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ePoster Display

489P - MEN1611 in combination with cetuximab: Targeting PIK3CA mutations in RAS-wild-type patient-derived colorectal cancer xenografts

Date

16 Sep 2021

Session

ePoster Display

Topics

Tumour Site

Colon and Rectal Cancer

Presenters

Stefania Capano

Citation

Annals of Oncology (2021) 32 (suppl_5): S530-S582. 10.1016/annonc/annonc698

Authors

S. Capano1, G. Merlino1, M. Bigioni1, P. Tunici1, F. Cottino2, E. Zanella2, V. Vurchio2, A. Bertotti3, L. Trusolino4, D.O. Laurent5, A. Pellacani6, M. Binaschi1

Author affiliations

  • 1 Experimental And Translational Oncology Department, Menarini Ricerche S.p.A, 00071 - Pomezia/IT
  • 2 Candiolo Cancer Institute, FPO IRCCS, 10060 - Candiolo/IT
  • 3 Department Of Oncology, University of Torino, 10060 - Candiolo/IT
  • 4 Department Of Oncology, University Of Torino, IRCCS Candiolo, 10060 - Candiolo/IT
  • 5 Oncology Therapeutic Area, Berlin Chemie AG/Menarini Ricerche S.p.A, Berlin/DE
  • 6 R&d Division, Menarini Ricerche S.p.A, Firenze/IT

Resources

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Abstract 489P

Background

In the management of metastatic colorectal cancer (mCRC) patients, the anti-EGFR antibody cetuximab has demonstrated a clinical benefit only in KRAS wild-type (wt) tumors. Although KRAS mutational status is an important biomarker to stratify patients for anti-EGFR therapy, still not all the patients harboring KRASwt benefit from this treatment. In addition, after an initial response, secondary resistance emerges due to genetic alterations in the PI3K and MEK pathways. Therefore PI3K inhibitors might be an effective therapeutic option in selected patients that have progressed to cetuximab. MEN1611 is a PI3K inhibitor in clinical development showing high activity against p110 α, β and ɣ isoforms and minimal inhibition of δ isoform.

Methods

In this work we investigate MEN1611 efficacy in combination with cetuximab in different patient derived xenograft (PDX) models obtained from mCRC patients characterized by N-KRASwt, BRAFwt and mutated PIK3CA. Mice were treated twice weekly with 20 mg/kg cetuximab (ip), daily with 6.5 mg/kg MEN1611 (os) or with their combination. No tolerability issues were observed with the described combination treatment.

Results

Two, among the established PDX models, were proven to be cetuximab resistant (in progressive disease -PD- according to mRECIST criteria). They harbored respectively H1047R (a driver mutation with allele frequency -AF- 17% in CRC patient population) or V344G PIK3CA mutation (AF 5%). In both models MEN1611 was ineffective (PD according to mRECIST), but, impressively, the combination was able to overcome cetuximab resistance inducing tumor- growth delay or disease stabilization, respectively, thus substantiating the potential utility of PI3K inhibition in mCRC.

Conclusions

In conclusion, in the selected genetic setting, the combination of MEN1611 with cetuximab displayed higher activity compared to single agents showing a synergistic effect in cetuximab-resistant PDX models. These data support the ongoing C-Precise phase Ib/II study investigating anti-tumor activity and safety of MEN1611 in combination with cetuximab in PIK3CAmut/N-K-RASwt/BRAFwt mCRC patients (NCT04495621).

Clinical trial identification

NCT04495621.

Editorial acknowledgement

Legal entity responsible for the study

Menarini Ricerche.

Funding

Menarini Ricerche.

Disclosure

All authors have declared no conflicts of interest.

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