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Olaparib and α-specific PI3K inhibitor alpelisib for patients with epithelial ovarian cancer: a dose-escalation and dose-expansion phase 1b trial
Open accessAbstract
Background Based on preclinical work, we found that combination of poly (ADP-ribose) polymerase (PARP) inhibitors with drugs that inhibit the homologous recombination repair (HRR) pathway (such as PI3K inhibitors) might sensitise HRR-proficient epithelial ovarian cancers to PARP inhibitors. We aimed to assess the safety and identify the recommended phase 2 dose of the PARP inhibitor olaparib in combination with the PI3K inhibitor alpelisib in patients with epithelial ovarian cancer and in patients with breast cancer. Methods In this multicentre, open-label, phase 1b trial following a 3 + 3 dose-escalation design, we recruited patients aged 18 years or older with the following key eligibility criteria: confirmed diagnosis of either recurrent ovarian, fallopian tube, or primary peritoneal cancer of high-grade serous histology; confirmed diagnosis of either recurrent ovarian, fallopian tube, or primary peritoneal cancer of any histology with known germline BRCA mutations; confirmed diagnosis of recurrent breast cancer of triple-negative histology; or confirmed diagnosis of recurrent breast cancer of any histology with known germline BRCA mutations. Additional patients with epithelial ovarian cancer were enrolled in a dose-expansion cohort. Four dose levels were planned: the starting dose level of alpelisib 250 mg once a day plus olaparib 100 mg twice a day (dose level 0); alpelisib 250 mg once a day plus olaparib 200 mg twice a day (dose level 1); alpelisib 300 mg once a day plus olaparib 200 mg twice a day (dose level 2); and alpelisib 200 mg once a day plus olaparib 200 mg twice a day (dose level 3). Both drugs were administered orally, in tablet formulation. The primary objective was to identify the maximum tolerated dose and the recommended phase 2 dose of the combination of alpelisib and olaparib for patients with epithelial ovarian cancer and patients with breast cancer. Analyses included all patients who received at least one dose of the study drugs. The trial is active, but closed to enrolment; follow-up for patients who completed treatment is ongoing. This trial is registered with ClinicalTrials.gov, number NCT01623349. Findings Between Oct 3, 2014, and Dec 21, 2016, we enrolled 34 patients (28 in the dose-escalation cohort and six in the dose-expansion cohort); two in the dose-escalation cohort were ineligible at the day of scheduled study initiation. Maximum tolerated dose and recommended phase 2 dose were identified as alpelisib 200 mg once a day plus olaparib 200 mg twice a day (dose level 3). Considering all dose levels, the most common treatment-related grade 3-4 adverse events were hyperglycaemia (five [16%] of 32 patients), nausea (three [9%]), and increased alanine aminotransferase concentrations (three [9%]). No treatment-related deaths occurred. Dose-limiting toxic effects included hyperglycaemia and fever with decreased neutrophil count. Of the 28 patients with epithelial ovarian cancer, ten (36%) achieved a partial response and 14 (50%) had stable disease according to Response Evaluation Criteria in Solid Tumors 1.1. Interpretation Combining alpelisib and olaparib is feasible with no unexpected toxic effects. The observed activity provides preliminary clinical evidence of synergism between olaparib and alpelisib, particularly in epithelial ovarian cancer, and warrants further investigation. Funding Ovarian Cancer Dream Team (Stand Up To Cancer, Ovarian Cancer Research Alliance, National Ovarian Cancer Coalition), Breast Cancer Research Foundation, Novartis.
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“In cancer cells, the PI3K/AKT pathway may be activated as a survival mechanism in response to the DNA damage caused by olaparib.”
From Celastrol attenuates the invasion and migration and augments the anticancer effects of olaparib in prostate cancer (2024) · cites this paper as [41]
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Citations
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ResultSelf-citationNiraparib Maintenance Therapy in Platinum-Sensitive, Recurrent Ovarian Cancer
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“The promise of PARPis in the management of EOC is tempered, however, by the fact that EOCs with intrinsic, de novo, HRR proficiency respond less than HRR-deficient carcinomas (5, 6).”
