Pharmacokinetic, pharmacodynamic and biomarker evaluation of transforming growth factor-β receptor I kinase inhibitor, galunisertib, in phase 1 study in patients with advanced cancer

Purpose Transforming growth factor-beta (TGF-β) signaling plays a key role in epithelial-mesenchymal transition (EMT) of tumors, including malignant glioma. Small molecule inhibitors (SMI) blocking TGF-β signaling reverse EMT and arrest tumor progression. Several SMIs were developed, but currently o...

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Autores: Rodón, Jordi, Carducci, Michael, Sepulveda-Sánchez, Juan M., Azaro, Analía, Calvo, Emiliano|||0000-0003-4921-829X, Seoane Suárez, Joan|||0000-0002-6541-5974, Braña, Irene|||0000-0002-1068-9601, Sicart, Elisabet, Gueorguieva, Ivelina, Cleverly, Ann, Pillay, Nischalan|||0000-0003-0579-4105, Desaiah, Durisala, Estrem, Shawn T., Paz-Ares, Luis|||0000-0002-3327-3246, Holdhoff, Matthias, Blakeley, Jaishri, Lahn, Michael M.., Baselga Torres, Josep
Tipo de recurso: artículo
Fecha de publicación:2014
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:185143
Acceso en línea:https://ddd.uab.cat/record/185143
https://dx.doi.org/urn:doi:10.1007/s10637-014-0192-4
Access Level:acceso abierto
Palabra clave:TGF-β inhibitor
Galunisertib
First-in-Human Dose
Glioma
Pharmacokinetics
Pharmacodynamics
Descripción
Sumario:Purpose Transforming growth factor-beta (TGF-β) signaling plays a key role in epithelial-mesenchymal transition (EMT) of tumors, including malignant glioma. Small molecule inhibitors (SMI) blocking TGF-β signaling reverse EMT and arrest tumor progression. Several SMIs were developed, but currently only LY2157299 monohydrate (galunisertib) was advanced to clinical investigation. Design The first-in-human dose study had three parts (Part A, dose escalation, n = 39; Part B, safety combination with lomustine, n = 26; Part C, relative bioavailability study, n = 14). Results A preclinical pharmacokinetic/pharmacodynamic (PK/PD) model predicted a therapeutic window up to 300 mg/day and was confirmed in Part A after continuous PK/PD. PK was not affected by co-medications such as enzyme-inducing anti-epileptic drugs or proton pump inhibitors. Changes in pSMAD2 levels in peripheral blood mononuclear cells were associated with exposure indicating target-related pharmacological activity of galunisertib. Twelve (12/79; 15 %) patients with refractory/relapsed malignant glioma had durable stable disease (SD) for 6 or more cycles, partial responses (PR), or complete responses (CR). These patients with clinical benefit had high plasma baseline levels of MDC/CCL22 and low protein expression of pSMAD2 in their tumors. Of the 5 patients with IDH1/2 mutation, 4 patients had a clinical benefit as defined by CR/PR and SD ≥6 cycles. Galunisertib had a favorable toxicity profile and no cardiac adverse events. Conclusion Based on the PK, PD, and biomarker evaluations, the intermittent administration of galunisertib at 300 mg/day is safe for future clinical investigation.