, %
Endocrine Therapy*
Tamoxifen	96(63%)	184(61%)	280(62%)
Aromatase Inhibitor	127(83%)	266(88%)	393(86%)
Fulvestrant	79(52%)	162(54%)	241(53%)
Endocrine therapy sensitivity†	106(69%)	236(78%)	342(75%)
Chemotherapy	137(90%)	269(89%)	406(89%)
Endocrine therapies for metastatic disease, median (range)§	1 (0–6)	2 (0–9)	2 (0–9)
Chemotherapies for metastatic disease, median (range)	2 (0–7)	2 (0–9)	2 (0–9)
Targeted Therapy
CDK4/6 inhibitor	45(29%)	87(29%)	132(29%)
mTOR inhibitor	49(32%)	97(32%)	146(32%)
‡AKT inhibitor§	23(15%)	4(1%)	27(6%)
Therapeutic clinical trial	52(34%)	95(32%)	147(32%)

^*Any endocrine therapy in adjuvant or metastatic setting;

^†≥24 months of adjuvant endocrine therapy or ≥6 months treatment duration on any metastatic endocrine therapy;

^§p<0.05;

^‡NCT01226316 was a first in human, phase I, multipart study of the AKT inhibitor, AZD5363, in advanced solid tumors. This study had many cohorts including individual molecularly selected cohorts for PIK3CA- AKT1-, and PTEN- mutant tumors. Four AKT1-wild type patients were treated on NCT01226316, 1 PIK3CA- and 2 PTEN -mutant breast cancers and 1 other patient for reasons unknown.