Form 8-K Lipocine Inc. For: Jun 23
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UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
WASHINGTON, D.C. 20549
FORM 8-K
CURRENT REPORT
Pursuant to Section 13 or 15(d) of
The Securities Exchange Act of 1934
Date of Report (Date of Earliest Event Reported):
June 23, 2021
LIPOCINE INC.
(Exact name of registrant as specified in its charter)
Commission File No. 001-36357
| Delaware | 99-0370688 |
| (State or other jurisdiction of incorporation) | (IRS Employer Identification Number) |
675 Arapeen Drive, Suite 202
Salt Lake City, Utah 84108
(Address of principal executive offices) (Zip Code)
Registrant’s telephone number, including area code: (801) 994-7383
Former name or former address, if changed since last report: Not Applicable
______________________
Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:
| ¨ | Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425) |
| ¨ | Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12) |
| ¨ | Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b)) |
| ¨ | Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c)) |
Securities registered pursuant to Section 12(b) of the Act:
| Title of each class | Trading Symbol(s) | Name of each exchange on which registered |
| Common Stock, par value $0.0001 per share | LPCN | The NASDAQ Stock Market LLC |
Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (17 CFR § 230.405) or Rule 12b-2 of the Securities Exchange Act of 1934 (17 CFR § 240.12b-2).
Emerging growth company ¨
If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ¨
| Item 8.01 | Other Events |
On June 23, 2021, the Company issued a press release announcing presentations at The International Liver Congress™ 2021 Digital Event being held June 23-26, 2021. The press release is filed as Exhibit 99.1 and is incorporated herein by reference.
Additionally, the Company is presenting data at The International Liver Congress™ 2021, the annual meeting of the European Association for the Study of the Liver (“EASL”), Digital Event, on June 23-26, 2021. The Company’s materials to be included are filed as Exhibits 99.2, 99.3, 99.4 and 99.5.
| Item 9.01 | Financial Statements and Exhibits. |
| (d) | Exhibits |
The following exhibits are filed with this report:
SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
| LIPOCINE INC. | ||||
| Date: | June 23, 2021 | By: | /s/ Mahesh V. Patel | |
| Mahesh V. Patel | ||||
| President and Chief Executive Officer | ||||
Exhibit 99.1
Lipocine Announces Presentations at The International Liver Congress™ 2021 Digital Event
SALT LAKE CITY, June 23, 2021-- Lipocine Inc. (Nasdaq: LPCN), a clinical-stage biopharmaceutical company focused on metabolic and endocrine disorders, today announced that clinical data will be presented at The International Liver Congress™ 2021, the annual meeting of the European Association for the Study of the Liver (“EASL”), Digital Event, on June 23-26, 2021.
| 1. | Title: Oral LPCN 1144 treatment significantly reduced liver fat and key liver injury markers in biopsy confirmed NASH subjects:
Results of a Phase 2 randomized controlled study Low Testosterone in Males may Warrant Liver Health Assessment Intervention Session Type: Poster Session Category: NAFLD: Therapy |
Date: June 23, 2021 8:00 a.m. E.T. to 6:00 p.m. E.T
ePoster Session: June 25, 2021 11:30 a.m. E.T.
| 2. | Title: High prevalence of low normal or overtly hypogonadal levels of testosterone observed in histologically established NASH
subjects in LiFT Study Session Type: Poster Session Category: NAFLD: Therapy |
Date: June 23, 2021 8:00 a.m. E.T. to 6:00 p.m. E.T
| 3. | Title: LPCN 1144 improves body composition in biopsy-confirmed NASH patients Session Type: Poster Session Category: Late Breaker: General Hepatology |
Date: June 23, 2021 8:00 a.m. E.T. to 6:00 p.m. E.T
About Lipocine
Lipocine Inc. is a clinical-stage biopharmaceutical company focused on metabolic
and endocrine disorders using its proprietary drug delivery technologies. Lipocine's clinical development pipeline includes: TLANDO,
LPCN 1144, TLANDO XR, LPCN 1148, LPCN 1154 and LPCN 1107. TLANDO, a novel oral prodrug of testosterone containing testosterone undecanoate,
has received tentative approval from the FDA for conditions associated with a deficiency of endogenous testosterone, also known as hypogonadism,
in adult males. LPCN 1144, an oral prodrug of bioidentical testosterone, recently completed a proof-of-concept clinical study demonstrating
the potential utility in the treatment of non-cirrhotic NASH. LPCN 1144 is currently being studied in a Phase 2 clinical study.
