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LPCN US Equity

Lipocine Inc.Health Care · Pharmaceutical Preparations · CIK 1535955 · FY ends Dec 31
$2.05
+0.01 (+0.49%)
USD · as of 2026-08-19 · marketstack

LPCN · 10-K · period ended 2022-12-31

← all LPCN documents
filed 2023-03-10 · EDGAR original ↗

Our rendering of the filing — original pagination and typography are not reproduced, and tables are reduced to their short label cells (the figures live on FA). Nothing is summarized: every line below is the filing's own text.

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UNITED

STATES

SECURITIES

AND EXCHANGE COMMISSION

WASHINGTON,

D.C. 20549

FORM

10-K

or

Commission

File Number: 001-36357

LIPOCINE

INC.

(Exact

name of registrant as specified in its charter)

675 Arapeen Drive, Suite 202, Salt Lake City, Utah 84108

(Address of Principal Executive Offices) (Zip Code)

801-994-7383

(Registrant’s

telephone number, including area code)

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

Securities

registered pursuant to Section 12(g) of the Act: None

Indicate

by check mark if the registrant is a well-known seasoned issuer, as defined in Rule 405 of the Securities Act. Yes ☐ No ☒

Indicate

by check mark if the registrant is not required to file reports pursuant to Section 13 or Section 15(d) of the Securities Exchange Act.

Yes ☐ No ☒

Indicate

by check mark whether the registrant (1) has filed all reports required to be filed by Section 13 or 15(d) of the Securities Exchange

Act of 1934 during the preceding 12 months (or such shorter period that the registrant was required to file such reports) and (2) has

been subject to such filing requirements for the past 90 days. Yes: ☒ No ☐

Indicate

by check mark whether the registrant has submitted electronically every Interactive Data File required to be submitted pursuant to Rule

405 of Regulation S-T (§220.405 of this chapter) during the preceding 12 months (or for such shorter period that the registrant

was required to submit such files). Yes ☒ No ☐

Indicate

by check mark whether the registrant is a large accelerated filer, an accelerated filer, a non-accelerated filer, a smaller reporting

company, or an emerging growth company. See the definitions of “large accelerated filer,” “accelerated filer,”

“smaller reporting company,” and “emerging growth company” in Rule 12b-2 of the Exchange Act:

Large accelerated filer ☐

Accelerated filer ☐

Non-accelerated filer ☒

Smaller reporting company ☒

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. ☐

Indicate

by check mark whether the registrant has filed a report on and attestation to its management’s assessment of the effectiveness

of its internal control over financial reporting under Section 404(b) of the Sarbanes-Oxley Act (15 U.S.C. 7262(b)) by the registered

public accounting firm that prepared or issued its audit report. ☐

If

securities are registered pursuant to Section 12(b) of the Act, indicate by check mark whether the financial statements of the registrant

included in the filing reflect the correction of an error to previously issued financial statements. ☐

Indicate

by check mark whether any of those error corrections are restatements that required a recovery analysis of incentive-based compensation

received by any of the registrant’s executive officers during the relevant recovery period pursuant to § 240.10D-1(b). ☐

Indicate

by check mark whether the registrant is a shell company (as defined in Rule 12b-2 of the Act). Yes ☐ No ☒

Outstanding

Shares

The

aggregate market value of the common stock held by non-affiliates of the registrant was $69.2 million as of June 30, 2022. For purposes

of calculating the aggregate market value of shares of our common stock held by non-affiliates as set forth on the cover page of this

Annual Report on Form 10-K, we have assumed that all outstanding shares are held by non-affiliates, except for shares held by each of

our executive officers, directors and 10% or greater stockholders. However, this assumption should not be deemed to constitute an admission

that all executive officers, directors and 10% or greater stockholders are, in fact, affiliates of our company, or that there are not

other persons who may be deemed to be affiliates of our company. Further information concerning shareholdings of our officers, directors

and principal stockholders is included or incorporated by reference in Part III, Item 12 of this Annual Report on Form 10-K.

As

of March 7, 2023, the registrant had 88,510,791 shares of common stock outstanding.

DOCUMENTS

INCORPORATED BY REFERENCE:

None

TABLE

OF CONTENTS

Page

PART I

Item 1. Business 4

Item 1A. Risk Factors 23

Item 1B. Unresolved Staff Comments 53

Item 2. Properties 53

Item 3. Legal Proceedings 53

Item 4. Mine Safety Disclosures 53

PART II

Item 6. Reserved 54

Item 7A. Quantitative and Qualitative Disclosures About Market Risk 64

Item 8. Financial Statements and Supplementary Data 65

Item 9A. Controls and Procedures 95

Item 9B. Other Information 95

Item 9C. Disclosure Regarding Foreign Jurisdictions that Prevent Inspections 96

PART III

Item 10. Directors, Executive Officers and Corporate Governance 97

Item 11. Executive Compensation 100

Item 14. Principal Accountant Fees and Services 108

PART IV

Item 15. Exhibits and Financial Statement Schedules 108

FORWARD-LOOKING

STATEMENTS

THIS

ANNUAL REPORT ON FORM 10-K, IN PARTICULAR “ITEM 7. MANAGEMENT’S DISCUSSION AND ANALYSIS OF FINANCIAL CONDITION AND RESULTS

OF OPERATION,” AND “ITEM 1. BUSINESS,” CONTAINS FORWARD-LOOKING STATEMENTS WITHIN THE MEANING OF SECTION 27A OF THE

SECURITIES ACT OF 1933, AS AMENDED, AND SECTION 21E OF THE SECURITIES EXCHANGE ACT OF 1934, AS AMENDED, that involve risks and uncertainties.

