Ibrutinib: From Molecule to Medicine
Küçük Resim Yok
Tarih
2014
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
İbrutinib: Molekülden İlacaBruton tirozin kinaz (BTK) inhibitörü Ibrutinib (PCI-32765), BTK üzerine irreversibl kovalan bağlanarak BCR aktivitesini yönlendiren yeni bir hedeflenmiş tedavi ajanıdır. Ibrutinib, kronik enfositik lösemi (KLL)'de tümör mikroçevresini hücresel moleküler elemanlar üzerinden myelosupresyona yol açmaksızın etkiler. Oral ibrutinib relaps/refrakter veya yeni tanı B-hücre malinitelerinde değişik klinik çalışmalarda test edilmektedir. KLL, mantle hücreli lenfoma (MCL) ve Waldenstrom makroglobulinemi (WM) hastalıklarında ibrutinib klinik çalışmaları devam etmektedir. Ibrutinib, klinik deneyimi özellikle relaps/refrakter KLL alanında progresyonsuz yaşam süresi (PFS) ve genel yaşam süresi (OS) iyileşmeleri ile birlikte hastalık kontrolü sağlamak amaçlı şekillenmiştir. Bu yazının amacı, ibrutinib tedavisinin farmakofizyolojik temellerine değinmek ve konu ile ilgili klinik çalışma deneyimlerini aktarmaktır. B-lenfoproliferatif hastalıkların tedavi şemaları, etkinliği artırmak ve hastaları gereksiz toksisiteden korumak üzerine odaklı olarak güncellenmeye devam edecektir
Bruton's tyrosine kinase (BTK) inhibitor Ibrutinib (PCI-32765) is a novel targeted-therapeutic agent modulating BCR, which serves as a covalent irreversible inhibitor of BTK. Ibrutinib significantly alters the composition of the tumor microenvironment in CLL, affecting soluble as well as cellular molecular elements without myelosupression. Ibrutinib is clinically developed as an orally administered anti-cancer agent with lead indications in relapse/refractory and in treatment-naïve patients with B-cell malignancies as a single agent. the clinical activities of Ibrutinib as a drug were shown in the B-cell malignancies, especially in patients with CLL, mantle cell lymphoma (MCL), and Waldenstrom's macroglobulinemia (WM). Ibrutinib has generated the most extensive results so far in patients with CLL, predominately refractory or relapsed CLL where durable disease control as well as improved progression-free survival (PFS) and overall survival (OS) has been observed. the aim of this review is to outline the pharmacophysiological basis of Ibrutinib treatment as well as the current clinical experience based on the trials. the treatment algorithms of B-lymphoproliferative diseases will continue to be revised to a more personalized approach to treat with improved efficacy devoid of unnecessary toxicity
Bruton's tyrosine kinase (BTK) inhibitor Ibrutinib (PCI-32765) is a novel targeted-therapeutic agent modulating BCR, which serves as a covalent irreversible inhibitor of BTK. Ibrutinib significantly alters the composition of the tumor microenvironment in CLL, affecting soluble as well as cellular molecular elements without myelosupression. Ibrutinib is clinically developed as an orally administered anti-cancer agent with lead indications in relapse/refractory and in treatment-naïve patients with B-cell malignancies as a single agent. the clinical activities of Ibrutinib as a drug were shown in the B-cell malignancies, especially in patients with CLL, mantle cell lymphoma (MCL), and Waldenstrom's macroglobulinemia (WM). Ibrutinib has generated the most extensive results so far in patients with CLL, predominately refractory or relapsed CLL where durable disease control as well as improved progression-free survival (PFS) and overall survival (OS) has been observed. the aim of this review is to outline the pharmacophysiological basis of Ibrutinib treatment as well as the current clinical experience based on the trials. the treatment algorithms of B-lymphoproliferative diseases will continue to be revised to a more personalized approach to treat with improved efficacy devoid of unnecessary toxicity
Açıklama
Anahtar Kelimeler
Onkoloji
Kaynak
Uluslararası Hematoloji-Onkoloji Dergisi
WoS Q Değeri
Scopus Q Değeri
Cilt
253