TLANDO XR, a novel oral prodrug of testosterone, originated and is being developed by Lipocine as a next-generation oral testosterone
product with potential for once-daily dosing. In a phase 2 clinical evaluation when administered as once daily or twice daily TLANDO
XR met the typical primary and secondary end points. LPCN 1148 is an oral prodrug of bioidentical testosterone targeted for the treatment
of cirrhosis. LPCN 1154 is an oral neurosteriod targeted for the treatment of depressive disorders. LPCN 1107 is potentially the first
oral hydroxyprogesterone caproate product candidate indicated for the prevention of recurrent preterm birth and has been granted orphan
drug designation by the FDA. For more information, please visit www.lipocine.com.
Forward-Looking Statements
This release contains "forward-looking statements" that are made pursuant to the safe harbor provisions of the Private
Securities Litigation Reform Act of 1995 and include statements that are not historical facts regarding Lipocine's product candidates
and related clinical trials, the timing of completion of clinical trials and studies, the availability of additional data, outcomes of
clinical trials of our product candidates, the potential uses and benefits of our product candidates, and our product development efforts.
Investors are cautioned that all such forward-looking statements involve risks and uncertainties, including, without limitation, the
risk that the FDA will not approve any of our products, risks related to our products, expected product benefits not being realized,
clinical and regulatory expectations and plans not being realized, new regulatory developments and requirements, risks related to the
FDA approval process including the receipt of regulatory approvals, the results and timing of clinical trials, patient acceptance of
Lipocine's products, the manufacturing and commercialization of Lipocine's products, and other risks detailed in Lipocine's filings with
the SEC, including, without limitation, its Form 10-K and other reports on Forms 8-K and 10-Q, all of which can be obtained on the SEC
website at www.sec.gov. Lipocine assumes no obligation to update or revise publicly any forward-looking statements
contained in this release, except as required by law.
Contact:
Morgan Brown
Executive Vice President & Chief Financial Officer
Phone: (801) 994-7383
Investors:
Hans Vitzthum
Phone: (617) 535-7743
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. [email protected] or [email protected] † 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
EASL 2021 Jun 23 – 26, 2021 Oral LPCN 1144 treatment significantly reduced liver fat and key liver injury markers in biopsy confirmed NASH subjects: a Phase 2 randomized controlled study Presenter: Kilyoung Kim, PhD Exhibit 99.3
Background & Aim • Non - alcoholic steatohepatitis (NASH) is a common cause of liver disease and is on a trajectory to become the most common indication for liver transplantation in Western Europe and the United States. • In large multi - ethnic cross - sectional studies, low testosterone (T) levels are independently predictive of fatty liver. (1,2) • Hepatic steatosis (measured by MRI - PDFF), together with serum transaminase levels, specifically alanine aminotransferase (ALT) and aspartate aminotransferase (AST), are predictive of liver pathology and histology in NASH subjects. • LPCN 1144 is an oral prodrug of endogenous Testosterone (T) under development for treatment of noncirrhotic NASH. – Therapy with vitamin E has previously been 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). • Here, we present the topline liver fat and key liver injury marker results post 12 weeks of treatment. 2 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