BackgroundInfluentialSecondary mutations as a mechanism of cisplatin resistance in BRCA2-mutated cancers
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Homologous Recombination Deficiency: Exploiting the Fundamental Vulnerability of Ovarian Cancer
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“The rationale for the combination of a PI3Ki with a PARPi was based on preclinical work performed initially in breast cancer models showing in vivo synergy of this combination(10, 11).”
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“The rationale for the combination of a PI3Ki with a PARPi was based on preclinical work performed initially in breast cancer models showing in vivo synergy of this combination(10, 11).”
BackgroundSelf-citationSecondary BRCA1 Mutations in BRCA1 -Mutated Ovarian Carcinomas with Platinum Resistance
Swisher, E. M., Sakai, W., Karlan, B. Y., Wurz, K., Urban, N. D., & Taniguchi, T. (2008) · Cancer Research · doi:10.1158/0008-5472.can-08-0088 · Cited by 459
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“Even in EOC that harbor PIK3CA mutations, responses are infrequently seen with PI3Ki monotherapy; monotherapy ORR in PIK3CA mutated cancers was 0% in one trial(30) with responses observed only with combinations of PI3Kis with other, mainly cytotoxic, agents(30).”
BackgroundSelf-citationKondrashova, O., Nguyen, M., Shield‐Artin, K., Tinker, A. V., Teng, N. N. H., Harrell, M. I., Kuiper, M. J., Ho, G., Barker, H. E., Jasin, M., et al. (2017) · Cancer Discovery · doi:10.1158/2159-8290.cd-17-0419 · Cited by 419
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“In the previously published olaparib/buparlisib trial(14), the objective response rate of olaparib/buparlisib was 29% in patients with gBRCAmut and 12% in patients with gBRCAwt.”
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“It is also important to underscore that PI3Kis, as monotherapy, have very modest activity in EOC(28, 29).”
BackgroundBayesian Dose‐Finding in Phase I/II Clinical Trials Using Toxicity and Efficacy Odds Ratios
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“There is a well-established monotonic doseefficacy relationship for olaparib (19) as well as similar monotonic dose-efficacy relationships for alpelisib (20) and other PI3K inhibitors (21).”
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“platinum resistant gBRCAmut EOC(3, 6)) and gBRCAwt EOC (i.”
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“It is also important to underscore that PI3Kis, as monotherapy, have very modest activity in EOC(28, 29).”
BackgroundSelf-citationPhosphoinositide 3-kinase inhibitors induce DNA damage through nucleoside depletion
Juvekar, A., Hu, H., Yadegarynia, S., Lyssiotis, C. A., Ullas, S., Lien, E. C., Bellinger, G., Son, J., Hok, R. C., Seth, P., et al. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1522223113 · Cited by 93 · cited 2×
“Specifically, PI3Ki disproportionately affects the nonoxidative pentose phosphate pathway that delivers ribose-5-phosphate required for synthesis of ribonucleotides, ultimately leading to a decrease in all four nucleotide triphosphates(13).”
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“Of note, alpelisib, in combination with endocrine therapy (fulvestrant) showed promising results in hormone receptor-positive HER2 negative breast cancer with PIK3CA mutations in the recently reported phase 3, global, double-blind SOLAR-1 study (15).”
BackgroundThe Promise of Combining Inhibition of PI3K and PARP as Cancer Therapy
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“Mechanistically, downregulation of BRCA1/2 appears to be mediated by ERK-dependent activation of the ETS transcription factor, which suppresses BRCA1/2 gene transcription, thereby causing a deficiency in HRR and concomitant PARPi sensitivity (10, 12).”
BackgroundMoore, K. N., Secord, A. A., Geller, M. A., Miller, D. S., Cloven, N. G., Fleming, G. F., Hendrickson, A. E. W., Azodi, M., DiSilvestro, P., Oza, A. M., et al. (2018) · Journal of Clinical Oncology · doi:10.1200/jco.2018.36.15_suppl.5514 · Cited by 29 · cited 1×
“Even in EOCs that are gBRCAwt but HRD positive and platinum resistant, the response to PARPi niraparib monotherapy in the recently reported QUADRA study was only 10%(26).”
