NASDAQ: ENTX

Osteoporosis is a chronic, progressive disorder in which bone resorption exceeds formation, resulting in decreased bone strength and increased susceptibility to fracture. Osteoporosis is a major and growing public health issue, responsible for over two million fractures annually in the United States. After age 50, one in three women and one in five men will suffer an osteoporosis-related fracture in their remaining lifetime. Osteoporotic fractures lead to chronic pain, decreased quality of life, increased disability, and contribute to premature death. Studies show that up to 20-24% of hip fracture patients die within one year of the fracture. The total medical cost of osteoporotic fractures is projected to increase from $57 billion in 2018 to $95 billion by 2040, largely due to the aging population. Postmenopausal women are at higher risk of developing osteoporosis-related fractures, particularly in the hip, spine, and wrist. The mechanism for low bone mineral density (“BMD”) in postmenopausal women is primary estrogen deficiency, which leads to accelerated bone loss, especially in the first five to ten years after menopause.

The three approved anabolic drugs, including Forteo®, are indicated for the treatment of very high-risk osteoporosis patients as first line therapy and as second line treatment in osteoporosis patients who cannot tolerate or progress on other osteoporosis drugs. Despite the superior efficacy of anabolic drugs, existing treatments require daily or monthly subcutaneous injections and are estimated to be used in a minority of very high-risk patients. EB613 is intended to provide an oral anabolic treatment earlier in an osteoporosis patient’s journey to increase skeletal mass, reduce the risk of fracture, limit the disease progression, and decrease disability and mortality. Our mission with EB613 is to democratize anabolic treatment and enable wider access to both patients and healthcare practitioners.

We have completed a comprehensive nonclinical and clinical package for the EB613 program, including three Phase 1 comparative studies with Forteo® and three Phase 2 clinical studies. EB613 has been safely administered to a total of 270 study participants, including postmenopausal women with low BMD or osteoporosis (n=118 on EB613, n=43 on placebo), healthy volunteers, and male and female patients with hypoparathyroidism.

EB613 completed a Phase 2, 6-month, 161-patient, placebo-controlled study that met all biomarker and BMD endpoints without significant safety concerns in women with postmenopausal osteoporosis or low BMD. In April 2024, Phase 2 data was published in the Journal of Bone and Mineral Research (JBMR). EB613 produced rapid dose-proportional increases in biochemical markers of bone formation, reductions in markers of bone resorption, and increased lumbar spine, total hip, and femoral neck BMD. At 6 months of treatment, EB613 2.5mg produced comparable total hip BMD increases as those that have been reported for Forteo® at 6 months.

In September and April 2025, the effects of EB613 on trabecular and cortical bone indices based on a 3D-Shaper DXA post-hoc analysis of Phase 2 results were presented at the American Society for Bone and Mineral Research (“ASBMR”) 2025 Annual Meeting and at the 2025 World Congress on Osteoporosis (WCO-IOF-ESCEO), respectively. The data using 3D-DXA modelling showed evidence of an early effect on both trabecular and cortical bone of the proximal femur. Mechanistically, the findings suggest that bone strengthening and fracture resistance may occur rapidly with EB613.

In October 2025, we reported clinical data from a post-hoc analysis of our Phase 2 trial of EB613 at the 2025 North American Menopause Society (NAMS) Annual Meeting in a poster presentation titled “EB613 (Oral PTH[1-34] Tablets) Increases BMD Over Six Months in Early Postmenopausal Women with Low Bone Mass or Osteoporosis: A Phase 2 Randomized Trial (P-66)”. In this analysis of the Phase 2 data, EB613 produced significant and consistent gains in BMD at the spine, femoral neck and hip in women within 10 years of menopause and in women more than 10 years post-menopause.

Since 2023, we have advanced a simplified formulation of EB613 that builds on clinical experience with the multi-tablet formulation which was used in Phase 1 and Phase 2 clinical studies. At the ASBMR Annual Meeting in September 2025, preclinical data for EB613 single tablet formulation from a cross-over pharmacokinetic mini-pig study was presented. This pre-clinical data showed comparable PK to the multiple tablet formulation of EB613. The preliminary results from the ongoing Phase 1b PK study (ENT-11-2023) demonstrate PK comparability between the multiple tablet formulation and the simplified single-tablet formulation of EB613 and Forteo®.

8

Regulatory Background

Initial approvals of drugs for the treatment of osteoporosis have historically required a placebo-controlled trial demonstrating reduction in the risk of fractures as the primary outcome measure in women with postmenopausal osteoporosis. The regulatory requirement for using fracture as the primary efficacy endpoint is challenging due to the patient types who would need to be studied: (1) very high risk patients may be randomized to placebo in a clinical trial, which poses an ethical concern; and (2) evaluation of moderate risk patients would require a very large sample size to evaluate treatment effectiveness. The last drug approval for osteoporosis occurred in 2019.

In the United States, the Foundation for the National Institute of Health-American Society for Bone and Mineral Research-Study to Advance BMD as a Regulatory Endpoint (FNIH-ASBMR-SABRE, previously known as the FNIH-Bone Quality Project [FNIH-BQP], hereinafter “SABRE”) was launched in 2013. This initiative was established as a public-private partnership with the FDA to study whether change in BMD at the lumbar spine, total hip or femoral neck in a placebo-controlled trial of an osteoporosis drug was predictive of vertebral, nonvertebral, hip and all clinical fracture risk reduction. SABRE aims to change the framework for how clinical trials of new anti-osteoporosis drugs are conducted and to promote innovation in the field of osteoporosis.