Methods 3 LiFT ( Li ver F at intervention with oral T estosterone)* (NCT04134091) * DEXA: Dual energy X - ray absorptiometry for measuring body composition ** OLE: Open Label Extension Study Study Design □ 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) ▪ Treatment A: 142 mg eq. T twice daily (n=18) ▪ Treatment B: 142 mg eq. T with tocopherol twice daily (n=19) ▪ Placebo twice daily (n=19) Key Endpoints: • Primary: Change in hepatic fat fraction via MRI - PDFF (W12) • Change in key liver injury markers (W12) • Change in body composition via DEXA (W20) • Change in NASH activity and fibrosis via liver biopsy scoring (W36) 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 (%) 20.06 16.73 20.87 ALT (U/L) 49.0 53.9 51.5 AST (U/L) 35.4 32.4 31.9
Results: Changes in Liver Fat and Key Liver Injury Markers at Week 12 from Baseline 4 Both LPCN 1144 treatment a rms reduced liver fat, ALT, and AST with statistical s ignificance † 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; † p < 0.05, †† p < 0.01, ns = not significant between treatment A and B < Changes in Liver Fat > < Changes in Key Liver Injury Markers >
Conclusions 5 LPCN 1144 treatment significantly improved the key non - invasive markers of liver health in male patients with biopsy confirmed NASH with fibrosis. Leveraging the largest, multi - modal proprietary clinical database of its kind to expand a robust pipeline of predictive algorithms with regulatory grade evidence. Developing novel transformative algorithms to transform healthcare. Commercially validated across 3 business models Experienced team Statistically significant reduction in liver fat was observed compared to placebo independent of hypogonadal status Statistically significant reduction in markers of liver injury were observed compared to placebo independent of hypogonadal status 68% on Treatment B had concurrent reductions of liver fat, ALT, and AST Adverse events in both the treatment arms were comparable to the placebo arm 01 02 03 04
B. J. BRUNO 1 ; K. PAPANGKORN 1 ; K. KIM 1 ; N. CHIDAMBARAM 1 ; M. V. PATEL 1 ; A. DELCONTE 2 ; A. J. SANYAL 3 1 Lipocine Inc., Salt Lake City, UT, USA 2 Saint Joseph’s University, Philadelphia, PA, USA 3 Virginia Commonwealth University, Richmond, VA, USA High Prevalence of Low Normal or Overtly Hypogonadal Levels of Testosterone Observed in Histologically Established NASH Subjects in LiFT Study INTRODUCTION • Nonalcoholic Steatohepatitis (NASH) is an advanced state of non - alcoholic fatty liver disease (“NAFLD”) and can progress to fibrotic or cirrhotic liver or result in hepatocellular carcinoma/liver cancer. • NASH prevalence is increasing; total disease burden is estimated to reach 27 million people by 2030. 1 • There is no FDA approved drug for NAFLD/NASH. • A study of liver disease in men undergoing androgen deprivation therapy (ADT) reported patients on ADT were significantly more likely to develop NAFLD. 2 • A previous single - arm study revealed that NAFL is highly prevalent in hypogonadal males (~66%). 3 • Furthermore, there is significant overlap in co - morbidities associated with NASH and hypogonadism in adult males. 4 - 7 • Currently, LPCN 1144 is being investigated for safety and efficacy in the phase 2 LiFT ("Liver Fat intervention with oral Testosterone") study (NCT04134091) CONCLUSIONS ▪ Men with hypogonadism have high rates of fatty liver in the LiFT study population ▪ The LiFT study demonstrates a high prevalence hypogonadism and low - normal levels of T in patients with suspected or biopsy - established NASH. ▪ Hypogonadism may be common even in the early stages of liver disease ▪ Men in the LiFT study with steatosis and/or inflammation on liver biopsy have lower levels of testosterone ▪ Male adult NASH patients may have compromised androgen signaling with possible associated symptoms of androgen deficiency such as sarcopenia, skeletal fragility, sexual/mood disorder, and/or anemia. ▪ The effect of oral T therapy on NASH is under investigation