P3, N=240, Completed, Ascletis Pharmaceuticals Co., Ltd. | Active, not recruiting --> Completed | Trial completion date: Mar 2026 --> Nov 2025

P1, N=30, Recruiting, Weill Medical College of Cornell University | Trial completion date: Nov 2026 --> Jan 2029 | Trial primary completion date: Nov 2025 --> Jan 2027

Using an AI-driven prediction model and in vitro/in vivo assays, fatty acid synthase inhibitor TVB-2640 is identified as a potential therapeutic agent for disrupting metabolic vulnerability and suppressing NSCLC BMs. These findings provide novel insights into NET-dependent cellular interactions that sustain the pro-metastatic microenvironment underlying NSCLC BMs, offering robust development of novel metabolism-based therapeutic strategies to combat this lethal complication.

Our study reveals a distinct lipid signature in gastric metaplasia characterized by TG and LD accumulation, providing novel therapeutic insights into targeting lipid metabolism to prevent GIM malignant transformation and reduce cancer risk.

P3, N=480, Completed, Huashan Hospital, Fudan University; Huashan Hospital, Fudan University

P1, N=40, Active, not recruiting, Sagimet Biosciences Inc.

While by far, several FAS inhibitors, including denifanstat and omeprazole, have demonstrated beneficial effects in clinical trials, no candidate has been approved by the FDA. We concluded here that targeting FAS is a feasible strategy to overcome chemoresistance, although more interdisciplinary efforts are needed to identify a potent, specific, and bioavailable FAS inhibitor for clinical applications.

Denifanstat (TVB-2640), the first-in-class selective FASN inhibitor with favorable pharmacokinetic properties, has demonstrated robust antitumor activity in preclinical models and encouraging results in early-phase clinical studies. Clinical evidence suggests that FASN blockade not only impairs tumor growth but also potentiates the efficacy of existing treatments, including chemotherapy and targeted agents, thereby supporting its integration into combination regimens. Future clinical optimization will require the identification of predictive biomarkers to guide patient selection and treatment stratification.

Our findings reveal that KAT2B suppresses de novo lipogenesis by interfering with HDAC5-LSD1 complex assembly, and highlight the potential of FASN inhibitors as a therapeutic strategy for RCC patients with low KAT2B expression.

P2, N=50, Recruiting, Wake Forest University Health Sciences | N=20 --> 50

Molecular docking and MD simulation studies with QNX-10 revealed the binding mode of the compound to the KR domain of FASN. Taken together, the study establishes compound QNX-10 to be a promising lead candidate for the development of anticancer therapeutics targeting the FASN enzyme.

P3, N=480, Completed, Ascletis Pharmaceuticals Co., Ltd. | Active, not recruiting --> Completed