The FNIH-ASBMR-SABRE working group obtained treatment group-level and patient-level BMD and fracture incidence data from the sponsors of most of the approved osteoporosis drug treatments including individual patient data from 53 clinical trials covering 176,750 individuals across seven osteoporosis drug classes (Black et al., 2020; Eastell et al., 2022; Vilaca & Eastell, 2024). Based on a meta-regression analysis to assess the relationship between change in total hip BMD (active-placebo) and the anti-fracture effect in randomized clinical trials for each fracture type, the SABRE group demonstrated that treatment-related change in total hip BMD is best associated with fracture reduction.

Since the end of our Phase 2 Meeting in December 2021, we have engaged in FDA Type C, D, and A Meetings in 2022, 2023, 2024, and 2025 to obtain clarity and alignment on total hip BMD as a primary endpoint and an appropriate data package to support a new drug application (“NDA”) for EB613 under a 505(b)(2) application.

Following Type C and Type D meetings with the FDA in March 2023, we announced the FDA’s concurrence that a 2-year, placebo-controlled phase 3 (registrational) study with total hip BMD as primary endpoint could support an NDA for EB613; however the SABRE BMD endpoint remained unqualified as a surrogate endpoint by FDA at that time. On the same day, we announced that we planned to continue our dialogue with the FDA and await the final qualification of the SABRE qualification and FDA’s guidance on the statistical evaluation of our BMD endpoint before initiating a Phase 3 study for EB613.

In March 2024, the ASBMR announced that the FDA had communicated to the SABRE project team that a ruling to qualify the treatment-related change in BMD as a surrogate endpoint for fractures in future trials of new anti-osteoporosis drugs would be provided within 10 months.

In June 2025, as part of our scientific bridging, we received a written concurrence from the FDA that comprehensive nonclinical developmental and reproductive toxicity (DART) studies are not required given the totality of evidence generated from Forteo®, published literature, and EB613 nonclinical studies. In May 2025, we received a written concurrence from the FDA that dedicated oral carcinogenicity studies are not warranted for EB613 given the totality of evidence generated from the literature and nonclinical studies conducted with EB613.

In July 2025, we announced that, in a written response to a Type A meeting request, the FDA agreed that an NDA filing for EB613 could be supported by a phase 3 study in women with postmenopausal osteoporosis, where change in total hip BMD is evaluated as the primary endpoint, and incidence of new or worsening vertebral fractures is evaluated as the key secondary endpoint at 24 months.

In December 2025, the FDA released the Determination for Qualification of BMD qualifying total hip BMD as a surrogate efficacy endpoint for fracture that could be used in future studies of new anti-osteoporosis therapies. FDA’s suggested a context of use (COU): “The percentage change from baseline at 24 months in total hip bone mineral density (BMD) assessed by dual-energy X-ray absorptiometry (DXA) can be used as a validated surrogate endpoint for the assessment of investigational therapies for postmenopausal women with osteoporosis at risk for fracture.”

In February 2026, we submitted to the FDA a clinical amendment that included the EB613 Phase 3 protocol, statistical analysis plan and open-label extension synopsis. Our planned multinational, randomized, double-blind, placebo-controlled Phase 3 study is expected to enroll approximately 750 postmenopausal women with osteoporosis and will evaluate the percentage change in total hip BMD from baseline to month 12 as the primary endpoint. The double-blind, placebo-controlled 12-month Phase 3 study and the scientific bridge to the listed drug, Forteo®, are planned to be submitted in support of the NDA. We also plan to conduct an open label extension study under separate protocol in which participants on EB613 and placebo would be randomized to either EB613 for an additional 12 months, or transition to a standard anti-resorptive drug. The extension study is expected to provide safety and efficacy data for EB613 at 24 months as a monotherapy and evaluate the sequence of 12 months of EB613 treatment sequenced to a standard anti-resorptive drug for an additional 12 months.

9

EB612 (PTH) Hypoparathyroidism Program

Our product candidate, EB612, is being developed as the first oral PTH(1-34) tablet peptide replacement therapy for patients with hypoparathyroidism. The FDA and the EMA have granted EB612 orphan drug designation for the treatment of hypoparathyroidism. Hypoparathyroidism is a rare, heterogeneous, endocrine disorder that leads to abnormally low calcium and high phosphorus levels in the blood and requires chronic PTH replacement therapy. Today, the only approved PTH replacement treatment, YORVIPATH® (developed by Ascendis Pharma), requires patients to administer daily injections, while investigational candidates may require weekly injections.

Entera previously demonstrated proof-of-concept clinical data for its EB612 program using an unmodified oral PTH(1-34) analog in a 16-week Phase 2 study in patients with hypoparathyroidism (JBMR, 2021). The study showed significant reduction in calcium supplement use and maintenance of serum calcium levels above the lower limit for hypoparathyroidism (>7.5 mg/dL) throughout the study. However, the trial required a four-times-daily regimen with doses of up to 9mg daily.

