18f - fac | Probe

Probes Breakthrough PET Probes

The [18F]FAC family of compounds are a breakthrough class of novel PET imaging probes that provide in vivo diagnostic assays to researchers and clinicians in the fields of oncology and immunology.

Why [18F]FAC?

  • Personalized medicine should be personal.
    PET imaging has seen dramatic and continued growth over the last 20 years, because it’s a powerful tool to examine specific biochemical, biological, and pharmaceutical processes non–invasively with high sensitivity, and without any significant mass effects due to administration of probes in trace amounts. We think it’s the key to accurate diagnosis and treatment management in the future, which means the PET probes used to examine the biology of disease shouldn’t be one-size-fits-all. We believe that novel probes that show real promise, like the [18F]FAC family of compounds and others, should get out of mice and into people, where they can do the real work to improve the quality of life.
  • The DNA salvage pathway is important.
    The DNA salvage pathway is involved in the production and maintenance of a balanced pool of deoxyribonucleoside triphosphates (dNTPs) for DNA synthesis. This pathway includes its rate limiting enzyme deoxycytidine kinase (dCK), for which SOFIE has a family of probes that are substrates for dCK. Intracellular dNTP pools reflect a balance between dNTP synthesis and degradation. This balance is tightly regulated in normal cells: insufficient amounts of dNTPs impair cell division and DNA repair; excess dNTPs or imbalances between the four dNTPs have genotoxic effects. Mammalian cells rely on two major pathways to produce and balance their intracellular dNTP pools: a) the de novo pathway that produces deoxynucleotides (dNs( from glucose and amino acids and b) the salvage pathway that recycles dNs from the extracellular milieu. In the cytosol, dCK phosphorylates these recycled dNs. Highly expressed in hematopoietic/lymphoid cells, in a subpopulation of lymphoid malignancies, and in a subpopulation of some solid tumors, dCK is essential for cancer nucleoside prodrugs such as Cytarabine and Gemcitabine, which require phosphorylation by dCK to become pharmacologically active in blocking malignant DNA replication and cell proliferation. [18F]FAC provides an in vivo assay of dCK enzyme activity.
  • It discovers new cancer therapeutics.
    Compared with conventional methods for examining pharmacological inhibition in vivo, PET provides quantitative, whole body readouts of target inhibition or availability by drugs. Researchers at UCLA used [18F]FAC for PET guided development of novel small molecule inhibitors of dCK. [18F]FAC enabled the screening of a library of Triangle-developed compounds to assess their capability to inhibit dCK in tumors vs. normal tissue and to use [18F]FAC to determine optimal drug dosing schedules. As a result, when combined with de novo pathway inhibition, the lead dCK inhibitors show dramatic efficacy against Acute Lymphoblastic Leukemia (ALL) xenografts, with negligible host toxicity. Researchers at UCLA are working to advance dCK inhibitors to the clinic where [18F]FAC will serve as a biomarker for target inhibition in patients.


UCLA is currently conducting a Phase I clinical trial to determine the accuracy of the in vivo assay of dCK enzyme activity with [18F]FAC PET by comparing results to the in vitro assay of dCK from resected tumor samples from patients with pancreatic, ovarian, and other cancers. For more information on referencing INDs, patient enrollment, and incorporating [18F]FAC into your clinical or preclinical research, please contact us.


  • [18F]FAC PET is under investigation for:
  • Treatment stratification – predicting patient response to nucleoside prodrugs
  • Determining dose schedules with nucleoside prodrugs


  • [18F]FAC PET is under investigation for:
  • Measuring immune response in drug discovery and development
  • Investigating and predicting efficacy of immunotherapies
  • Monitoring transplant rejection and graft–versus–host–disease
  • Diagnosis and staging of auto–immune disorders