Article

Pharmacodynamic, pharmacokinetic, and phase 1a study of bisthianostat, a novel histone deacetylase inhibitor, for the treatment of relapsed or refractory multiple myeloma

Yu-bo Zhou1,2, Yang-ming Zhang1,2,3, Hong-hui Huang4, Li-jing Shen4, Xiao-feng Han4, Xiao-bei Hu1, Song-da Yu1,5, An-hui Gao1, Li Sheng1, Ming-bo Su1, Xiao-li Wei1, Yue Zhang1, Yi-fan Zhang1,5, Zhi-wei Gao1,5, Xiao-yan Chen1,2,5, Fa-jun Nan1,2,3, Jia Li1,2, Jian Hou4
1 National Center for New Drug Screening, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China
2 University of Chinese Academy of Sciences, Beijing 100049, China
3 Yantai Key Laboratory of Nanomedicine & Advanced Preparations, Yantai Institute of Materia Medica, Yantai 264000, China
4 Department of Hematology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200127, China
5 Shanghai Center for Drug Metabolism and Pharmacokinetics Research, Shanghai 201203, China
Correspondence to: Fa-jun Nan: fjnan@simm.ac.cn, Jia Li: jli@simm.ac.cn, Jian Hou: houjian@medmail.com.cn,
DOI: 10.1038/s41401-021-00728-y
Received: 7 December 2020
Accepted: 27 June 2021
Advance online: 2 August 2021

Abstract

HDAC inhibitors (HDACis) have been intensively studied for their roles and potential as drug targets in T-cell lymphomas and other hematologic malignancies. Bisthianostat is a novel bisthiazole-based pan-HDACi evolved from natural HDACi largazole. Here, we report the preclinical study of bisthianostat alone and in combination with bortezomib in the treatment of multiple myeloma (MM), as well as preliminary first-in-human findings from an ongoing phase 1a study. Bisthianostat dose dependently induced acetylation of tubulin and H3 and increased PARP cleavage and apoptosis in RPMI-8226 cells. In RPMI-8226 and MM.1S cell xenograft mouse models, oral administration of bisthianostat (50, 75, 100 mg·kg-1·d-1, bid) for 18 days dose dependently inhibited tumor growth. Furthermore, bisthianostat in combination with bortezomib displayed synergistic antitumor effect against RPMI-8226 and MM.1S cell in vitro and in vivo. Preclinical pharmacokinetic study showed bisthianostat was quickly absorbed with moderate oral bioavailability (F% = 16.9%–35.5%). Bisthianostat tended to distribute in blood with Vss value of 0.31 L/kg. This distribution parameter might be beneficial to treat hematologic neoplasms such as MM with few side effects. In an ongoing phase 1a study, bisthianostat treatment was well tolerated and no grade 3/4 nonhematological adverse events (AEs) had occurred together with good pharmacokinetics profiles in eight patients with relapsed or refractory MM (R/R MM). The overall single-agent efficacy was modest, stable disease (SD) was identified in four (50%) patients at the end of first dosing cycle (day 28). These preliminary in-patient results suggest that bisthianostat is a promising HDACi drug with a comparable safety window in R/R MM, supporting for its further phase 1b clinical trial in combination with traditional MM therapies.

Keywords: multiple myeloma; HDAC inhibitor; bisthianostat; pharmacodynamics; pharmacokinetics; phase 1a clinical trial; antitumor drug

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