In June 2024, Phase 1 clinical data for EB612 was presented at the Endocrine Society ENDO 2024 Annual Meeting. The safety, pharmacokinetic (PK) and pharmacodynamic (PD) data reported from a Phase 1 clinical study supported twice a day dosing of EB612.

In December 2025, we announced new in vivo PK/PD data supporting the development of a proprietary long-acting PTH (LA-PTH) analog, which is being developed as part of a material transfer and collaboration agreement with OPKO Biologics, Inc., a subsidiary of OPKO Health, Inc. (“OPKO”), utilizing our N-Tab® platform. Preclinical findings demonstrated a markedly prolonged plasma half-life and sustained elevation of serum calcium levels for more than three days following administration of a single oralThese data support the development of a once-daily oral PTH tablet for patients with hypoparathyroidism. Based on these data, in February 2026, we announced the expansion of our collaboration with OPKO to jointly advance this LA-PTH program. We intend to accelerate pre-IND development of this program and currently expect to submit an IND application to the FDA late 2026.

For additional information regarding our collaboration agreement with OPKO, see Item 7. Management’s Discussion and Analysis of Financial Condition and Results of Operations—Recent Developments—License and Collaboration Agreement with OPKO, contained in this Annual Report.

EB618 Program (Oral GLP-1/Glucagon)

In September 2023, we entered into a research collaboration agreement (the “2023 Collaboration Agreement”) with OPKO. Under the terms of this agreement, OPKO agreed to supply its proprietary Oxyntomodulin (OXM) analogs for the development of oral tablet candidates using our proprietary N-Tab® platform. Under this agreement, we and OPKO have each agreed to be responsible for specific phases of development of the two oral peptides to the point of demonstrated in vivo feasibility.

OXM is a naturally occurring GLP-1/Glucagon dual agonist peptide hormone found in the small intestine that acts to suppress appetite, induce weight loss and has additional cardioprotective and anti-fibrotic attributes. The program focuses on developing the first oral dual agonist GLP-1/Glucagon peptide as a potential once-daily tablet treatment for patients with obesity, metabolic and fibrotic disorders using the N-Tab® platform. Currently, there are no approved dual GLP-1/Glucagon agonists available. OPKO previously reported that weekly injections of pegylated OXM demonstrated significant weight loss and reduction in HbA1, triglyceride and cholesterol levels in 113 obese and diabetic patients in a Phase 2B study. The OXM agonist peptide (OPK-88006) is a GLP-1/Glucagon dual agonist peptide that has been modified to maintain its long-acting profile while increasing its potential potency.

In September 2024, we and OPKO jointly announced topline PK/PD results for the OXM program. Oral OXM exhibited significant systemic exposure across two in vivo models, a favorable PK profile and bioavailability. The high plasma concentrations with prolonged systemic exposure were consistent with the reported half-life for semaglutide (Rybelsus®), the only approved oral GLP-1 analog. Oral OXM showed a statistically significant reduction in plasma glucose levels compared with placebo.

10

Given the scarcity of oral peptide treatments and potential safety challenges attributed to small molecule approaches, we believe oral OXM may address a significant number of patients suffering from chronic metabolic diseases

In March 2025, we entered into a collaboration and license agreement (the “2025 Collaboration Agreement”) with OPKO to collaborate with respect to the preclinical and clinical development and decision making related to the Oral OXM program for the treatment of obesity, metabolic and fibrotic disorders in humans (the “Program”). The Program combines OPKO’s OPK-88006 analog and Entera’s proprietary N-Tab® platform.

Under the 2025 Collaboration Agreement, we granted to OPKO an exclusive, sublicensable and non-transferable, worldwide license to certain of our intellectual property and technology solely to develop, manufacture, and commercialize any GLP-1/Glucagon dual agonist as an oral treatment form for the treatment of obesity, metabolic, cardiovascular, and fibrotic disorders in humans, and OPKO has granted to us a non-exclusive, non-sublicensable and non-transferable license to certain of its intellectual property and technology to the extent necessary for us to perform our obligations in relation to the Program, in each case subject to certain exceptions.

Under the terms of the 2025 Collaboration Agreement, we and OPKO will retain 40% and 60%, respectively, of all proceeds deriving from the Program and will be responsible for 40% and 60% of the Program’s development costs, respectively. Following the completion of the Phase 1 stage, we may continue to fund our 40% share of the Program to maintain our right to proceeds or to opt-out (the “Opt-Out”). If we Opt-Out, then we and OPKO will retain 15% and 85%, respectively, of all proceeds deriving from the Program, while OPKO will be solely responsible for ongoing development and commercialization funding of the Program.

In June 2025, a poster at ENDO2025 reported PK data from a mini-pig study of oral OPK-88006 (EB618), which showed plasma levels consistent with those reported in humans for the highest subcutaneous dose of Wegovy™ (semaglutide) weekly injection, a standard of care for the treatment of obesity.

As of late 2025, OPKO is planning to initiate a single ascending dose (SAD) and multiple ascending dose (MAD) Phase 1 clinical study with the subcutaneous injection formulation of OXM, with data expected by the end of 2026. We plan to file an IND for the oral OXM tablet formulation thereafter.