Forward-looking statements provide current expectations of future events based on certain assumptions and include any statement that

does not directly relate to any historical or current fact. Forward-looking statements may refer to such matters as products, product

benefits, pre-clinical and clinical development timelines, clinical and regulatory expectations and plans, REGULATORY DEVELOPMENTS AND

REQUIREMENTS, THE RECEIPT OF REGULATORY APPROVALS, THE EXPECTATIONS FOR AND RESULTS OF CLINICAL TRIALS, PATIENT ACCEPTANCE OF LIPOCINE’S

PRODUCTS, MANUFACTURING AND COMMERCIALIZATION OF LIPOCINE’S PRODUCTS, anticipated financial performance, future revenues or earnings,

business prospects, projected ventures, new products and services, anticipated market performance, future expectations for liquidity

and capital resources needs and similar matters. Such words as “may”, “will”, “expect”, “continue”,

“estimate”, “project”, “intend”, and “potential” and similar terms and expressions are

intended to identify forward looking statements. Forward-looking statements are not guarantees of future performance and our actual results

may differ significantly from the results discussed in the forward-looking statements. Factors that might cause such differences include,

but are not limited to, those discussed in Part I, Item 1A “Risk Factors” of this Form 10-K. Except as required by applicable

law, we assume no obligation to revise or update any forward-looking statements for any reason.

There

are a number of risks, uncertainties and other important factors that could cause our actual results to differ materially from the forward-looking

statements contained in this Annual Report on Form 10-K. Such risks, uncertainties and other important factors include, among others,

the risks, uncertainties and factors set forth in “Risk Factors,” and the following risks, uncertainties and factors:

● our ongoing and planned clinical trials;

● our ability to monetize non-core product candidates;

● significant competition in our industry;

● our intellectual property position;

● loss of key members of management;

● failure to successfully execute our strategy; and

● our failure to maintain effective internal controls.

There

may be other factors that may cause our actual results to differ materially from the forward-looking statements, including factors disclosed

in “Risk Factors” and “Management’s Discussion and Analysis of Financial Condition and Results of Operations.”

You should evaluate all forward-looking statements made in this Annual Report on Form 10-K in the context of these risks and uncertainties.

We

caution you that the risks, uncertainties and other factors referred to above may not contain all of the risks, uncertainties and other

factors that are important to you. In addition, we cannot assure you that we will realize the results, benefits or developments that

we expect or anticipate or, even if substantially realized, that they will result in the consequences or affect us or our business in

the way expected. All forward-looking statements in this Annual Report on Form 10-K apply only as of the date made and are expressly

qualified in their entirety by the cautionary statements included in this Annual Report on Form 10-K. We undertake no obligation to publicly

update or revise any forward-looking statements to reflect subsequent events or circumstances.

PART

I

ITEM 1. BUSINESS

General

Lipocine

Inc. (“Lipocine” or the “Company”) was originally incorporated on June 19, 1997, under the laws of the State

of Delaware.

We

are a biopharmaceutical company focused on leveraging our proprietary Lip’ral platform to develop differentiated products through

the oral delivery of previously difficult to deliver molecules, focused on treating Central Nervous System (“CNS”) disorders.

Our proprietary delivery technologies are designed to improve patient compliance and safety through orally available treatment options.

Our primary development programs are based on oral delivery solutions for poorly bioavailable drugs. We have a portfolio of differentiated

innovative product candidates that target high unmet needs for neurological and psychiatric CNS disorders, liver diseases, and hormone

supplementation for men and women.

We

entered into a license agreement for the development and commercialization of our product candidate, TLANDO®, an oral

testosterone replacement therapy (“TRT”) comprised of testosterone undecanoate (“TU”). TLANDO is a

registered trademark assigned to Antares. On October 14, 2021, we entered into the license agreement (the “Antares License

Agreement”) with Antares Pharma, Inc. (“Antares” or our “Licensee”), pursuant to which we granted to

Antares an exclusive, royalty-bearing, sublicensable right and license to develop and commercialize, upon final approval of TLANDO

from the United States Food and Drug Administration (“FDA”), the TLANDO product for TRT in the U.S. Any FDA required

post-marketing studies will also be the responsibility of our licensee, Antares. On March 28, 2022, approval was received from the

FDA for TLANDO as a TRT in adult males for conditions associated with a deficiency of endogenous testosterone, also known as

hypogonadism. On May 24, 2022, Halozyme Therapeutics (“Halozyme”) completed an acquisition of Antares Pharma Inc.

through a merger of a wholly owned subsidiary of Halozyme with and into Antares, with Antares continuing as the surviving

corporation and becoming a wholly owned subsidiary of Halozyme. On June 7, 2022, Halozyme announced the commercial launch of TLANDO,

an oral treatment indicated for TRT in adult males for conditions associated with a deficiency or absence of endogenous testosterone

(primary or hypogonadotropic hypogonadism).

Additional

clinical development pipeline candidates include: LPCN 1154 for postpartum depression (“PPD”); LPCN 2101 for epilepsy; and

LPCN 1148 comprising a novel prodrug of testosterone, testosterone laurate (“TL”), for the management of decompensated cirrhosis.

In addition to our CNS product candidates, we have non-core assets for which we expect to seek partnerships to enable further development

which we do not plan to devote significant resources to developing in the future without a partnership or out licensing agreement. These

non-core assets include LPCN 1148 which we intend to explore partnering once completion of the Phase 2 study is complete, LPCN 1144,

an oral prodrug of androgen receptor modulator for the treatment of non-cirrhotic non-alcoholic steatohepatitis (“NASH”)

which has completed Phase 2 testing; LPCN 1111, a next generation oral TRT product comprised of testosterone tridecanoate (“TT”)

with the potential for once daily dosing which has completed Phase 2 testing; and LPCN 1107, potentially the first oral hydroxy progesterone

caproate (“HPC”) product indicated for the prevention of recurrent preterm birth (“PTB”), which has completed

a dose finding clinical study in pregnant women and has been granted orphan drug designation by the FDA.

