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CC BY 4.0 · Indian J Med Paediatr Oncol
DOI: 10.1055/s-0044-1786017
Drug Review

Trilaciclib: A Novel Approach to Mitigate Chemotherapy-Induced Myelosuppression in Cancer Treatment

Mayank Kapoor 
1   Department of Medical Oncology, All India Institute of Medical Sciences (AIIMS), Rishikesh, Uttarakhand, India
,
Amit Sehrawat 
1   Department of Medical Oncology, All India Institute of Medical Sciences (AIIMS), Rishikesh, Uttarakhand, India
,
Deepak Sundriyal
1   Department of Medical Oncology, All India Institute of Medical Sciences (AIIMS), Rishikesh, Uttarakhand, India
› Author Affiliations Source of Funding None.
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Abstract

Trilaciclib, a novel cyclin-dependent kinase 4/6 inhibitor, has demonstrated the ability to protect bone marrow from chemotherapy toxicity, improving patients' quality of life (QoL). This review describes the mechanism of action, efficacy, and toxicity profile of trilaciclib. Trilaciclib halts retinoblastoma protein phosphorylation during the early G1 phase, preventing the transition from the G1/S phase and inducing the cell cycle arrest in the G1 phase, which protects the hematopoietic cell lineages. Trilaciclib is indicated by the United States Food and Drug Administration and National Comprehensive Cancer Network to decrease the incidence of chemotherapy-induced myelosuppression in adult patients before a platinum/etoposide or topotecan containing regimen for extensive stage small cell lung cancer. Its ease of administration as an intravenous infusion, given before starting chemotherapy, and the favorable side effect profile make it a better-tolerated drug, improving patient QoL.

Keywords

trilaciclib - neutropenia - CDK 4/6 inhibitor - chemotherapy-induced myelosuppression

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No prior submissions.


The manuscript has been read and approved by all the authors, that the requirements for authorship as stated earlier in this document have been met, and that each author believes that the manuscript represents honest work.


Patient Consent

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Publication History

Article published online:
30 April 2024

© 2024. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

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