Oral GLP-2

This program focuses on developing the first glucagon-like-peptide 2 (GLP-2) peptide tablet alternative for patients suffering from short bowel syndrome (SBS) and additional disorders involving mucosal inflammation and nutrient malabsorption. SBS is a rare and potentially life-threatening malabsorptive condition caused by a significant loss of functional bowel mass (secondary to congenital defects or disease-associated loss of absorption) or physical bowel mass (secondary to extensive intestinal resection). Approximately 30,000 patients across the United States and EU are living with SBS. SBS patients have a reduced ability to absorb nutrients and fluids and are at risk of malnutrition, unintended weight loss and additional symptoms due to the loss of essential vitamins and minerals. SBS is the most common cause of chronic intestinal failure, accounting for approximately 75% of chronic intestinal failure cases in adults and 50% of such events in children. Currently, the only approved GLP-2 agonist, which is marketed under the name Gattex® (teduglutide), requires daily sub-cutaneous injections. Zealand Pharma and Ironwood are developing long-acting GLP-2 therapies requiring once and twice weekly injections.

In May 2023, the results from our oral GLP-2 program were published in the International Journal of Peptide Research and Therapeutics, “Oral Delivery Technology Enabling Gastro-Mucosal Absorption of Glucagon-Like-Peptide-2 Analog (Teduglutide, Gattex®) - A Novel Approach for Injection-Free Treatment of Short Bowel Syndrome.” We believe GLP-2 represents a strong candidate for our N-Tab® platform and warrants further development as an injection-free alternative to patients suffering from SBS and other gastrointestinal disorders where GLP-2 plays a role.

In late 2023, Entera and OPKO completed a proof of concept single dose pharmacokinetic study in rodents. Oral GLP-2 tablets exhibited significant systemic exposure. Furthermore, plasma levels achieved with the oral tablet form of the GLP-2 analogue were approximately 10-fold higher than therapeutic plasma concentrations reported for subcutaneously administered teduglutide (Gattex® label). The pharmacokinetic analysis of the data obtained following the IV injections of the GLP-2 peptide showed the plasma half-life in rats to be approximately six times longer than the half-life reported for teduglutide in the same animal model. This data is consistent with previously reported PK data relating to OPKO’s GLP-2 peptide’s long-acting profile, which had initially been developed as a weekly subcutaneous injection.

11

In September 2025, pharmacokinetic data from a mini-pig study of OPK-8801003, our oral GLP-2 analog developed in collaboration with OPKO, were presented at the 47th European Society for Clinical Nutrition & Metabolism (ESPEN) Congress. The data demonstrated a plasma half-life of approximately 15 hours (approximately 18 time longer than teduglutide), which has a half-life of only 0.85 hours in the same species. Oral administration achieved peak plasma levels of ~200 ng/mL and maintained systemic exposure (AUC ≈ 2 h•μg/mL) for over 24 hours with low variability, supporting once-daily oral dosing.

Given the challenging compliance rates attributed to injectable GLP-2 therapy and heterogeneity of SBS patients, we believe a daily tablet format may address a significant unmet need in treating and titrating SBS patients more effectively than injectable alternatives.

Our Strategy

Our goal is to develop first-in-class oral peptides and protein replacement therapies for ignored, underserved, chronic medical conditions for which a tablet treatment has the potential to significantly shift a treatment paradigm. We are developing our product candidates to potentially become the first oral, single daily tablet peptide or protein replacement therapies designed to expand access for patients and healthcare practitioners. We aspire to continue to validate our platform across a variety of additional high value therapeutic proteins.

Our strategy to achieve these goals includes:

•
Advancing EB613, Potentially the First Oral Anabolic (Bone Building) Tablet, into Phase 3 for the Treatment of Osteoporosis: Building on our historical alignment with the FDA in July 2025 and the FDA’s 2025 broad qualification of BMD as a regulatory endpoint for anti-osteoporosis drugs, we submitted a clinical amendment to the FDA in February 2026, providing a streamlined Phase 3 protocol. We believe that EB613 may be the first osteoporosis program to be permitted by FDA to pursue a placebo controlled, BMD endpoint registrational Phase 3 study in support of an NDA. We view this potential outcome as a testament to the treatment gap and unmet need for a viable alternative for the millions of osteoporosis patients who, despite current guidelines and availability of highly efficacious injectable anabolic agents, remain undertreated. Entera currently retains global rights to EB613.

•
Advancing Potentially the First Oral LA-PTH Analog as a Once-Daily Tablet for Patients with Hypoparathyroidism as part of our Collaboration with OPKO: In 2015, we successfully completed a Phase 2a four-month trial in 19 patients with hypoparathyroidism, which demonstrated clinical benefit, including a statistically significant reduction in calcium supplementation, maintenance of calcium levels above the lower target level for Hypoparathyroidism patients (>7.5 mg/dL) throughout the study and statistically significant rapid decline in median serum phosphate levels two hours following the first dose, which was maintained for the duration of the study. The FDA and the European Medicines Agency (“EMA”) have granted EB612 orphan drug designation for the treatment of hypoparathyroidism. In 2025, we were testing the development of a proprietary LA-PTH analog utilizing our N-Tab® platform and preclinical findings demonstrated a markedly prolonged plasma half-life and sustained elevation of serum calcium levels for more than three days following administration of a single oral. These data support the development of a once-daily oral PTH tablet for patients with hypoparathyroidism. We currently expect to submit an IND application to the FDA in late 2026. We and OPKO each own 50% of the rights related to the LA-PTH hypoparathyroidism EB612 program. Our development expenses through Phase 1 are expected to be funded from the $8 million in proceeds received as part of OPKO’s equity investment in Entera in 2025.