The

following charts summarize the status of our product candidate development programs:

Corporate

Strategy

Our

goal is to become a leading biopharmaceutical company focused on leveraging our proprietary Lip’ral drug delivery technology platform

to develop differentiated products through oral delivery of previously difficult to deliver molecules for CNS disorders. The key components

of our strategy are to:

Advance

LPCN 1154 and other CNS product candidates. We intend to focus on the development of endogenous neuroactive steroids (“NAS”)

which have broad applicability in treating various CNS conditions where we can leverage our technology platform to develop highly differentiated

oral therapeutics. Our priority is on the development of LPCN 1154, a fast-acting oral antidepressant for postpartum depression (“PPD”)

with potential for outpatient use.

Support

our licensee in commercialization of our licensed oral TRT option. We believe the TRT market needs a differentiated, convenient oral

option. We have exclusively licensed rights to TLANDO to Antares for commercialization of TLANDO in the US. We plan to support our licensee’s

efforts to effectively enable the availability of TLANDO to patients in a timely manner, in addition to receiving milestone and royalty

payments associated with TLANDO commercialization as agreed to in the Antares License Agreement.

Develop

partnership(s) to continue the advancement of non-core pipeline assets. We continuously strive to prioritize our resources in seeking

partnerships of our pipeline assets. We are currently exploring partnering (i) LPCN 1144, our candidate for treatment of non-cirrhotic

NASH, (ii) LPCN 1148, for the management of decompensated cirrhosis, (iii) LPCN 1111, a once-a-day therapy candidate for

TRT, and (iv) LPCN 1107, our candidate for prevention of pre-term birth. We are also exploring the possibility of licensing LPCN 1021

(known as TLANDO in the United States) to third parties outside the United States, although no licensing agreement has been entered into

by the Company.

Our

Development Pipeline Product Candidates

Our

pipeline of clinical development candidates includes LPCN 1154 for postpartum depression (“PPD”), LPCN 2101 for epilepsy,

and LPCN 1148, an androgen therapy for the management of cirrhosis. We will continue to explore other product development candidates

targeting CNS indications with a significant unmet need. We will also continue efforts to enter into partnership arrangements for the

continued development and/or marketing of LPCN 1144, LPCN 1148, LPCN 1111, LPCN 1107 and TLANDO outside of the United States.

Our

products are based on our proprietary Lip’ral drug delivery technology platform. Lip’ral-based TLANDO was approved in March

2022. Lip’ral technology is a patented technology based on lipidic compositions which form an optimal dispersed phase in the gastrointestinal

environment for improved absorption of insoluble drugs. The drug loaded dispersed phase presents the solubilized drug efficiently at

the absorption site (gastrointestinal tract membrane) thus improving the absorption process and making the drug less dependent on physiological

variables such as dilution, gastro-intestinal pH and food effects for absorption. Lip’ral-based formulation enables improved solubilization

and higher drug-loading capacity, which can lead to improved bioavailability, reduced dose, faster and more consistent absorption, reduced

variability, reduced sensitivity to food effects, improved patient compliance, and targeted lymphatic delivery where appropriate.

Oral

Programs for CNS Disorders

Some

preferred endogenous or naturally occurring NAS present in central nervous system act as positive allosteric modulators (“PAM”)

of the GABAA receptor, the major biological target of the inhibitory neurotransmitter γ-aminobutyric acid (“GABAA”).

To improve oral delivery of these modulators, several synthetic NAS derivatives of endogenous GABAA receptor PAMs, have been

developed for therapeutic use in the past few decades.

We

believe through utilization of our proprietary technology we may have the ability to enable effective oral delivery of endogenous GABAA

receptor PAMs which historically had been deemed to be not orally bioavailable. As a novel drug class, NAS have received considerable

attention because of their potential to treat various neuropsychiatric conditions including depression, movement disorders, epilepsy,

anxiety, and neurodegenerative diseases. We have conducted Phase 1 pharmacokinetic (“PK”) studies for each of our two lead

NAS candidates which have demonstrated promising PK results, safety, and tolerability and we are evaluating additional undisclosed CNS-focused

candidates.

LPCN

1154: Product Candidate for PPD

Our

most advanced NAS candidate is LPCN 1154, a non-invasive, oral formulation of the neuroactive steroid brexanolone which we are developing

for the treatment of PPD. The FDA recently agreed with our proposal for establishing the efficacy of LPCN 1154 through a pivotal PK bridge

to an approved IV infusion brexanolone via a 505(b)(2) NDA filing. Based on feedback from the FDA, the company has initiated a pilot

PK bridge study of LPCN 1154, a prelude to a pivotal study required for NDA filing, and results from the pilot PK bridge study are expected

in the first half of 2023. We have previously completed an oral PK study and a food effect study with LPCN 1154.

PPD

PPD

(“Postpartum depression”), a type of major depressive disorder with onset either during pregnancy or within four weeks of

delivery, refers to depression persisting up to 12 months after childbirth. PPD can be clinically segmented by the severity of symptoms

and presence of a comorbidity, including epilepsy. Approximately 1 in 8 mothers suffers from PPD in the United States alone; this equates

to approximately 500,000 women being affected by PPD annually.

Disease

Overview - PPD

Associated

Risk Factors

Unmet

Medical Need

We

believe there is considerable unmet need within women with PPD due to lack of convenient and fast-acting oral therapies. Selective Serotonin

Reuptake Inhibitors (“SSRIs”) have been the traditional first-line choice for women with severe PPD requiring weeks for onset

of efficacy; therefore, a need for an oral treatment option with a faster onset of action remains a significant unmet need in treating

PPD, especially in women with epilepsy risk wherein psychiatric comorbidity is common and PPD rates are higher than the general population.

Injectable brexanolone (ZulressoTM, Sage Therapeutics) became the first FDA-approved treatment for postpartum depression. However, numerous

factors limit the utilization of injectable brexanolone such as method of administration, cost, and safety concerns. Administration of

injectable brexanolone requires a 60-hour continuous infusion in a supervised medical setting, a demanding ask for a mother with a newborn.

