Exhibit 99.1

1. Dhindsa et al., Diabetes Care 2010; Guay et al., Int J Impotent Res 2010; Rector et al., Gastroenterol 2008 2. a) Kim et al., BMC Gastroenterol 2012; b) Sumida et al., Gastroenterol Hepatol 2015; c) Sinclair et al., Liver Trans 2016 3. Younossi et al., Hepatol 2016 4. Lazo et al, Am J Endocrinol 2013 5. Patel et al., Ther Adv Gastroenterol 2016 Hypogonadism is Associated with NAFLD: LPCN 1144 MRI - PDFF Clinical Results INTRODUCTION ▪ Male hypogonadism (Testosterone, T, level less than 300 ng/dL) is an underappreciated co - morbidity in NAFLD/NASH ▪ Significant overlap of co - morbidities for NAFLD/NASH and hypogonadism 1 ▪ Testosterone (T) deficiency in male patients is prevalent across the pathological spectrum of NAFLD 2 ▪ Serum levels of free T are inversely related with severity of lobular inflammation, ballooning, NAFLD activity, and fibrosis 2.b) ▪ LPCN 1144 is a lymphatically delivered well tolerated oral prodrug of bioidentical testosterone targeting treatment for NASH Kilyoung Kim 1 , Burke Byrne 1 , Jonathan Baker 1 , Nachiappan Chidambaram 1 , Mahesh V. Patel 1 , Arun Sanyal 2 , and Michael Charlton 3 1 Lipocine Inc., Salt Lake City, UT, USA; 2 Virginia Commonwealth University, VA, USA; 3 University of Chicago, IL, USA RESULTS ▪ Higher prevalence of NAFLD was observed in hypogonadal males relative to general population, even after BMI stratification ▪ Morbidly obese hypogonadal males are highly likely to have NAFLD ▪ Appreciable % of patients experienced resolution of NAFLD while on LPCN 1144 treatment ▪ Substantial reductions of liver fat were achieved with LPCN 1144 therapy as early as ~8 weeks ▪ Interim LPCN 1144 results strongly suggest further evaluation to validate a histopathologic benefit in NASH patients M ETHODS □ NAFLD is Over Represented in Hypogonadal Males CONCLUSION REFERENCES Contact info: Kilyoung Kim, kk@lipocine.com or admin@lipocine.com ▪ In a pioneering MRI - PDFF based Liver Fat Study (LFS) in hypogonadal males, the prevalence of fatty liver and the impact of LPCN 1144 therapy was assessed ▪ LFS is an open - label, multi - center single arm study (N=36) with LPCN 1144 225mg BID ▪ Baseline liver fat (LF) % distribution ▪ The metabolic syndrome attribute prevalence in LFS were: 81% obese, 58% hypertriglyceridemia, 33% hypertensive, and 19% type 2 diabetes □ Hypogonadism Increased NAFLD Prevalence in Obese Males □ Substantial Reductions in Liver Fat % in Obese Hypogonadal NAFLD Males* □ LPCN 1144 Reduced Both Absolute and Relative Liver Fat % Post 8 Week Treatment † NAFLD identified by MRI - PDFF ≥ 5% in LPCN 1144 Liver Fat Study (hypogonadal males) †† 28% was estimated from reported 25% for general population diagnosed as NAFLD by imaging hepatosteatosis ≥ 5% liver fat 3 by accounting for male ratio to female in NAFLD = 1.1 ▪ NAFLD subjects with at least 8% and 10% baseline liver fat were evaluated for change from baseline ▪ NAFLD resolution was assessed by % of subjects with LF ≥ 5% at baseline to < 5% at ~8 weeks * Subjects available for MRI - PDFF scan for the interim analysis (~8 week) * Patients with MRI - PDFF ≥ 10% at BL ▪ NAFLD was resolved in 28% of patients on LPCN 1144 treatment □ Higher the Baseline Liver Fat, Better Reduction with LPCN 1144 Treatment* * NAFLD: identified by Ultrasonography in US general male population 4 ; ** Identified by MRI - PDFF ≥ 5% in hypogonadal males □ Liver Fat Reduction Responder Rates Clinically meaningful Relationship of MRI - PDFF % Reduction with Histological Response in NASH 5 * Based on NAFLD patients identified with MRI - PDFF ≥ 5% at BL Exhibit 99.1