•
Identifying and Developing Additional High Value Oral Peptides in Collaboration with Strategic Partners such as our Oxyntomodulin (Oral GLP-1/Glucagon) and Oral GLP-2 Programs: We intend to leverage our N-Tab® platform by applying it to the development of additional, proprietary peptides and therapeutic proteins. In collaboration with OPKO, we are currently focusing on the development of the first oral OXM, a dual targeted GLP1/glucagon peptide, in tablet form, for the treatment of metabolic disorders and have completed a proof of concept for an oral GLP-2 peptide tablet as an injection-free alternative for patients suffering from rare malabsorption conditions, such as short bowel syndrome. We and OPKO own 40% and 60%, respectively, of the rights related to the OXM EB618 program.

•
Establishing Select Global and Regional Development and Commercial Partnerships: Our N-Tab® platform and intellectual property are designed to generate a pipeline of product candidates across various therapeutic indications. We intend to explore opportunities to diversify and shorten the preclinical and clinical development of these candidates in a capital-efficient manner, including selectively pursuing research and clinical development partnerships with biopharmaceutical companies with specific domain expertise as well as with biopharmaceutical companies with proven commercial footprints to de-risk our late-stage programs.

12

PTH

Parathyroid hormone (PTH) is an 84-amino acid hormone that regulates calcium and phosphate homeostasis and bone metabolism in the body. The effects of PTH on bone depends on the duration of exposure. The physiological pulses help encourage bone turnover through activation of both osteoblasts and osteoclasts, the two main types of cells responsible for bone remodeling. In the absence of adequate parathyroid function producing these pulses, it is difficult for the body to regulate homeostatic processes, and osteoporosis may ensue. The synthetic analog of PTH, human parathyroid hormone (1-34) peptide, Forteo® (teriparatide), has been approved in the United States and the EU (Forsteo®) and has been a mainstay anabolic (bone forming) therapy for the treatment of osteoporosis patients since 2002 and 2003, respectively. Forteo® requires a daily subcutaneous injection.

EB613: Potentially the First Oral PTH(1-34) Anabolic Tablet Treatment for Post-Menopausal Women with Osteoporosis

EB613 is the first once daily PTH(1-34, teriparatide) tablet treatment and has the same amino acid sequence as Forteo® (teriparatide daily subcutaneous injection), a leading anabolic agent which has been marketed for 24 years and achieved peak annual sales of $1.7 billion prior to patent expiration in 2018.

Osteoporosis is a chronic, progressive disorder in which bone resorption exceeds formation, resulting in decreased bone strength and increased susceptibility to fracture. Postmenopausal women are at higher risk of developing osteoporosis-related fractures, particularly in the hip, spine, and wrist. The mechanism for low BMD in postmenopausal women is primary estrogen deficiency, which leads to accelerated bone loss, especially in the first five to ten years after menopause. The bone remodeling cycle can be separated into two distinct processes: (i) bone resorption, where cells called osteoclasts function in the resorption of mineralized tissue; and (ii) bone formation, where cells called osteoblasts are responsible for bone matrix synthesis and subsequent mineralization of the bone. In healthy individuals, bone resorptions matched by new bone formation. Osteoporosis develops as the balance between bone resorption by osteoclasts and bone formation by osteoblasts is not maintained, and not enough bone tissue is formed, leading to frail and fracture-prone bones.

Prevalence

The Bone Health & Osteoporosis Foundation estimates that approximately 10 million Americans have osteoporosis and that an additional 44 million have low bone mass. More than two million osteoporosis-related fractures occur annually in the United States, and more than 70% of these occur in women. In U.S. women 55 years of age and older, the hospitalization burden, including hospital costs of osteoporotic fractures, is greater than that of myocardial infarction, stroke, or breast cancer. Worldwide, osteoporosis affects an estimated 200 million women, according to the International Osteoporosis Foundation (the “IOF”) and causes more than 8.9 million fractures annually, which is equivalent to an osteoporotic fracture occurring approximately every three seconds. The IOF has estimated that 1.6 million hip fractures occur worldwide each year, and by 2050 this number could reach between 4 to 6 million. The IOF estimates that, in Europe alone, the annual cost of osteoporotic fractures could surpass €76 billion by 2050.

Current Osteoporosis Treatment Paradigm

The goal of pharmacological treatment of osteoporosis is to maintain or increase bone mass and strength and to prevent fractures throughout a patient’s life. It is critical to identify patients who have significant bone loss. Pharmacologic therapy is strongly recommended for patients with a BMD T-score of -2.5 or lower in the spine, femoral neck, total hip, or 1/3 radius.