Besides associated privacy concerns and social stigma, inpatient treatment may also require separation of the mother and child for a few

days, which may be difficult to the already strained mother-infant bond and may present breast feeding challenges. Moreover, the pharmacotherapy

costs coupled with inpatient treatment/childcare costs limits its accessibility and affordability to women most in need of the therapy.

Finally, due to concerns about the safety of injectable Zulresso including excessive sedation or loss of consciousness, Zulresso has a

Black Box Warning in its label and is only available through a restricted distribution program (REMS), and sites need significant time

to become treatment ready.

We believe LPCN 1154 targets the unmet need for a convenient oral treatment with faster onset of action or rapid relief.

LPCN

2101: NAS for Epilepsy

We

are currently evaluating an additional NAS candidate, LPCN 2101, for women with epilepsy (“WWE”). We have completed pre-clinical

and Phase 1 studies for LPCN 2101 which demonstrated promising PK results, safety and tolerability. In July 2022 our IND was accepted

by the FDA for LPCN 2101 for adults with epilepsy and we plan to initiate a Phase 2 IND opening proof-of-concept study to evaluate the

safety, tolerability, and efficacy of LPCN 2101 in 2023 subject to the availability of additional resources.

Disease

Overview – Epilepsy

Epilepsy

is defined by the 1) occurrence of at least two unprovoked seizures more than 24 hours apart, 2) occurrence of one unprovoked seizure

and a probability of further seizures occurring over the next 10 years, and/or 3) diagnosis of an epilepsy syndrome. Patients with epilepsy

are more likely to be comorbid with other conditions, including depression and anxiety.

Patients

with epilepsy have increased risk of mortality due to direct effects of seizures (e.g., status epilepticus, car accidents) and indirect

effects of seizures (e.g., suicide, cardiovascular effects.)

Epilepsy

is a disorder of the brain that causes seizures, affecting the physical, mental, and social well-being of persons, and is associated

with a 2 to 3 times greater mortality rate compared with the general population. About 60-65% of epilepsy is idiopathic and about 30%

of patients are refractory (i.e., epilepsy not well managed with currently available Anti-Seizure Medications (“ASMs”). Epilepsy

is the most common neurological disorder during pregnancy.

It

is estimated that approximately 900,000 child-bearing (“CB”) age women suffer from active epilepsy in the U.S. Women of CB

age with epilepsy face many additional challenges due to hormonal influences on seizure activity and endocrine function throughout the

different phases of their reproductive cycles. Elevated estrogen or decreased progesterone levels can exacerbate seizure frequency. Often,

these women experience hormonal and endogenous NAS imbalances, coupled with fluctuations in the blood levels of ASMs that impact control

of seizures, efficacy of oral contraceptives, any coexisting anxiety and/or depression and any associated sleep impairment. Epileptic

patients are 5-20 times more likely to develop depression.

Clinical

segmentation can be categorized by epilepsy type, comorbidities and patient subgroups. Categorization of focal epilepsy, generalized

epilepsy, combined focal and generalized epilepsy, and unknown epilepsy can guide the choice of ASM. Special patient subgroups, including

WWE of CB age and elderly patients, require special care and management of epilepsy. Comorbidities such as depression and anxiety may

be co-treated with therapies that do not aggravate seizures and have no drug interaction with the ASM used for epilepsy. While lowest

effective dose and monotherapy are preferred, management of patients with epilepsy is focused on controlling seizures, avoiding adverse

events, and maintaining quality of life. Despite a wide range of ASMs available, about 30 % of all people with epilepsy still fail to

respond to treatment effectively. Women with epilepsy face specific challenges throughout their lifespan because of seizures, ASMs, and

hormonal fluctuations.

Women

with epilepsy were once counseled to avoid pregnancy, but epilepsy is no longer considered a contraindication to pregnancy. Caregivers

for WWE in the preconception phase either intending to start a family (planning pregnancy) or using contraception to prevent an unplanned

pregnancy face significant challenges to balance seizure control efficacy with the selection and dosage of ASMs and ASM-related risks

such as, among other risks, fetal-neonatal toxicity, contraception failure, and psychiatric side effects.

Several

ASMs are known to have teratogenic effects on the developing fetus (converging evidence from registry studies indicates that teratogenic

risks are highest with valproate, followed by carbamazepine and topiramate). Other commonly prescribed ASMs, including older generation

agents, such as phenobarbital and phenytoin, have been associated with higher risks as compared with lamotrigine, levetiracetam, clonazepam

and gabapentin (Vajda et al., 2014; Voinescu and Pennell, 2015). Moreover, risks associated with ASMs are considerable early in pregnancy;

therefore, it is necessary that WWE of CB age undergo counseling, monitoring, and adjustment to the most appropriate ASM prior to becoming

pregnant. It is preferable that WWE of CB age discuss seizure control with their doctor for at least 6 months before conception and,

if possible, cease ASM therapy or use the lowest effective dose of a single anticonvulsant according to the type of epilepsy and the

fetal toxicity of the ASM. Anxiety, depression, lack of adherence to ASM, and/or contraception failure may be experienced by women who

are worried about unplanned pregnancy or are late in confirming pregnancy, planned or unplanned. ASMs can reduce the efficacy of oral

contraceptives, compounding this problem.

Complex,

multidirectional interactions between female hormones, seizures, and ASMs exist. Most hormones act as NAS and can thus modulate

brain excitability. Any changes in endogenous or exogenous hormone levels can affect the occurrence of seizures, either directly or

via PK interactions that modify the plasma levels of ASMs (Harden, 2008). The PK interactions between oral contraceptives and ASMs

are bidirectional (Johnston and Crawford, 2014). The efficacy of hormonal contraception may be diminished for women taking CYP-P450

enzyme inducing ASMs. Epilepsy is not a medical condition in which contraceptives are contraindicated. Contraceptive failure,

possibly related to ASMs, may be responsible for up to 1 in 4 unplanned pregnancies in WWE (~12.5% of all WWE pregnancies), versus a

rate of 1% in healthy women.

