TLC-1180 protonophore program
phase 1drug program · high · Mon Oct 20 2025 00:00:00 GMT+0000 (Coordinated Universal Time)
Evaluate TLC-1180 for obesity and metabolic disease, including weight loss with preservation of lean mass when combined with semaglutide.
Small-molecule protonophore; Phase 1 single- and multiple-ascending-dose trial in healthy subjects assessing safety, tolerability, pharmacokinetics, and pharmacodynamics.
Phase 1 clinical trial record published for single and multiple doses in healthy subjects.
A 2025 publication title reports that TLC-1180 with semaglutide enhanced weight loss and preserved lean mass in DIO mice.
TLC-2716 LXR inverse agonist program
phase 2drug program · high · Mon Aug 12 2024 00:00:00 GMT+0000 (Coordinated Universal Time)
Treat hypertriglyceridemia, dyslipidemia, NAFLD/MASH-related metabolic disease, and residual atherosclerotic cardiovascular disease risk by reducing triglyceride-rich lipoproteins and liver steatosis.
Oral gut- and liver-restricted LXR inverse agonist; Phase 1 trial in healthy participants and Phase 2a randomized, double-blind, placebo-controlled trial in subjects with hypertriglyceridemia and NAFLD.
Phase 2a study evaluating two dose levels in subjects with hypertriglyceridemia and NAFLD.
Phase 1 14-day treatment was well tolerated and produced placebo-adjusted reductions up to 38.5% in plasma triglycerides and 61% in postprandial remnant cholesterol; human liver organoids showed reduced lipid accumulation and suppressed inflammatory and fibrotic gene expression.
TLC-6740 obesity and diabetes program
phase 1drug program · medium · Sat Apr 22 2023 00:00:00 GMT+0000 (Coordinated Universal Time)
Evaluate TLC-6740 in healthy subjects and in subjects with obesity, with or without type 2 diabetes mellitus.
Phase 1/1b study with single- and multiple-ascending doses in healthy subjects, followed by assessment of safety, tolerability, and pharmacokinetics in subjects with obesity with or without diabetes.
Phase 1/1b clinical trial record published.
TLC-3595 ACC2 inhibitor program
phase 2drug program · medium · Wed Mar 08 2023 00:00:00 GMT+0000 (Coordinated Universal Time)
Improve insulin resistance and support treatment of disorders associated with impaired fatty acid oxidation, including severe heart failure models with cardiac lipid accumulation.
Oral selective small-molecule ACC2 inhibitor; Phase 2a trial in participants with insulin resistance and preclinical pharmacological inhibition in murine ATGL knockout severe heart failure model.
Phase 2a clinical study evaluating daily oral doses in participants with insulin resistance.
In ATGL knockout mice, TLC-3595 promoted mitochondrial fatty acid oxidation, reduced cardiac lipid accumulation and remodeling, and improved cardiac function, locomotor activity, and survival.
ACMSD inhibition for MASLD/MASH
preclinicalresearch program · medium
Enhance hepatic de novo NAD+ synthesis to treat MASLD/MASH by reducing fibrosis, inflammation, and DNA damage.
Pharmacological inhibition of ACMSD tested in primary rodent hepatocytes, Huh7 cells, induced pluripotent stem cell-derived human liver organoids, and mouse MASLD/MASH models.
Preclinical Journal of Hepatology publication reporting ACMSD inhibition effects in mouse and human liver organoid steatohepatitis models.
ACMSD inhibition increased liver NAD+, enhanced mitochondrial respiration, reduced DNA damage, and reversed MASLD/MASH features including fibrosis and inflammation in preclinical models.
Human liver organoid metabolic liver disease research
exploratoryresearch program · medium
Define the genetic basis of metabolic liver disease and support tailored therapeutic development using human liver organoids.
En masse human liver organoid study; OrsoBio team members collaborated with Professor Takebe on the Cell study.
Cell publication highlighted on OrsoBio site and linked as a PDF.
The supplied material describes the study as the first use of en masse human liver organoids to define the genetic basis of metabolic liver disease and potential for tailored therapeutic development.