in the ongoing LiFT study. RESULTS METHODS ▪ A Phase 2, randomized double - blind, placebo - controlled, multi - center, 36 - week study (LiFT) with oral LPCN 1144 in male NASH subjects (N=56) ▪ 181 subjects underwent biopsy and had serum T concentration measured or a history of hypogonadism ▪ 56 biopsy - confirmed NASH subjects were randomized ▪ All available baseline data was analyzed to identify the prevalence of hypogonadism and/or low T levels (using LC - MS/MS). ▪ Definitions: • Hypogonadism: Baseline T < 300 ng/dL, or historical diagnosis of hypogonadism • Subjects with a historical diagnosis of hypogonadism did not have T measured in screening • Low - normal testosterone: < 400 ng/dL • Fatty liver: ≥ 5% liver fat on MRI - PDFF • Suspected NASH: Subjects were eligible for biopsy based on liver stiffness by transient elastography, elevated liver injury markers, and/or medical history AIM To investigate the prevalence of hypogonadism and low testosterone (T) levels at baseline for the LiFT study. REFERENCES 1 Estes et al. Modeling the Epidemic of Nonalcoholic Fatty Liver Disease Demonstrates an Exponential Increase in Burden of Disease. Hepatol 2018, 67:123 - 133 2 Gild et al. Liver Disease in Men Undergoing Androgen Deprivation Therapy for Prostate Cancer. J Urol 2018, 200:573 - 581 3 Albhaisi et al. LPCN 1144 resolves NAFLD in hypogonadal males. Hepatol Commun 2020, 4(10):1430 - 1440 4 Rector et al. Non - alcoholic fatty liver disease and the metabolic syndrome: An update. World J Gastroenterol 2008, 14(2): 185 - 192 5 Guay et al. Hypogonadism in men with erectile dysfunction may be related to a host of chronic illnesses. Int J Impotence Res 2010, 22: 9 - 19 6 Kim et al. Male hypogoandsim and liver disease. Contemp Endocrinol 2017, pp. 219 - 234 7 Sarkar et al. Low Testosterone Is Associated With Nonalcoholic Steatohepatitis and Fibrosis Severity in Men. Clin Gastroenterol Hepatol 2021, 19:400 - 402 □ Prevalence of Fatty Liver in Hypogonadism or Vice - Versa All Subjects (N=56) Placebo (n=19) All Subjects (N=56) Placebo (n=19) Treatment A (n=18) Treatment B (n=19) Treatment A (n=18) Treatment B (n=19) CONTACT INFORMATION Benjamin J. Bruno, PharmD, PhD. [email protected] or [email protected] □ Prevalence of Hypogonadism in Biopsied Subjects Healthy: No fibrosis and NAS = 0; 1 point: either fibrosis 1 or NAS = 1; 2+ points: Fibrosis + NAS is ≥ 2 □ Prevalence of low - normal T (< 400 ng/dL) 78% 73% 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100% All biopsied subjects with T measured (suspected NASH) Randomized (biopsy-established NASH) % of Subjects □ T levels are lower in subjects with NAS >1 □ T levels are lower in subjects with inflammation or steatosis but not ballooning 472 465 309 40% 50% 71% 0% 10% 20% 30% 40% 50% 60% 70% 80% 0 100 200 300 400 500 600 700 % Hypogonadal Testosterone (ng/dL) T % Hypogonadal p = 0.002 p = 0.025 90% 57% 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100% Hypogonadal men: % with fatty liver Fatty liver men: % with hypogonadism % of Subjects 87 97 87 152 n = 3 5 7 12 124 164 n = 10 51 39 34 p = 0.004 p = 0.002 p = 0.042 n = 6 91 37 104 134 41 56 p < 0.001 n = 11 n = 30 n = 24 n = 69 p < 0.001 p < 0.001 NAS 0 - 1 NAS 2 NAS 3 NAS 4+ Grade 0 1 2 n = 69 44 21 p = NS Grade 0 1 2 3 Grade 0 1 2 p = 0.009 p < 0.001 Exhibit 99.4
