J2H Biotech announced on December 16 that its investigational treatment for metabolic dysfunction-associated steatohepatitis (MASH), 'J2H-1702', demonstrated simultaneous improvements in liver fat, liver enzymes, fibrosis, and metabolic markers in a Phase 2a clinical trial, proving its potential as a next-generation therapy.
This study, conducted by J2H Biotech at 11 medical institutions in Korea with 87 patients at risk of MASH, confirmed multi-pathology improvements within a short 12-week period using non-invasive imaging techniques. J2H-1702 is an oral small molecule compound with 11β-HSD1 inhibitory activity. Based on its liver-targeting properties, it exerts a complex mechanism that simultaneously regulates steatosis, metabolism, and fibrosis.
The study was designed as a randomized, double-blind, placebo-controlled trial, with patients divided into placebo, 50mg, 100mg, and 200mg dosing groups. Imaging assessments such as MRI-PDFF and MRE were performed alongside blood-based biomarker analyses. Clinical results showed that patients who received higher doses of J2H-1702 experienced greater improvements in liver fat and liver enzyme levels. Liver fat content measured by MRI-PDFF decreased in a dose-dependent and statistically significant manner compared to placebo. ALT, a key indicator of liver function, also showed statistically significant improvements in the two higher dose groups. AST showed an overall trend toward improvement.
Despite the short study duration, clear changes were observed in fibrosis markers. No patients in the placebo group experienced a reduction in liver stiffness of 30% or more from baseline as measured by MRE, whereas 10% of patients in the drug-treated groups did. The proportion of patients with a reduction of 15% or more in liver stiffness from baseline reached 45% in the drug-treated groups.
Blood biomarker tests also showed a consistent overall decrease in fibrosis markers such as Pro-C3, TIMP-1, PIIINP, HA, and ELF. Significant improvements were also confirmed in the high-dose group based on FibroScan-derived steatosis (CAP) and liver stiffness (VCTE) assessments. The detection of short-term improvement signals in fibrosis, which typically requires long-term treatment, strongly suggests the drug's potential anti-fibrotic effect.
Improvement signals were also observed in metabolic markers. LDL cholesterol (bad cholesterol) and total cholesterol (TC) decreased significantly compared to placebo in the 50mg low-dose group, with clear reductions observed at all doses. The 200mg group showed a trend toward increased HDL cholesterol (good cholesterol). Body weight and BMI decreased significantly in the 200mg group, and waist circumference was also reduced. Among patients with baseline HbA1c levels of 6.5% or higher, those in the high-dose group experienced a reduction in this marker. HOMA-IR, an indicator of insulin resistance, also consistently improved in the drug-treated groups, suggesting the drug's potential for direct metabolic regulation.
The safety profile of J2H-1702 was similar to that of placebo. No drug-related serious adverse events were reported during the 12-week period, and the overall incidence of adverse events was very low and mild. There were no imbalanced safety signals in any dosing group, indicating that a safety foundation for long-term clinical development has been established.
Kim Jaeseon, CEO of J2H Biotech, stated, "Based on these clinical results, we are preparing for a global Phase 2b trial targeting patients with moderate to severe MASH. In the next study, we plan to directly confirm fibrosis improvement through tissue biopsy. We are also exploring joint development and combination therapy possibilities with domestic and global pharmaceutical companies, and accelerating global development of the oral idiopathic pulmonary fibrosis (IPF) treatment J2H-2302."
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