Unmet

need to treat WWE in CB age

It

is estimated that approximately 900,000 CB age women suffer from active epilepsy in the U.S. Women of CB age with epilepsy face many

additional challenges such as hormonal influences on seizure activity and endocrine function throughout the different phases of their

reproductive cycles, and approximately 30% of patients with epilepsy cannot be efficiently controlled with available ASMs making consideration

of newer pharmacological treatment development options important.

Managing

uncontrolled seizures in WWE of CB age is the primary aim during preconception, pregnancy, and postpartum phases. Therefore, uncompromised

ASM efficacy with acceptable variability and less or no drug-drug interactions achieved with lowest possible monotherapy dose to address

fetal toxicity concerns remain highly unmet needs. Moreover, control of seizures including prevention of breakthrough seizures is critical

when planning for pregnancy and also during pregnancy, as it can also lead to undesired falls or auto-accidents and compromise freedom

to drive.

Select

ASMs have the potential to induce contraception failures, reproductive hormone imbalance, anxiety, and depression. There remains an unmet

need for an ASM without the aforementioned downsides, with no to low fetal-neonatal toxicity and without any breast-feeding concerns

as well as potential to treat associated comorbidities.

While

over 30 molecules have been approved for the treatment of epilepsy in the U.S., no epilepsy drug has been specifically approved for WWE

of CB age. We believe our endogenous NASs as GABAA PAMs, while targeting the goal of seizure control, also have the potential

for additional benefits in psychiatric disorders comorbidities (e.g., anxiety and/or depression) and sleep impairment. Moreover, these

oral endogenous NAS could potentially address some of the fetal toxicity concerns related to unplanned or planned pregnancy in WWE. (1)

LPCN

1148: Oral Product Candidate for the Management of Decompensated Cirrhosis

We

are currently evaluating LPCN 1148 comprising testosterone laurate (“TL”) for the management of decompensated cirrhosis.

We believe LPCN 1148 targets unmet needs for subjects with cirrhosis including improvement in the quality of life of patients while on

the liver transplant waiting list, prevention or reduction in the occurrence of new decompensation events such as hepatic encephalopathy

(“HE”), and improvement in post liver transplant survival, including outcomes and costs.

We

are currently conducting a Phase 2 proof of concept (“POC”) study (NCT04874350) in male cirrhotic subjects to evaluate the

therapeutic potential of LPCN 1148 for the management of sarcopenia. The ongoing Phase 2 POC study is a prospective, multi-center, randomized,

placebo-controlled study in male sarcopenic cirrhotic patients. Subjects will be randomized 1:1 to 1 of 2 arms. The treatment arm

is an oral dose of LPCN 1148, and the second arm is a matching placebo. The primary endpoint is change in skeletal muscle index at week

24 with key secondary endpoints including change in liver frailty index, rates of breakthrough HE, and number of waitlist events, including

all-cause mortality. Total treatment is expected to be 52 weeks. Enrollment in the Phase 2 study was completed in the fourth quarter

of 2022 and top-line 24-week results are expected in mid-2023.

Possible

outcomes of interest from the Phase 2 study include clinical outcomes such as overall survival and new decompensation events (including

HE and/or ascites occurrences), rates of survival to transplant, rates of hospitalizations, infections, etc., muscle changes such as

muscle mass, body composition, myosteatosis (muscle fat), functional capacity changes such as liver frailty index (“LFI”),

patient reported outcomes (“PROs”), and biochemical markers including hematocrit for anemia status, albumin, creatinine/kidney

function, etc.

Disease

Overview – Cirrhosis

There

are over 2 million cases of cirrhosis worldwide, with over 500,000 people living with decompensated cirrhosis in the U.S. and nonalcoholic

fatty liver disease is the most rapidly increasing indication for liver transplant. 62% of those on the liver transplant (“LT”)

waitlist are male and the economic burden (approximately $812,500/transplant) is high and continues to increase. Each year about half

of the approximately 17,000 people in U.S. on the LT waitlist undergo transplant, while nearly 3,000 patients either die or are removed

from the list because they were “too sick to transplant.”

Liver

cirrhosis is defined as the histological development of regenerative nodules surrounded by fibrous bands. Cirrhotic patients typically

have a years-long silent, asymptomatic phase (compensated cirrhosis) until decreasing liver function and increasing portal pressure move

the patient into the symptomatic phase (decompensated cirrhosis). Transition to decompensated cirrhosis is marked by clinical events

including ascites, encephalopathy, jaundice, and/or variceal hemorrhage. Decompensated subjects survive on average less than 2 years.

Common causes of liver cirrhosis include alcoholic liver disease, nonalcoholic fatty liver disease (“NAFLD”), chronic hepatitis

B and C, primary biliary cirrhosis (“PBC”), primary sclerosing cholangitis (“PSC”) and cryptogenic.

Common

complications in cirrhotic patients may include: compromised liver function, portal hypertension, varices in GI tract with internal bleeding,

edema, ascites, hepatic encephalopathy, compromised immunity with post-transplant acute rejection risk, high sodium levels, increased

bilirubin, low albumin level, insulin resistance with impaired peripheral uptake of glucose, depression, accelerated muscle disorder

in the form of sarcopenia, myosteotosis, and frailty with compromised energetics, bone diseases (e.g., osteoporosis), high alkaline phosphatase

(“ALP”), cachexia, malnutrition, weight loss (>5%), symptoms of hypogonadism such as abnormal hair distribution, anemia,

sexual dysfunction, testicular atrophy, muscle wasting, fatigue, osteoporosis, gynecomastia, inflammation with elevated cytokines, and

infection risk leading to hospital admissions and possibly death.