BackgroundSelf-citation
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“therapy in breast cancer [228] and other advanced solid tumors [229, 230], as well as in combination with either trastuzumab-emtansine [231], fulvestrant [232–235], letrozole [236–239], nab-paclitaxel [240], olaparib [241], or trastuzumab + LJM716 [242], in breast cancer, and in combination with either imatinib [243],…”
BackgroundRecent advances in therapeutic strategies for triple-negative breast cancer
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PARP and PARG inhibitors in cancer treatmentPreprint
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“A phase I clinical trial revealed synergistic effects between olaparib and the PI3K inhibitor alpelisib in epithelial ovarian cancer, which are most likely based on HR suppression through reduced RAD51 protein levels and RAD51 foci formation (Konstantinopoulos et al. 2019).”
Metadata
- Authors
- Konstantinopoulos, P. A., Barry, W. T., Birrer, M., Westin, S. N., Cadoo, K. A., Shapiro, G. I., Mayer, E. L., O'Cearbhaill, R. E., Coleman, R. L., Kochupurakkal, B., Whalen, C., Curtis, J., Farooq, S., Luo, W., Eismann, J., Buss, M. K., Aghajanian, C., Mills, G. B., Palakurthi, S., Kirschmeier, P., Liu, J., Cantley, L. C., Kaufmann, S. H., Swisher, E. M., D'Andrea, A. D., Winer, E., Wulf, G. M., & Matulonis, U. A.
- Affiliations
- Dana-Farber Cancer Institute (US)
- Massachusetts General Hospital (US)
- The University of Texas MD Anderson Cancer Center (US)
- Memorial Sloan Kettering Cancer Center (US)
- Beth Israel Deaconess Medical Center (US)
- Oregon Health & Science University (US)
- Weill Cornell Medicine (US)
- Mayo Clinic (US)
- University of Washington (US)
- Corresponding author
- Konstantinopoulos, Panagiotis A
- ORCID
- Konstantinopoulos, Panagiotis A
- Birrer, Michael
- Westin, Shannon N
- Cadoo, Karen A
- Shapiro, Geoffrey I
- Mayer, Erica L
- O'Cearbhaill, Roisin E
- Coleman, Robert L
- Kochupurakkal, Bose
- Farooq, Sarah
- Buss, Mary K
- Aghajanian, Carol
- Mills, Gordon B
- Palakurthi, Sangeetha
- Liu, Joyce
- Cantley, Lewis C
- Kaufmann, Scott H
- Swisher, Elizabeth M
- Winer, Eric
- Wulf, Gerburg M
- Matulonis, Ursula A
- Venue
- The Lancet Oncology
- Publisher
- Elsevier BV
- Published
- 2019-04
- Volume
- 20
- Issue
- 4
- Pages
- 570-580
- ISSN
- 1470-2045 (ISSN-L)
- PMC
- PMC7025391
- OpenAlex
- W2921991537
- Cited by
- 263
- References
- 33
- Citations by year
- 2026: 13 · 2025: 29 · 2024: 33 · 2023: 38 · 2022: 48 · 2021: 46 · 2020: 38 · 2019: 17
- FWCI
- 15.67
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet Oncology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Breast Cancer Research Foundation
- Topics
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Health Sciences › Medicine › Oncology › Ovarian cancer diagnosis and treatment
- Keywords
- olaparib, alpelisib, PI3K inhibitors, PARP inhibitors, epithelial ovarian cancer, breast cancer, triple-negative breast cancer, homologous recombination repair, BRCA mutations, high-grade serous ovarian cancer, combination therapy, maximum tolerated dose, recommended phase 2 dose, drug safety, dose escalation, dose expansion, recurrent cancer, PARP inhibitor resistance
- MeSH terms
- Poly(ADP-ribose) Polymerase Inhibitors, Carcinoma, Ovarian Epithelial, Phosphoinositide-3 Kinase Inhibitors, Aged, Antineoplastic Combined Chemotherapy Protocols, Dose-Response Relationship, Drug, Female, Humans, Middle Aged, Mutation, Ovarian Neoplasms, Phthalazines, Piperazines, Thiazoles, Genome, Human, Treatment Outcome, Maximum Tolerated Dose, Drug-Related Side Effects and Adverse Reactions
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