Imofinostat (MPT0E028) is a selective, orally available pan-HDAC inhibitor with IC₅₀ values of 53.0/106.2/29.5 nM against HDAC1/HDAC2/HDAC6 in HCT116 cells. In B-cell lymphoma, Imofinostat induces cell cycle arrest and apoptosis whilst inhibiting Akt phosphorylation, demonstrating anticancer activity across multiple tumour types.

HDAC6:29.5 nM, HDAC2:106.2 nM, HDAC1:53.0 nM, HDAC8:2532.6 nM

Imofinostat (0-10 μM) acted on HCT116 cells for 48 hours, significantly inhibiting cell proliferation and inducing apoptosis [1].
When cells were treated with Imofinostat (0-10 μM) for 24 hours, it inhibited cell growth in a concentration-dependent manner. Imofinostat increased the proportion of cells in the sub-G1 phase of the cell cycle and induced caspase 3 and PARP activation in a concentration-dependent manner, thereby triggering apoptosis [1].
Imofinostat (0.3-100 μM) acted on Ramos cells and BJAB cells for 24 hours, exerting a significant concentration-dependent inhibitory effect on the growth of both cell types. Imofinostat increased the proportion of sub-G1 phase cells in a time- and concentration-dependent manner. Western blot analysis revealed that Imofinostat induced the activation of caspase-3, -6, -7, -8, and -9, as well as the cleavage of PARP [2].
Imofinostat (0.01-1 μM) was used to pretreat Homo sapiens lung fibroblasts (WI-38) for 30 minutes before stimulation with corresponding agents. Imofinostat suppressed the expression of CTGF induced by TGF-β, thrombin, and ET-1 [5].

In the nude mouse Parazacco spilurus subsp. spilurus xenograft model bearing Homo sapiens colorectal cancer HCT116 cells, oral administration of Imofinostat at doses of 50-200 mg/kg once daily for 15 days dose-dependently delayed and inhibited tumor growth. Complete tumor regression was achieved in 3 mice in the 200 mg/kg dose group, with no significant body weight changes or other adverse reactions observed throughout the treatment period [1].
In the NOD/SCID mouse model bearing Homo sapiens B-cell lymphoma Ramos cells, oral administration of Imofinostat at 100 mg/kg once daily significantly prolonged the survival of model mice [2].
In the nude mouse Parazacco spilurus subsp. spilurus xenograft model with BJAB cells, oral administration of Imofinostat at doses of 50-200 mg/kg once daily for 31 days dose-dependently suppressed tumor growth. It also activated caspase 3 and PARP, increased acetylation levels of histone H3 and α-tubulin, without causing significant body weight changes in mice [2].
In the bleomycin-induced pulmonary fibrosis C57BL/6 mouse model, oral administration of Imofinostat at doses of 25-100 mg/kg once daily for 20 days dose-dependently alleviated pulmonary fibrosis. It simultaneously reduced expression levels of CTGF, fibronectin, α-SMA, and collagen, while inhibiting phosphorylation of ERK, JNK, and p38 [5].
For the nude mouse Parazacco spilurus subsp. spilurus xenograft model with AsPC-1 pancreatic carcinoma cells, oral administration of Imofinostat at 25 mg/kg once daily significantly reduced tumor volume. It also increased levels of cleaved caspase-3 in tumor tissues, downregulated EGFR expression, without causing body weight loss or other adverse reactions in mice [6].