HE,

a significant decompensation event in patients with cirrhosis, is a brain dysfunction caused by liver insufficiency and/or portal systemic

shunting. Because the damaged liver cannot function normally (as in cirrhosis), neurotoxins such as ammonia are inadequately removed

from systemic circulation and travel to the brain, where they affect neurotransmission. This can cause episodes of HE, which may present

as alterations in consciousness, cognition, and behavior that range from minimal to severe. Overt HE occurs in 30% to 40% of patients

with cirrhosis at some point during the clinical course of their disease. As the burden of chronic liver disease and cirrhosis is increasing,

the frequency of HE is also increasing.

Our

Partnership Pipeline Product Candidates

We

continue to pursue opportunities for partnering arrangements for the continued development and/or marketing of LPCN 1144, LPCN 1148,

LPCN 1111, LPCN 1107 and TLANDO outside of the U.S. We do not currently anticipate conducting any further significant development activities

with respect to these products and product candidates, without the participation of a partner. There can be no guarantee that we will

be able to identify or enter into partnering arrangements on terms that are beneficial to us or at all. Even if we do enter into partnering

arrangements, such arrangements may not be sufficient to successfully develop and commercialize these products.

TLANDO:

An Oral Product for Testosterone Replacement Therapy

As

previously described, under the Antares License Agreement, we granted to Antares an exclusive, royalty-bearing, sublicensable right and

license to develop and commercialize TLANDO, our product for TRT in the U.S. TLANDO received FDA approval on March 28, 2022. Any FDA

requirement to conduct certain post-marketing studies will be the responsibility of our licensee, Antares. On May 24, 2022, Halozyme

Therapeutics completed an acquisition of Antares Pharma Inc. through a merger of a wholly owned subsidiary of Halozyme with and into

Antares, with Antares continuing as the surviving corporation and becoming a wholly owned subsidiary of Halozyme.

Proof-of-concept

for TLANDO was initially established in 2006, and subsequently TLANDO was licensed in 2009 to Solvay Pharmaceuticals, Inc., which

was then acquired by Abbott Products, Inc. (“Abbott”). Following a portfolio review associated with the spin-off of

AbbVie Inc. by Abbott in 2011, the rights to TLANDO were reacquired by us. All obligations under the prior license agreement have

been completed except that Lipocine will owe Abbott a perpetual 1% royalty on net sales of TLANDO. Such royalties are limited to $1

million in the first 2 calendar years following product launch, after which period there is no cap on royalties and no maximum

aggregate amount. If generic versions of any such product are introduced, then royalties are reduced by 50%. TLANDO was commercially

launched on June 7, 2022. During the year ended December 31, 2022, we incurred royalty expense of approximately $12,000 resulting

from the commercial launch of TLANDO in 2022.

Under

the Pediatric Research Equity Act (“PREA”), since TLANDO received full FDA approval, under the Antares Licensing Agreement

Antares will need to address the PREA requirement to assess the safety and effectiveness of TLANDO in pediatric patients. The FDA may

also require certain post-marketing studies to be conducted which will also be the responsibility of our licensee, Antares.

Upon

execution of the Antares License Agreement, Antares paid us an initial payment of $11.0 million. Antares will also make additional payments

of $5.0 million to us on each of January 1, 2025, and January 1, 2026, provided that certain conditions are satisfied. We are also eligible

to receive milestone payments of up to $160.0 million in the aggregate, depending on the achievement of certain sales milestones in a

single calendar year with respect to products licensed by Antares under the Antares License Agreement. In addition, we will receive tiered

royalty payments at rates ranging from percentages in the mid-teens to up to 20% of net sales of TLANDO in the United States, subject

to certain minimum royalty obligations. Further, on October 14, 2021, we assigned our Manufacturing Agreement, dated August 27, 2013,

by and between the Company and Encap Drug Delivery (the “Manufacturing Agreement”) to Antares as part of the Antares License

Agreement.

We

are exploring the possibility of licensing LPCN 1021 (known as TLANDO in the United States) to third parties outside the United States,

although no licensing agreement has been entered into by the Company. If and when an agreement is made with a partner, such arrangement

would likely be contingent upon obtaining acceptable cost of goods by securing an agreement with a new manufacturer in addition to obtaining

local regulatory approval. No assurance can be given that any license agreement will be completed, or, if an agreement is completed,

that such an agreement would be on terms favorable to us.

LPCN

1144: An Oral Prodrug of Bioidentical Testosterone Product Candidate for the Treatment of NASH

We

are exploring the possibility of partnering LPCN 1144 to a third party, although no partnering agreement has been entered into by the

Company. No assurance can be given that any license agreement will be completed, or, if an agreement is completed, that such an agreement

would be on terms favorable to us.

Disease

Overview – NASH

NASH

is a more advanced state of non-alcoholic fatty liver disease (“NAFLD”) and can progress to a cirrhotic liver or liver failure,

require liver transplant, and can result in hepatocellular carcinoma/ liver cancer, and death. Progression of NASH to end stage liver

disease will soon surpass all other causes of liver failure requiring liver transplantation. Importantly, beyond these critical conditions,

NASH and NAFLD patients additionally suffer heightened cardiovascular risk and, in fact, die more frequently from cardiovascular events

than from liver disease. NAFLD/NASH is becoming more common due to its strong correlation with obesity and metabolic syndrome, including

components of metabolic syndrome such as diabetes, cardiovascular disease and high blood pressure. In the U.S., 20% to 30% of the population is estimated to suffer from NAFLD and 15% to 20% percent of this group progress to NASH, which is a substantially large population

that lacks effective therapy. NASH is a silent killer that affects millions in the U.S. Diagnoses have been on the rise and are expected

to increase dramatically in the next decade. Approximately 50% of NASH patients are in adult males. In men, especially with comorbidities

associated with NAFLD/NASH, testosterone deficiency has been associated with an increased accumulation of visceral adipose tissue and

insulin resistance, which could be factors contributing to NAFLD/NASH. There is currently no approved therapy for the treatment of NASH

although there are several drug candidates currently under development with many having clinical failures to date.

