Literature DB >> 34559360

A Phase 1b Trial of Prexasertib in Combination with Standard-of-Care Agents in Advanced or Metastatic Cancer.

Kathleen N Moore1,2, David S Hong3, Manish R Patel4,5, Shubham Pant6,3, Susanna V Ulahannan6,4, Suzanne Jones4, Funda Meric-Bernstam3, Judy S Wang4,5, Raid Aljumaily6,4, Erika P Hamilton4,7, Erika S Wittchen8, Xuejing Wang9, Aimee Bence Lin9, Johanna C Bendell4,7.   

Abstract

BACKGROUND: The checkpoint kinase 1 (CHK1) inhibitor prexasertib exhibited modest monotherapy antitumor activity in prior trials, suggesting that combination with chemotherapy or other targeted agents may be needed to maximize efficacy.
OBJECTIVES: The aim of this study was to determine the recommended phase II dose and schedule of prexasertib in combination with either cisplatin, cetuximab, pemetrexed, or 5-fluorouracil in patients with advanced and/or metastatic cancer, and to summarize preliminary antitumor activity of these combinations. PATIENTS AND METHODS: This phase Ib, nonrandomized, open-label study comprised dose-escalation phase(s) with multiple sub-arms evaluating different prexasertib-drug combinations: Part A, prexasertib + cisplatin (n = 63); Part B, prexasertib + cetuximab (n = 41); Part C, prexasertib + pemetrexed (n = 3); Part D, prexasertib + 5-fluorouracil (n =8). Alternate dose schedules/regimens intended to mitigate toxicity and maximize dose exposure and efficacy were also explored in sub-parts.
RESULTS: In Part A, the maximum tolerated dose (MTD) of prexasertib in combination with cisplatin (75 mg/m2) was declared at 80 mg/m2, with cisplatin administered on Day 1 and prexasertib on Day 2 of a 21-day cycle. The overall objective response rate (ORR) in Part A was 12.7%, and 28 of 55 evaluable patients (50.9%) had a decrease in target lesions from baseline. The most frequent treatment-related adverse events (AEs) in Part A were hematologic, with the most common being white blood cell count decreased/neutrophil count decreased, experienced by 73.0% (any grade) and 66.7% (grade 3 or higher) of patients. In Part B, an MTD of 70 mg/m2 was established for prexasertib administered in combination with cetuximab (500 mg /m2), both administered on Day 1 of a 14-day cycle. The overall ORR in Part B was 4.9%, and 7 of 31 evaluable patients (22.6%) had decreased target lesions compared with baseline. White blood cell count decreased/neutrophil count decreased was also the most common treatment-related AE (56.1% any grade; 53.7% grade 3 or higher). In Parts A and B, hematologic toxicities, even with the addition of prophylactic granulocyte colony-stimulating factor, resulted in frequent dose adjustments (> 60% of patients). In Part C, evaluation of prexasertib + pemetrexed was halted due to dose-limiting toxicities in two of the first three patients; MTD was not established. In Part D, the MTD of prexasertib in combination with 5-fluorouracil (label dose) was declared at 40 mg /m2, both administered on Day 1 of a 14-day cycle. In Part D, overall ORR was 12.5%.
CONCLUSIONS: This study demonstrated the proof-of-concept that prexasertib can be combined with cisplatin, cetuximab, and 5-fluorouracil. Schedule was a key determinant of the tolerability and feasibility of combining prexasertib with these standard-of-care agents. Reversible hematologic toxicity was the most frequent AE and was dose-limiting. Insights gleaned from this study will inform future combination strategies for the development of prexasertib and next-generation CHK1 inhibitors. CLINICALTRIALS. GOV IDENTIFIER: NCT02124148 (date of registration 28 April 2014).
© 2021. The Author(s), under exclusive licence to Springer Nature Switzerland AG.

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Year:  2021        PMID: 34559360     DOI: 10.1007/s11523-021-00835-0

Source DB:  PubMed          Journal:  Target Oncol        ISSN: 1776-2596            Impact factor:   4.493


  27 in total

1.  RNAi screening of the kinome identifies modulators of cisplatin response in ovarian cancer cells.

Authors:  Shilpi Arora; Kristen M Bisanz; Lourdes A Peralta; Gargi D Basu; Ashish Choudhary; Raoul Tibes; David O Azorsa
Journal:  Gynecol Oncol       Date:  2010-09       Impact factor: 5.482

2.  A phase 1 dose-escalation study of checkpoint kinase 1 (CHK1) inhibitor prexasertib in combination with p38 mitogen-activated protein kinase (p38 MAPK) inhibitor ralimetinib in patients with advanced or metastatic cancer.

