K. KIM 1 ; B. J. BRUNO 1 ; K. PAPANGKORN 1 ; N. CHIDAMBARAM 1 ; M. V. PATEL 1 ; A. DELCONTE 2 ; M. CHARLTON 3 ; M. E. RINELLA 4 ; A. J. SANYAL 5 1 Lipocine Inc., Salt Lake City, UT, USA; 2 Saint Joseph’s University, Philadelphia, PA, USA; 3 University of Chicago Medicine, Hepatolo gy , Chicago, IL, USA; 4 Northwestern Medicine Digestive Health Center, Hepatology, Chicago, IL, USA; 5 Virginia Commonwealth University, Internal Med ici ne, Richmond, VA, USA Oral LPCN 1144 treatment significantly reduced liver fat and key liver injury markers in biopsy confirmed NASH subjects: a phase 2 randomized controlled study ( LiFT ) ADD YOUR LOGOS HERE INTRODUCTION • Non - alcoholic Steatohepatitis (NASH) is a common liver disease and NASH cirrhosis is predicted to be the most common etiology for liver transplantation. • In large cross - sectional studies, low testosterone (T) levels are independently predictive of fatty liver. 1,2 • Hepatic steatosis (assessed by MRI - PDFF) together with serum transaminase levels, specifically alanine aminotransferase (ALT) and aspartate aminotransferase (AST), may be predictive of liver histopathology in NASH subjects. • LPCN 1144 is an oral prodrug of endogenous Testosterone (T) under development for treatment of noncirrhotic NASH. • Therapy with tocopherol has been previously shown to improve biochemical (ALT) and histological features of NASH albeit in a non - diabetic population. 3,4 • Currently, LPCN 1144 is being investigated for safety and efficacy in a 36 - week randomized, double - blind, paired biopsy, placebo - controlled phase 2 LiFT ("Liver Fat intervention with oral Testosterone") study (NCT04134091). CONCLUSIONS ▪ 12 - week treatment with LPCN 1144 significantly improved non - invasive markers of liver health in male patients with biopsy confirmed NASH with fibrosis. ▪ LPCN 1144’s treatment potential for NASH resolution and/or fibrosis improvement is under evaluation in the ongoing LiFT trial. RESULTS METHOD • A Phase 2, randomized double - blind, placebo - controlled, multi - center study with oral LPCN 1144 in subjects with NASH for 36 weeks (N=56) • Randomization (1:1:1) x Treatment A: 142 mg eq. T twice daily (n=18) x Treatment B: 142 mg eq. T with tocopherol twice daily (n=19) x Placebo twice daily (n=19) • Key endpoints: x Primary: Change in hepatic fat fraction via MRI - PDFF (W12) x Change in key liver injury markers (W12) x Change in body composition via DEXA (W20) x Change in NASH activity and fibrosis via liver biopsy scoring (W36) AIM To present the topline liver fat and key liver injury marker results post 12 weeks of treatment. REFERENCES 1 Kim et al . A low level of serum total testosterone is independently associated with nonalcoholic fatty liver disease. BMC Gastroenterol 2012, 12:69 2 Albhaisi et al . LPCN 1144 resolves NAFLD in hypogonadal males. Hepatol Commun 2020, 4(10):1430 - 1440 3 Sanyal et al . Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med 2010, 362(18):1675 - 85 4 Hoofnagle et al . Vitamin E and changes in serum alanine aminotransferase levels in patients with non - alcoholic steatohepatitis. Aliment Pharmacol Ther 2013, 38(2):134 - 143 □ Demographics and Baseline Characteristics □ Absolute Changes in Liver Fat (MRI - PDFF) CONTACT INFORMATION Kilyoung Kim, PhD. kk@lipocine.com or admin@lipocine.com † Two missing data at week 12 (one in placebo and one in treatment A) were multiple - imputed ‡ Among subjects with baseline liver fat ≥ 5% * p < 0.05, ** p < 0.01, *** p < 0.001 vs placebo; ns = not significant between treatment A and B LPCN 1144 treatments significantly reduced liver fat (% of MRI - PDFF) regardless of hypogonadal status (T < 300 ng/dL) in biopsy - confirmed NASH male subjects □ Absolute Changes in Key Liver Injury Markers LPCN 1144 treatments significantly reduced key liver injury markers (ALT and AST) regardless of hypogonadal status (T < 300 ng/dL) in biopsy - confirmed NASH male subjects † All Subjects: Placebo n=17, Treatment A n=16, Treatment B n=19 ‡ Eugonadal subjects (T ≥ 300 ng/dL): Placebo n=11, Treatment A n=8, Treatment B n=7 □ Summary Both LPCN 1144 treatment arms met the primary endpoint with statistical significance * DEXA: Dual energy X - ray absorptiometry ** OLE: Open label extension study for additional 36 weeks Parameter Placebo Treatment A Treatment B Randomized Subjects (N) 19 18 19 Completed WK 12 (N) 18 18 19 Age (years) 53.6 51.3 53.4 BMI (kg/m 2 ) 37.3 36.9 34.5 Diabetes (%) 52.6 72.2 57.9 Hypertension (%) 68.4 66.7 57.9 Hepatic Fat Fraction (%) 20.1 16.7 20.9 ALT (U/L) 49.0 53.9 51.5 AST (U/L) 35.4 32.4 31.9 □ Relative Changes in Liver Fat and Responder Rate * p < 0.05, ** p < 0.01, *** p < 0.001 vs placebo; ns = not significant between treatment A and B † Two missing data at week 12 (one in placebo and one in treatment A) were multiple - imputed ‡ Based on subjects with baseline liver fat ≥ 5% without imputation of two missing MRI - PDFF data at week 12 Greater than 70% of subjects had responded to LPCN 1144 treatments at week - 12 from baseline, showing significant improvement in liver fat compared to placebo □ Longitudinal Changes in Key Liver Injury Markers * p < 0.05, ** p < 0.01, *** p < 0.001 vs placebo; † p < 0.05, †† p < 0.01 vs Treatment A Continued reduction in ALT and AST was observed in LPCN 1144 treatments □ Concurrent Reduction of Liver Fat and Liver Injury Markers 68% of subjects on treatment B showed concurrent reductions in liver fat, ALT, and AST Exhibit 99.2