The

critical pathophysiologic mechanisms underlying the development and progression of NASH include reduced ability to handle lipids, increased

insulin resistance, injury to hepatocytes and liver fibrosis in response to hepatocyte injury. NASH patients have an excessive accumulation

of fat in the liver resulting primarily from a caloric intake above and beyond energy needs. A healthy liver contains less than 5% fat,

but a liver in someone with NASH can contain more than 20% fat. This abnormal liver fat contributes to the progression to NASH, a liver

necro-inflammatory state that can lead to scarring, also known as fibrosis, and, for some, can progress to cirrhosis and liver failure.

Current

Status

We

have recently completed the LiFT Phase 2 clinical study in biopsy-confirmed non-cirrhotic NASH subjects. The LiFT clinical study was

a prospective, multi-center, randomized, double-blind, placebo-controlled multiple-arm study in biopsy-confirmed hypogonadal and eugonadal

male NASH subjects with grade F1-F3 fibrosis and a target NAFLD Activity Score ≥ 4 with a 36-week treatment period. The LiFT clinical

study enrolled 56 biopsy confirmed NASH male subjects. Subjects were randomized 1:1:1 to one of three arms (Treatment A is a twice daily

oral dose of 142 mg testosterone equivalent, Treatment B is a twice daily oral dose of 142 mg testosterone equivalent formulated with

217 mg of d-alpha tocopherol equivalent, and the third arm is twice daily matching placebo).

The

primary endpoint of the LiFT clinical study was change in hepatic fat fraction via MRI-PDFF and exploratory liver fat/marker end

points post 12 weeks of treatment. Additionally, key secondary endpoints post 36 weeks of treatment included assessment of histological

change for NASH resolution and/or fibrosis improvement (biopsy) as well as liver fat data (MRI-PDFF). The LiFT clinical study

was not powered to assess statistical significance of any of the secondary endpoints. Other important endpoints included the following:

change in liver injury markers, anthropomorphic measurements, lipids, insulin resistance and inflammatory/fibrosis markers; as well as

patient reported outcomes.

Treatments

with LPCN 1144 post 12 weeks of treatment in the LiFT study resulted in robust liver fat reduction, assessed by MRI-PDFF, and

showed improvement of liver injury markers with no observed tolerability issues.

Liver

biopsies were performed at baseline (“BL”) and after 36 weeks of treatment (“EOS”). Prespecified biopsy analyses

included NASH Clinical Research Network (“CRN”) scoring as well as a continuous paired (“Paired Technique”) and

digital technique (“Digital Technique-Fibronest”). All biopsy analyses were performed on the same slides and the reads for

the 3 techniques were done independently. Analysis sets included the NASH Resolution Set (all subjects that have BL and EOS biopsy

with NASH at BL [NAS ≥4 with lobular inflammation score ≥ 1 and hepatocyte ballooning score ≥1 at BL] (n=37)), the Biopsy Set

(all subjects with baseline and EOS biopsies (n=44)), and the Safety Set (all randomized subjects (n=56)).

Both

LPCN 1144 treatment arms met with statistical significance the pre-specified accelerated approval regulatory endpoint of NASH resolution

with no worsening of fibrosis based on NASH CRN scoring. Additionally, both treatment arms showed substantial improvement of the observed

NASH activity in steatosis, inflammation, and ballooning.

During

the 36 weeks of treatment, LPCN 1144 was well tolerated with an overall safety profile comparable to placebo. Additionally, subjects

were given the option to have access to LPCN 1144 through an open label extension (“OLE”) study. The extension study enabled

the collection of additional data on LPCN 1144 for up to a total of 72 weeks of therapy, as well as data for 36 weeks of therapy for

those subjects on placebo in the LiFT study. Key results from the OLE study are as follows:

● Observed liver histology improvements support further development

In

November 2021, the FDA granted Fast Track Designation to LPCN 1144 as a treatment for non-cirrhotic NASH. The Fast Track program is designed

to accelerate the development and expedite the review of products, such as LPCN 1144, which are intended to treat serious diseases and

for which there is an unmet medical need.

We

had a written only response from FDA for a LPCN 1144 Type C meeting with the FDA in January 2022 to discuss the development path forward

with LPCN 1144. The FDA acknowledged that the NDA submission of LPCN 1144 would be via 505(b)2 regulatory pathway and agreed that no

additional non-clinical studies are needed to support an NDA submission. The FDA acknowledged that in the LiFT study subjects achieved

improvements in key components associated with NASH histopathology after 36-weeks of treatment with LPCN 1144 in adult males and agreed

that the proposed multicomponent primary surrogate endpoint is acceptable for seeking approval under the accelerated approval pathway.

The FDA agreed that the proposed primary multicomponent surrogate endpoint, NASH resolution with no worsening of fibrosis, is acceptable

for seeking approval under the accelerated approval pathway and the FDA recommended a Phase 3 trial with a study duration of 72 weeks.

In July 2022, Lipocine held an End of Phase 2 meeting with FDA for LPCN 1144 in NASH. The FDA recommended a Phase 2 dose ranging study

be conducted to identify the optimal dose prior to conducting a pivotal study. The FDA agreed to the proposed unique testosterone ester,

testosterone laurate, for future clinical studies.

LPCN

1111: A Next-Generation Long-Acting Oral Product Candidate for TRT

We

are in the process of scaling up the manufacturing process and generation of supplies of LPCN 1111 to enable potential partners to conduct

pivotal studies for registration. We are exploring the possibility of partnering LPCN 1111 to a third party, although no partnering agreement

has been entered into by the Company. No assurance can be given that any license agreement will be completed, or, if an agreement is

completed, that such an agreement would be on terms favorable to us.