Authors:  Johanna C Bendell; Helge G Bischoff; Jimmy Hwang; Hans Christian Reinhardt; Thomas Zander; Xuejing Wang; Scott Hynes; Celine Pitou; Robert Campbell; Philip Iversen; Daphne L Farrington; Katherine Bell-McGuinn; Michael Thomas
Journal:  Invest New Drugs       Date:  2019-11-09       Impact factor: 3.850

3.  LY2606368 Causes Replication Catastrophe and Antitumor Effects through CHK1-Dependent Mechanisms.

Authors:  Constance King; H Bruce Diaz; Samuel McNeely; Darlene Barnard; Jack Dempsey; Wayne Blosser; Richard Beckmann; David Barda; Mark S Marshall
Journal:  Mol Cancer Ther       Date:  2015-07-03       Impact factor: 6.261

4.  Chk1/2 inhibition overcomes the cisplatin resistance of head and neck cancer cells secondary to the loss of functional p53.

Authors:  Mayur A Gadhikar; Maria Rita Sciuto; Marcus Vinicius Ortega Alves; Curtis R Pickering; Abdullah A Osman; David M Neskey; Mei Zhao; Alison L Fitzgerald; Jeffrey N Myers; Mitchell J Frederick
Journal:  Mol Cancer Ther       Date:  2013-07-09       Impact factor: 6.261

Review 5.  Prexasertib, a checkpoint kinase inhibitor: from preclinical data to clinical development.

Authors:  Gesuino Angius; Silverio Tomao; Valeria Stati; Patrizia Vici; Vincenzo Bianco; Federica Tomao
Journal:  Cancer Chemother Pharmacol       Date:  2019-09-11       Impact factor: 3.333

Review 6.  CHEK again: revisiting the development of CHK1 inhibitors for cancer therapy.

Authors:  S McNeely; R Beckmann; A K Bence Lin
Journal:  Pharmacol Ther       Date:  2013-10-15       Impact factor: 12.310

7.  Evaluation of Prexasertib, a Checkpoint Kinase 1 Inhibitor, in a Phase Ib Study of Patients with Squamous Cell Carcinoma.

Authors:  David S Hong; Kathleen Moore; Manish Patel; Stefan C Grant; Howard A Burris; William N William; Suzanne Jones; Funda Meric-Bernstam; Jeffrey Infante; Lisa Golden; Wei Zhang; Ricardo Martinez; Sameera Wijayawardana; Richard Beckmann; Aimee Bence Lin; Cathy Eng; Johanna Bendell
Journal:  Clin Cancer Res       Date:  2018-04-11       Impact factor: 12.531

8.  Phase I Study of LY2606368, a Checkpoint Kinase 1 Inhibitor, in Patients With Advanced Cancer.

Authors:  David Hong; Jeffrey Infante; Filip Janku; Suzanne Jones; Ly M Nguyen; Howard Burris; Aung Naing; Todd M Bauer; Sarina Piha-Paul; Faye M Johnson; Razelle Kurzrock; Lisa Golden; Scott Hynes; Ji Lin; Aimee Bence Lin; Johanna Bendell
Journal:  J Clin Oncol       Date:  2016-04-04       Impact factor: 44.544

9.  Therapeutic targeting of Chk1 in NSCLC stem cells during chemotherapy.

Authors:  M Bartucci; S Svensson; P Romania; R Dattilo; M Patrizii; M Signore; S Navarra; F Lotti; M Biffoni; E Pilozzi; E Duranti; S Martinelli; C Rinaldo; A Zeuner; M Maugeri-Saccà; A Eramo; R De Maria
Journal:  Cell Death Differ       Date:  2011-11-25       Impact factor: 15.828

Review 10.  G2 checkpoint abrogation and checkpoint kinase-1 targeting in the treatment of cancer.

Authors:  N Bucher; C D Britten
Journal:  Br J Cancer       Date:  2008-01-29       Impact factor: 7.640

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  4 in total

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Review 3.  Therapeutic Targeting of DNA Damage Response in Cancer.

Authors:  Wonyoung Choi; Eun Sook Lee
Journal:  Int J Mol Sci       Date:  2022-02-01       Impact factor: 5.923

Review 4.  Targeting the DNA Damage Response and DNA Repair Pathways to Enhance Radiosensitivity in Colorectal Cancer.

Authors:  Siyao Deng; Tijana Vlatkovic; Moying Li; Tianzuo Zhan; Marlon R Veldwijk; Carsten Herskind
Journal:  Cancers (Basel)       Date:  2022-10-05       Impact factor: 6.575

  4 in total

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