sorafenib

AntiHCC assay suggested 19 analogues showed better inhibitory activity than sorafenib on HepG2, SK-Hep-1, and Huh7 cells...In vivo, dimer 10 at 30 and 60 mg/kg inhibited tumor weight up to 64 % and 69 % without detectable toxicity, and IHC analysis confirmed in vivo target engagement. This study identified compound 10 as a potential antiHCC agent targeting CDK2, and warrants further investigation.

P2/3, N=87, Not yet recruiting, Nanfang Hospital, Southern Medical University

FAM83A promotes MASH pathogenesis by interacting with RAF1 to activate ERK signaling, thereby stimulating fatty acid and cholesterol biosynthesis. Targeting this axis may offer therapeutic potential for MASH and metabolic dyslipidemia.

OS can be accurately predicted in patients with HCC receiving sorafenib by combining certain radiomics features with clinical metadata, centered primarily on baseline characteristics.

Collectively, our findings underscore the pivotal role of Sh/TgE in modulating drug particle size within CSD matrices through distinct mechanisms. Furthermore, our study underscores the potential of P188-mediated CSD formulations in augmenting the dissolution rate and bioavailability of poorly soluble drugs by minimizing drug particle size and sustaining drug supersaturation, thereby enhancing the efficacy of sorafenib in treating liver cancer.

The combination of ANPEP silencing and sorafenib treatment showed a synergistic effect in inhibiting liver cancer progression. Finally, clinical data and mouse models demonstrated that chronic stress drove liver tumor progression via ANPEP-regulated SLC3A2. These findings reveal unanticipated communication between chronic stress and metabolic reprogramming during liver cancer progression, providing potential therapeutic implications for liver cancer.

Subsequently, multiple hepatic metastases and pelvic dissemination developed, and conventional chemotherapy including bevacizumab was ineffective...Switching to sorafenib led to further progression, but reintroduction of LVB reduced Tg levels...The patient has survived seven years since recurrence, including six years on LVB. The tumor behaved similarly to poorly differentiated thyroid carcinoma, with Tg levels reflecting disease activity and LVB demonstrating the potential for long-term tumor control.

These results challenge the assumption that all VEGFR-targeting TKIs are equivalent post-ICI and suggest lenvatinib may be superior to sorafenib following anti-VEGF-based immunotherapy. While prospective randomised trials are still needed, these real-world data offer valuable guidance for clinicians and help refine treatment sequencing in advanced HCC.

Our findings suggest that ZnS inhibits autophagy, promotes ferroptosis, and enhances sensitivity to sorafenib in HCC cells through the lncRNA TCONS-00026762/AKR1C1 axis.

TKIs reduce stiffness and malignancy in HCC. MRE is a promising tool for early treatment response evaluation.

However, compound 4f displayed a unique antiproliferative potency on HepG2 cells (7.9 µM) and a promising cytotoxicity in MCF-7 (13.5 µM), compared to sorafenib with IC50 values of 2.1 and 2.3 µM against MCF-7 and HepG-2 cancer cells. Compound 4f treatment induced total apoptosis in the HepG2 cancer cells by 36.3-fold, arresting the cell proliferation at the G1-phase by 83.4%. Accordingly, compounds 4l and 4f exhibited target-oriented chemotherapeutic activity against liver cancer.

During maintenance therapy with sorafenib combined with ITI, median relapse-free survival (mRFS) was also not reached, with 12- and 24-month RFS rates of 73.7% (14/19) and 57.9% (11/19), respectively. The sorafenib combined with ITI regimen is an effective maintenance therapy for FLT3-ITD (+) AML, significantly reducing relapse risk and prolonging survival.