LPCN

1111: is a next-generation, novel ester prodrug of testosterone comprised of testosterone tridecanoate (“TT”) which uses

our proprietary delivery technology to enhance solubility and improve systemic absorption. We completed a Phase 2b dose finding study

in hypogonadal men in the third quarter of 2016. The primary objectives of the Phase 2b clinical study were to determine the starting

Phase 3 dose of LPCN 1111 along with safety and tolerability of LPCN 1111 and its metabolites following oral administration of single

and multiple doses in hypogonadal men. Good dose-response relationship was observed over the tested dose range in the Phase 2b study.

Additionally, the target Phase 3 dose met primary and secondary end points. Overall, LPCN 1111 was well tolerated with no drug-related

severe or serious adverse events reported in the Phase 2b study.

In

February 2018 we had a meeting with the FDA to discuss these pre-clinical results and to discuss the Phase 3 clinical study and path

forward for LPCN 1111. Based on the results of the FDA meeting and additional pre-clinical studies conducted after the FDA meeting, we

have proposed a Phase 3 protocol for LPCN 1111 and have solicited FDA feedback. Based on initial FDA feedback, we expect the Phase 3

clinical trial design to follow the International Council for Harmonisation of Technical Requirements for Pharmaceuticals for Human Use

(“ICH”) guidelines and we expect the trial will include at least a 3-month efficacy treatment period and a 1-year safety

component for approximately 100 subjects. We are currently seeking further clarification from FDA with respect to the total subject LPCN

1111 exposure information needed for an NDA filing. We continue to refine the Phase 3 protocol and plan to request FDA approval of the

protocol once it is finalized. Additionally, the FDA previously requested that a food effect and a phlebotomy study be completed, and

that ambulatory blood pressure monitoring (“ABPM”) be included as part of the Phase 3 clinical study. We are currently transferring

the manufacturing of LPCN 1111 to a third-party contract manufacturer and scaling up the formulation after which we anticipate the next

steps for a partner developing LPCN 1111 may be to conduct a food effect/phlebotomy study with LPCN 1111. Under the terms of the Antares

License Agreement, Antares had been granted an option to license LPCN 1111, exercisable on or before March 31, 2022, for further development

and, should LPCN 1111 receive FDA approval, commercialization. On April 1, 2022, the Company entered into the First Amendment to the

License Agreement (the “Amendment”), pursuant to which the License Agreement was amended to extend the deadline by which

Antares was to exercise its option to license LPCN 1111 to June 30, 2022. As consideration for the Company’s agreement to the Amendment,

Antares paid the Company a non-refundable cash fee of $500,000 in April 2022. On June 30, 2022, Antares’ option to license LPCN

1111 expired and was not exercised.

LPCN

1107: An Oral Product Candidate for the Prevention of Preterm Birth

We

are exploring the possibility of partnering LPCN 1107 to a third party, although no partnering agreement has been entered into by the

Company. No assurance can be given that any partnership agreement will be completed, or, if an agreement is completed, that such an agreement

would be on terms favorable to us.

We

believe LPCN 1107 has the potential to become the first oral hydroxyprogesterone caproate (“HPC”) product indicated for the

reduction of risk of PTB (delivery less than 37 weeks) in women with singleton pregnancy who have a history of singleton spontaneous

PTB. Prevention of PTB is a significant unmet need as approximately 11% of all U.S. pregnancies result in PTB, a leading cause of neonatal

mortality and morbidity.

Current

Status

We

have completed a multi-dose PK dose selection study in pregnant women. The objective of the multi-dose PK selection study was to

assess HPC blood levels in order to identify the appropriate LPCN 1107 Phase 3 dose. The multi-dose PK dose selection study was an

open-label, 4-period, 4-treatment, randomized, single and multiple dose PK study in pregnant women with 3 dose levels of LPCN 1107

and the IM HPC (Makena®). The study enrolled 12 healthy pregnant women (average age of 27 years) with a gestational age of

approximately 16 to 19 weeks. Subjects received three dose levels of LPCN 1107 (400 mg BID, 600 mg BID, or 800 mg BID) in a

randomized, crossover manner during the first 3 treatment periods and then received 5 weekly injections of HPC during the fourth

treatment period. During each of the LPCN 1107 treatment periods, subjects received a single dose of LPCN 1107 on Day 1 followed by

twice daily administration from Day 2 to Day 8. Following completion of the 3 LPCN 1107 treatment periods and a washout period,

all subjects received 5 weekly injections of HPC. Results from this study demonstrated that average steady state HPC levels

(Cavg0-24) were comparable or higher for all 3 LPCN 1107 doses than for injectable HPC. Additionally, HPC levels as a function

of daily dose were linear for the 3 LPCN 1107 doses. Also, unlike the injectable HPC, steady state exposure was achieved for all

3 LPCN 1107 doses within 7 days.

A

traditional PK/PD based Phase 2 clinical study in the intended patient population is not expected to be required prior to entering into

Phase 3. Therefore, based on the results of our multi-dose PK study we had an End-of-Phase 2 meeting and subsequent guidance meetings

with the FDA to define a pivotal Phase 2b/3 development plan for LPCN 1107. However, these discussions may be updated based on recent

developments with Covis’ Makena® as described below. We have completed a food effect study to characterize the dosing regimen

for the pivotal study. We plan to submit a pivotal clinical study protocol to the FDA.

The

FDA has granted orphan drug designation to LPCN 1107 based on a major contribution to patient care. Orphan designation qualifies Lipocine

for various development incentives, including tax credits for qualified clinical testing, and a waiver of the prescription drug user

fee when we file our NDA.

Recent

Competition Update

On

October 5, 2020, the FDA’s Center for Drug Evaluation and Research (“CDER”) proposed that Makena be withdrawn from

the market because the PROLONG trial failed to verify the clinical benefit of Makena and concluded that the available evidence does not

show Makena is effective for its approved use.

CDER

Source: SEC EDGAR (public domain) · 10-K for the period ended 2022-12-31, filed 2023-03-10 · accession 0001493152-23-007178

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