S. MEHRABAN 1 , B. J. BRUNO 1 , K. KIM 1 , K. PAPANGKORN 1 , N. CHIDAMBARAM 1 , M. V. PATEL 1 , A. DELCONTE 2 1 Lipocine Inc., Salt Lake City, UT, USA 2 Saint Joseph’s University, Philadelphia, PA, USA LPCN 1144 improves body composition in biopsy - confirmed NASH patients INTRODUCTION • Non - alcoholic Steatohepatitis (NASH) is a common cause of liver disease and rapidly rising to be the leading etiology for liver transplantation (1) • Sarcopenia, loss of muscle mass, occurs in 20 - 60% of patients with liver disease and reduces survival of cirrhotic patients (2) • There is an unmet need for addressing adverse body composition in advanced liver disease • A decrease in free Testosterone (T) and increase in Sex Hormone Binding Globulin (SHBG) are reported with progression of NAFLD (3) • LPCN 1144 is an oral prodrug of endogenous T under development for treatment of noncirrhotic NASH • Previously, LPCN 1144 has showed to reduce hepatic fat fraction, AST and ALT levels in noncirrhotic NASH subjects compared to placebo (p<0.001 and <0.05,respectively) CONCLUSIONS ▪ LPCN 1144 significantly improved body composition in biopsy - confirmed NASH male subjects ▪ Similar to the results shown in cirrhotic patients, oral testosterone resulted in significant improvement in APLM and reduction in WBFM in non - cirrhotic NASH subjects (4) ▪ This significant impact of LPCN 1144 on body composition can be beneficial in end stage diseases such as cirrhosis ▪ Larger longitudinal investigations are warranted to confirm these effects in end stage diseases RESULTS METHOD • The ongoing LiFT (Liver Fat intervention with oral Testosterone) study is a randomized, double - blind, paired biopsy, placebo - controlled, phase 2 study in men with NASH (NCT04134091) (N=56) • Biopsy - confirmed NASH subjects were randomized 1:1:1 to three arms: x Treatment A: 142 mg eq. oral T twice daily x Treatment B: 142 mg eq. oral T with tocopherol twice daily x O ral matching placebo twice daily • Body composition parameters were evaluated in all subjects with available baseline and week 20 Dual Energy X - ray Absorptiometry (DEXA) scans (N=38), including changes in: x A ppendicular Lean M uscle M ass (APLM) x W hole Body F at M ass (WBFM) x W hole Body L ean M ass (WBLM) • Other key outcomes measured at week 12 included changes in: x SHBG AIM To present topline body composition results post 20 weeks of treatment with oral testosterone . REFERENCES 1 . Bhanji RA et al . Sarcopenia in hiding: the risk and consequence of underestimating muscle dysfunction in nonalcoholic steatohepatitis. Hepatology. 2017 Dec;66(6):2055 - 65. 2. S. Dasarathy . Etiology and Management of Muscle Wasting in Chronic Liver Disease. Curr Opin Gastroenterol. 2016, 32(3): 159 – 165. 3. Fujihara et al . High sex hormone - binding globulin concentration is a risk factor for high fbrosis - 4 index in middle - aged Japanese men. Endoc J. 2019, 66 (7): 637 - 645. 4. Sinclair M , et al . Testosterone therapy increases muscle mass in men with cirrhosis and low testosterone: a randomised controlled trial. Journal of hepatology. 2016 Nov 1;65(5):906 - 13. □ Demographics and Baseline Characteristics All Subjects (N=56) Placebo (n=19) All Subjects (N=56) Placebo (n=19) Treatment A (n=18) Treatment B (n=19) Treatment A (n=18) Treatment B (n=19) CONTACT INFORMATION Shadi Mehraban, MD, PhD. [email protected] or [email protected] □ Percentage of subjects with increase in WBFM and decrease in WBLM LPCN 1144 treatment reduced progression of adverse muscle composition compared to placebo. □ Responders with decrease in WBFM and increase in WBLM 64% of the subjects receiving LPCN 1144 compared to 15.4% in the placebo arm had favorable body composition changes. □ Absolute Change from Baseline in SHBG LPCN 1144 significantly decreased SHBG levels from baseline at 12 weeks compared to placebo. Free T is expected to increase after treatment with LPCN 1144. □ Relative change in Appendicular Lean Muscle Mass All Subjects (N=56) Placebo (n=19) All Subjects (N=56) Placebo (n=19) Treatment A (n=18) Treatment B (n=19) Treatment A (n=18) Treatment B (n=19) □ Relative Change in Whole Body Fat Mass LPCN 1144 treatment significantly elevated APLM, and significantly reduced WBFM in biopsy - confirmed NASH subjects after 20 weeks compared to placebo. □ Relative Change in Whole Body Lean Mass Exhibit 99.5
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