13

Current osteoporosis drugs may be divided into two categories: antiresorptive and anabolic. Drugs that inhibit bone resorption (or bone degradation) include oral and injectable options such as estrogen (for postmenopausal women), oral and intravenous bisphosphonates, selective estrogen receptor modulators (SERMs), the RANK-ligand inhibitor (denosumab) and (salmon) calcitonin. According to the American Association of Clinical Endocrinology (AACE) 2020 Guidelines, injectable anabolic agents, such as teriparatide, abaloparatide or romosozumab, can be considered as an initial therapy for patients who are at very high fracture risk (which include women who have had multiple vertebral fractures or hip fractures and high-risk patients who have very low T-scores), and who have had an inadequate response to antiresorptive therapies. For patients undergoing treatment, stable or increasing BMD at the spine and hip indicates a satisfactory response. The three currently approved osteoanabolic drugs that stimulate bone formation all require daily or monthly subcutaneous injections: teriparatide (PTH(1-34)), Forteo®); abaloparatide (a PTH-related protein analog, Tymlos®)); and romosozumab (an antibody that inhibits sclerostin and also inhibits bone resorption, Evenity®). According to surveys with osteoporosis practitioners including primary care, gynecology, endocrinology and rheumatology, we estimate that less than 15% of currently treated osteoporosis patients agree to or have access to injectable osteoanabolic treatment despite guideline recommendations, their efficacy versus the anti-resorptive drugs and the approval of lower cost injectable generics.

There are currently no FDA-approved oral anabolic treatments for osteoporosis. EB613 is positioned to potentially be the first, once daily osteoanabolic tablet treatment for women with high-risk post-menopausal osteoporosis.

Phase 1 Safety, PK and PD Data for Oral PTH(1-34) Tablet Programs

We have completed a comprehensive nonclinical and clinical package for EB613, including three Phase 1 studies and three Phase 2 clinical studies. In the clinical development program, EB613 has been administered collectively to a total of 270 subjects in Phase 1 (n = 117) and Phase 2 (n = 153) studies. EB613 was well-tolerated, and no new drug-related adverse events (AEs) were identified in the Phase 1 and Phase 2 studies, at doses of up to 9 mg daily.

Across Phase 1 studies, the PK profile of EB613 has been characterized by a rapid increase in plasma PTH(1-34) levels, with peak concentrations of the drug observed within 30 minutes after dose and a rapid decline thereafter. The blood half-life of PTH(1-34) in humans is less than five minutes (see Forteo® USPI). Due to this very short elimination time and a short absorption phase, PTH(1-34) levels decrease below the limit of quantitation within two hours after drug administration. As a result, no drug accumulation is expected with once daily tablet dosing.

14

EB613 Phase 2 Study in Post-Menopausal Women with Low Bone Mass and Osteoporosis

This Phase 2 clinical trial of EB613 was a dose-ranging, placebo-controlled, double-blind study in 161 postmenopausal women with osteoporosis or low BMD conducted at four leading medical centers in Israel. The trial evaluated 0.5 mg to 2.5 mg daily tablets on BMD, pharmacodynamic bone markers, including P1NP and Osteocalcin-bone formation markers, CTX - a bone resorption marker, and various safety endpoints.

Safety

The most common drug-related AEs reported were headache, nausea, dizziness and presyncope. There were no treatment emergent hypercalcemia adverse events, and serial serum chemistry evaluations found no increase in mean calcium or changes in calcium exceeding predefined limits in patients treated with EB613 2.5 mg daily tablets.

There were no reported drug-related SAEs. All adverse events were mild or moderate in intensity.

15

Bone Biomarkers (PD Effect)

The primary bone biomarker endpoint of the Phase 2 clinical study—change in P1NP at Month 3—was met. Statistically significant increases were observed in P1NP (key anabolic marker) at Month 1 (p<0.001), Month 2 (p<0.005) and Month 3 (p<0.05) for the 2.5 mg EB613 dose group. Similar to the increase in P1NP, a significant increase in Osteocalcin was also observed in the 2.5 mg group after 3 months (P <0.01). A statistically significant decrease also occurred in Serum CTX (marker of resorption) from baseline to Month 6 (p<0.01). The decrease in bone resorption (CTX) resulting from EB613 daily tablets indicates a potential dual mechanism of action for EB613 with preferential stimulation of ostoblastic activity over osteoblastic activity.

Bone Mineral Density

Dose-related changes in BMD were also observed at the total hip (TH), femoral neck (FN) and lumbar spine (LS) locations with a linear regression showing a statistically significant dose response at all sites; TH (p=0.008), FN (p=0.001), and LS (p<0.0001).

Increases in TH (2.07%) and FN (2.92%) BMD in the 2.5 mg EB613 daily tablet titrated group were greater than those previously reported with Forteo® at six months (0.1% and 0.3%) (Leder, 2015).

At 6 months of treatment, EB613 2.5mg produced comparable total hip BMD increases as those that have been reported for Forteo® at 6 months.

16

Furthermore, in a post hoc analysis using FDA-approved 3D-DXA, EB613 showed early effects on both trabecular and cortical bone of the proximal femur. The outcomes were comparable with those reported for Forteo and Tymlos on cortical bone indices at 6 months.

