07-05-2025
Bluejay Therapeutics Reports First Preclinical Data for Liver-Targeted Fatty Acid Synthase (FASN) Inhibitor BJT-188 Being Investigated for the Treatment of Metabolic Dysfunction-Associated Steatohepat
Bluejay Therapeutics
BJT-188 demonstrated liver-specific potency with minimal exposure to other tissues
The data are being presented at the European Association for the Study of the Liver (EASL) Congress 2025
REDWOOD CITY, Calif., May 07, 2025 (GLOBE NEWSWIRE) -- Bluejay Therapeutics, a clinical-stage biopharmaceutical company dedicated to developing potentially life-changing therapeutics for serious viral and liver diseases, today announced preclinical data on BJT-188, a liver-targeted fatty acid synthase (FASN) inhibitor being investigated for the treatment of metabolic dysfunction-associated steatohepatitis (MASH). BJT-188 demonstrated potent FASN inhibition in preclinical models, with reduced systemic exposure that may help minimize toxicities. BJT-188 is a product of Bluejay Therapeutics' Liver-Targeting Advanced Platform (L-TAP) that integrates molecular modeling and drug design to create novel therapeutics with optimized liver-targeted distribution profiles.
The data are being presented in a poster at the European Association for the Study of the Liver (EASL) Congress 2025. The poster is also available on Bluejay's website.
"MASH represents a serious and growing global health challenge,' said Hassan Javanbakht, Ph.D., Chief Scientific Officer of Bluejay Therapeutics. 'While FASN inhibitors offer therapeutic potential, many have been limited by systemic side effects. Our preclinical data suggest that BJT-188 may potentially overcome these challenges by reducing systemic exposure while maintaining therapeutic efficacy in the liver. We are now moving the program into IND-enabling studies."
Preclinical Characterization of BJT-188
This study evaluated the intrinsic potency of BJT-188 versus denifanstat, an investigational FASN inhibitor, by measuring in vitro inhibition of de novo lipogenesis (DNL) in primary rat, mouse and human hepatocytes. BJT-188 inhibited DNL in primary human hepatocytes with an EC₅₀ of 20.4 ± 9.9 nM and demonstrated comparable potency in rat and mouse hepatocytes.
In vivo, a single oral dose of BJT-188 in rats demonstrated rapid and preferential accumulation in the liver, with similar liver targeting observed in mice. Liver-to-plasma and liver-to-skin ratios were significantly more favorable for BJT-188 compared to denifanstat. The minimal exposure to skin and other peripheral tissues suggests a lower risk of alopecia, a side effect reported with denifanstat.
Additionally, in an in vivo rat study, BJT-188 inhibited palmitate formation in a dose-dependent manner, reaching up to 98% inhibition of DNL at the highest dose tested (60 mg/kg). Palmitate is the primary fatty acid produced during DNL.
