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FCF Funded Projects

AI-Driven Deorphanization of SLC16A14

Icahn School of Medicine at Mount Sinai

2026 | Active

Goal: Uncover the function of SLC16A14, a protein uniquely expressed in fibrolamellar carcinoma (FLC) and absent from normal tissues and other cancers

Principal Investigator: Avner Schlessinger, PhD

Grant length: One year

Study overview: Prior FCF-funded research demonstrated that the transporter protein, SLC16A14, is essential for FLC cell survival and appears to be regulated by FLC’s DNAJ-PKAc fusion protein, making it an attractive therapeutic target. However, the molecule(s) transported by SLC16A14 remain unknown, classifying it as an “orphan” transporter.

Dr. Schlessinger’s team will use advanced artificial intelligence, structural modeling, and computational biology approaches to predict the three-dimensional structure of SLC16A14, identify substrate-binding sites, and determine the molecule(s) transported. The investigators will also conduct virtual screening of metabolites, prescription drugs, and chemical libraries to identify compounds that may inhibit SLC16A14 function.

Successful completion of the project will:

  • Identify the substrate(s) transported by SLC16A14, providing critical insight into its biological role in FLC.
  • Identify chemical tool compounds and inhibitors that could disrupt SLC16A14 function.
  • Establish a foundation for future therapeutic development targeting this FLC-specific protein.