EB612: First Oral Long-Acting PTH(1-34) Peptide Tablet for the Treatment of Hypoparathyroidism

Hypoparathyroidism is a rare condition in which the body either fails to produce sufficient PTH or the PTH produced lacks normal biologic activity. Individuals with a deficiency of parathyroid hormone may exhibit hypocalcemia and hyperphosphatemia. Hypocalcemia can cause weakness, muscle cramps, excessive nervousness, headaches and uncontrollable twitching and tetany. Hyperphosphatemia can result in soft tissue calcium deposition, which may lead to severe issues, including damage to the circulatory and central nervous systems. In contrast to osteoporosis, longer persistence of PTH in plasma is a desirable property for the treatment of hypoparathyroidism. Here, hormone replacement therapy is warranted.

17

Prevalence

It is estimated that hypoparathyroidism affects approximately 200,000 people across the United States, the European Union and Japan, with approximately 43% of cases characterized as mild, 39% characterized as moderate, and 18% characterized as severe.

Limitations of current treatments for hypoparathyroidism

Historically, the treatments for hypoparathyroidism have been calcium supplements, vitamin D supplements and phosphate binders. Although calcium and vitamin D can help alleviate hypocalcemia, their chronic use can result in many serious side effects.

An injectable form of full length human PTH (1-84) marketed under the name Natpara®, was approved for the treatment of hypoparathyroidism in 2015. However, it was recalled in 2019 due to a plastic particulate and was permanently phased out globally at the end of 2024. TransCon PTH, once-daily injectable, long-acting prodrug of parathyroid hormone (PTH(1-34)) developed by Ascendis Pharma A/S was FDA Approved in August 2023 and EU Approved in November 2023. Eneboparatide, once-daily injectable long-acting parathyroid hormone 1 (PTH1) receptor agonist, developed by Amolyt Pharma (acquired by AstraZeneca 2024) reported topline data that the primary endpoint for its Phase 3 study was met in March 2025. A long acting once weekly injectable PTH peptide prodrug (MBX2109) developed by MBX Biosciences, Inc. reported positive Phase 2 topline data in 2025. Finally, oral small molecule PTHR1 5(SEP786) developed by Septerna Inc, discontinued a Phase I trial in February 2025 due to safety and is expected to advance another small molecule into Phase 1 in 2026.

EB612

Our current product candidate for hypoparathyroidism, EB612, is the first oral long acting PTH(1-34) hormone replacement treatment developed in a tablet form. We believe that EB612 may have inherent advantages as compared to injectable and small molecule approaches in terms of potential superior safety and flexibility to provide more individualized treatment in this heterogeneous disease.

18

Phase 2a Clinical Trial

In 2015, we successfully completed a multicenter Phase 2a clinical trial of an older, multitablet formulation of EB612 in hypoparathyroidism patients. This study demonstrated the safety and tolerability of EB612 administered four times daily for 16 weeks to patients with hypoparathyroidism. In this study, patients were titrated up to a maximum of 12 EB612 0.75 mg tablets a day (total daily dose of 9 mg) according to each subject’s albumin-adjusted serum calcium (ACa), and supplement treatment regimen. Of the 19 enrolled patients, 17 completed the trial. No drug-related serious adverse events were reported and most of the adverse events were not considered study drug-related. The study achieved its primary and secondary endpoints, including a reduction in calcium supplements, reductions in serum phosphate and 24-hour urine calcium excretion, maintenance of ACa within the reference range, and an improvement in quality of life.

Planned Additional Clinical Development and Regulatory Pathway

We have since developed a new generation of EB612 based on new intellectual property of our N-Tab® platform, which we have designed to optimize its PK profile and the potential for reduced daily dosing. We initiated a PK study in May 2023, which tested various potential drug candidates based on our new platform, including several which could be developed for the treatment of hypoparathyroidism. In April 2024, we submitted pharmacokinetic (PK) and early PD Data from a Phase 1 study evaluating an unmodified PTH(1-34) peptide and a new generation of Entera’s N-Tab® platform to the Endocrine Society Annual Meeting (ENDO 2024). In June 2024, we presented Phase 1 clinical data at the ENDO 2024 Annual Meeting, supporting a BID (twice-daily) tablet dose to Phase 2 development in patients with hypoparathyroidism.

In December 2025, we announced new in vivo PK/PD data supporting the development of a proprietary LA-PTH analog utilizing our N-Tab® platform in partnership with OPKO. Preclinical findings demonstrated a markedly prolonged plasma half-life and sustained elevation of serum calcium levels for more than three days following administration of a single oral tablet, in contrast to unmodified PTH(1-34) controls, which showed no calcium response. These data support the development of a once-daily oral PTH tablet for patients with hypoparathyroidism.

Intellectual Property

Our success depends in part on our ability to protect the proprietary nature of our product candidates, technology, and know-how; operate without infringing on the proprietary rights of others and preventing others from infringing on our proprietary rights. We seek to protect our proprietary position by, among other methods, seeking patent protection in the United States and in certain other jurisdictions for our product candidates and other technology that we consider important to the development of our business, where such protection is available. We believe that our success will depend in part on our ability to obtain patent protection for our intellectual property. We also intend to rely on trade secret protection, know-how and the exploitation of in-licensing opportunities to develop our proprietary position.

19

Patent Rights

As of March 23, 2026, our global patent portfolio included issued patents and patent applications. We believe that the granted patents as well as certain of the pending claims contained in our patent applications, if issued in substantially the same form, would cover our proprietary platform (N-Tab®) and the candidates used in various pipeline programs as indicated in the table below.

In addition, during 2025 we further strengthened the patent protection for our EB612 and GLP1/Glucagon product candidates through the in-licensing of composition-of-matter patent applications from OPKO. The composition-of-matter patent applications relating to EB612 and GLP1/Glucagon are expected to expire in 2046 and 2045, respectively, not considering any patent term extensions that may be obtained.

Subject Mater

# Pending Applications

# Issued Patents

Geographical Scope

Nominal Patent Term

EB613

79

51

United States, Europe, Japan, China, Canada, Singapore, United Arab Emirates, Israel, Brazil, Mexico, South Africa, India, Australia, New Zealand, Russia, South Korea and Hong Kong

2029 - 2044

EB612

73

44

United States, Europe, Japan, China, Canada, Singapore, United Arab Emirates, Israel, Brazil, Mexico, South Africa, India, Australia, New Zealand, Russia, South Korea and Hong Kong

2029 - 2044

GLP-1/Glucagon

58

8

United States, Europe, Japan, China, Canada, Singapore, United Arab Emirates, Israel, Brazil, Mexico, South Africa, India, Australia, New Zealand, Russia, South Korea and Hong Kong

2036 - 2044

GLP-2

57

8

United States, Europe, Japan, China, Canada, Singapore, United Arab Emirates, Israel, Brazil, Mexico, South Africa, India, Australia, New Zealand, Russia, South Korea and Hong Kong

2036 - 2044

Platform

(N-Tab®)

131

56

United States, Europe, Japan, China, Canada, Singapore, United Arab Emirates, Israel, Brazil, Mexico, South Africa, India, Australia, New Zealand, Russia, South Korea and Hong Kong

2029 - 2044

Issued patents and any patent that may issue from the pending patent applications are currently expected to expire by the Nominal Patent Term as noted in the above table, assuming national phase filings are timely effected. The nominal patent term does not include potential patent term extension and/or patent term adjustment when applicable.

The term of individual patents depends upon the legal term for patents in the countries in which they are granted. In most countries, including the United States, the patent term is generally 20 years from the earliest claimed filing date of a non-provisional patent application in the applicable country. In the United States, a patent’s term may, in certain cases, be lengthened by patent term adjustment, which compensates a patentee for administrative delays by the United States Patent and Trademark Office, or USPTO, in examining and granting a patent or may be shortened if a patent is terminally disclaimed over a commonly owned patent or a patent naming a common inventor and having an earlier expiration date. The Drug Price Competition and Patent Term Restoration Act, or the Hatch-Waxman Act, permits a patent term extension of up to five years beyond the expiration date of a U.S. patent as partial compensation for the useful patent term lost, if any, during the FDA regulatory review process. However, a patent term extension cannot extend the remaining term of a patent beyond a total of 14 years from the date of the product’s approval by the FDA. The patent term extension period is generally one-half the time between the effective date of the IND and the submission date of the NDA for the product, plus the time between the submission date of the NDA and the approval of the application. Only one patent applicable to an approved drug is eligible for the extension and the application for the extension must be submitted within 60 days of regulatory approval of the approved drug and prior to the expiration of the patent. Only those claims covering the approved drug, a method for using it or a method for manufacturing it may be extended. Moreover, we may not receive an extension because of, for example, failing to apply within applicable deadlines, failing to apply prior to expiration of relevant patents or otherwise failing to satisfy applicable requirements. Similar provisions are available in the EU and certain other foreign jurisdictions to extend the term of a patent that covers an approved drug. However, the length of any extension, if granted, could be less than we request. In December 2025 an opposition was filed by an anonymous entity against our European patent EP3256113 ('113 patent). The granted claims of the '113 patent are directed to an old-generation product that is not currently under development.

20

Trade Secrets

In addition to patent rights, we also rely on unpatented trade secrets and know-how to protect our proprietary technology. However, trade secrets can be difficult to protect. We seek to protect our proprietary technology, in part, by entering into confidentiality agreements with our employees, consultants, contractors, manufacturers, outside scientific collaborators and sponsored researchers, members of our board of directors (the “Board”), technical review board and other advisors upon their engagement. These agreements generally provide that all confidential information developed or made known to the individual during the individual’s relationship with us is to be kept confidential and not to be disclosed to third parties except in specific limited circumstances. We also generally require signed confidentiality or material transfer agreements from any company that is to receive our confidential information. In the case of employees, consultants, and contractors, the agreements also generally provide that all inventions conceived by the individual while rendering services to us shall be assigned to us as our exclusive property. There can be no assurance, however, that we have entered into agreements with all applicable parties, that all persons who we desire to sign such agreements will sign, or if they do, that such agreements will not be breached, that we would have adequate remedies for any breach, or that our unpatented trade secrets or know-how will not otherwise become known or be independently developed by competitors. Additionally, to the extent that our commercial partners, collaborators, employees, and consultants use intellectual property owned by others in their work for us, disputes may arise as to the rights in related or resulting know-how and inventions. For this and a more comprehensive discussion of risks related to our intellectual property, see “