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Item 1. Business

2025-03-11 compared with 2024-03-08 · 364 added, 401 removed, 263 unchanged (74% of the section changed)

Ovid is a biopharmaceutical company that is dedicated to meaningfully improving the lives of people affected by certain epilepsies and brain conditions with seizure symptoms.

We believe that addressing these disorders represents a substantial scientific, medical and commercial opportunity.

Over the last decade, scientific understanding of the underlying biology of neuronal hyperexcitability and the related pathophysiology of epilepsy and many neurological disorders has improved.

This understanding of disease, coupled with advances in preclinical research tools, is improving the predictive potential of translational research, and thereby, may increase the probability of successful clinical development of anti-seizure medicines (“ASMs”).

Emerging science also indicates that addressing the underlying causes of hyperexcitability may have therapeutic applications in broad neurological disease well beyond epilepsy.

The large global epilepsy market opportunity reflects significant unmet medical need and economic potential.

Epilepsy therapeutics today represent an approximately $8 billion market globally.

Evidence supporting the opportunity includes the number of recent acquisitions of epilepsy assets and companies, several of which have been acquired for values greater than $1.0 billion.

The unmet need of people affected by seizures remains significant.

Approximately three million Americans live with epilepsies today and approximately 50 million people suffer from epilepsy worldwide.

We have proven capabilities and expertise in the successful clinical development of ASMs.

We have applied our knowledge to build a differentiated pipeline of medicines with potential first-in-class or best-in-class drug mechanisms of action (“MoA”) to treat epilepsies and brain disorders with seizure symptoms.

Our pipeline has produced three programs with potential first-in-class MoAs, and one program with a potential best-in-class MoA.

Currently, three of these programs are in clinical trials in humans.

The fourth is in preclinical studies and is anticipated to advance into human safety studies in 2024.

An overview of these programs includes:

• Soticlestat , a novel cholesterol 24 hydroxylase (“CH24”) inhibitor, which is currently being evaluated in two pivotal Phase 3 trials for Dravet syndrome and Lennox-Gastaut syndrome by Takeda Company Limited (“Takeda”).

Takeda purchased our rights to soticlestat, and is conducting the pivotal trials.

We maintain a significant financial interest in the potential approval and commercialization of soticlestat via potential regulatory and commercial milestones of up to $660.0 million and net sales-based royalty payments from low double digits up to 20%.

We sold a 13% stake in the royalty, regulatory and commercial milestone payments that we are eligible to receive from Takeda to Ligand Pharmaceuticals Incorporated for $30.0 million.

• OV888 (GV101), a highly selective inhibitor of rho associated coiled-coil containing protein kinase 2 (“ROCK2”), which is being developed as a potential first-in-class medicine to treat cerebral cavernous malformations (“CCM”), of which seizures are among common symptoms.

OV888 (GV101) is completing a Phase 1 double-blind, multiple-ascending dose trial and is expected to initiate its Phase 2 program in 2024.

A higher dose cohort has been added to the Phase 1 trial and no serious adverse events have been observed.

• OV329 , a highly potent next-generation GABA-aminotransferase inhibitor (“GABA-AT”), that is thought to potentially deliver preferable seizure reduction and dosing relative to prior medicines in the class.

An oral formulation of OV329 is currently being evaluated in a Phase 1 study that uses biomarkers for efficacy and target engagement.

An intravenous formulation of OV329 is also in development for acute seizures and is expected to enter human safety studies in 2025.

• OV350 , a potential first-in-class direct activator of the central nervous system (“CNS”), specific K-Cl co-transporter (“KCC2”) and is the most advanced of a unique portfolio of drugs leads which are direct KCC2 activator compounds.

Oral and intravenous (“IV”) formulations of several of these compounds have been prepared and have demonstrated activity in multiple preclinical disease models.

We expect to file the first investigational new drug application (“IND”) from this portfolio in 2024.

We believe this portfolio has the potential to deliver multiple INDs over the years to come.

Collectively, these development programs are anticipated to create a range of value-creating milestones in the near- and mid-term for investors.

The Opportunity:

Epilepsies and Neurological Disorders

Although it is one of the earliest known maladies documented by humanity four millennia ago, epilepsy remains a common, and often intractable, medical diagnosis.

Approximately 50 million people globally experience epilepsy, including an estimated three million adults living with epilepsy in the United States.

While modern drug discovery efforts have produced more than 30 ASMs over the last 100 years, a substantial number of epilepsy patients continue to experience breakthrough seizures that can cause enduring damage to the brain.

Individuals who suffer from rare forms of refractory epilepsies may experience persistent seizure rates ranging from 50 - 90%.

The seizures they suffer can have a devastating impact both upon patients and their families, by triggering permanent motor, cognitive and developmental delays, as well as epileptogenesis, which is a cascade of seizures begetting more seizures.

Some patients with developmental epileptic encephalopathies experience even greater rates of refractory seizures that are resistant to drug therapy.

With an estimated 70% of epilepsy diagnoses occurring in people less than 20 years of age, the need to treat seizures early and effectively is critical to mitigate worsening and permanent later-life disabilities.

Ovid is a biopharmaceutical company that is dedicated to developing small molecule medicines for brain conditions with significant unmet need.

These potential medicines targeting the central nervous system (“CNS”) are designed to potentially halt the course of brain disease by quelling neural hyper-excitation and alleviating the most impactful patient symptoms.

We seek to address fundamental biological targets in the brain that are implicated in neuronal hyperexcitability, such as neurotransmitters and dysregulated ion channels.

By mitigating excessive neuronal hyper-excitation with differentiated medicines, we believe we can unlock substantial scientific, therapeutic and commercial opportunities across a range of neurological and psychiatric conditions that have few therapeutic options today, both impacting patients’ lives and creating long-term stockholder value.

Over the last decade, scientific understanding of the underlying biology of neuronal hyperexcitability and the related pathophysiology of epilepsies, psychoses, and other brain conditions has significantly advanced.

Today, the underpinnings of many monogenic epilepsies and seizure disorders are becoming better understood and can be linked to mutations in specific molecular transporters, ion channels and receptors.

Additionally, science is beginning to illuminate the systemic and damaging effects of over-excitation on neural networks, including its relationship to cell inflammation, stress, and apoptosis.

This improved understanding of the genesis and pathophysiology of disease, coupled with advances in preclinical research tools, is enhancing the predictive potential of translational research, and is thereby improving the probability of successful clinical development of CNS medicines.

Additionally, emerging scientific evidence suggests that hyperexcitability of neurons is implicated in a broad range of conditions well beyond seizures and psychoses.

Therefore, ameliorating excessive neural hyperexcitability may offer therapeutic relevance and applications in a broad array of brain disorders, including certain psychiatric, neurodegenerative and neurodevelopmental conditions, and other brain traumas.

Despite the scientific advances mentioned above, the unmet need for people living with seizures, epilepsies, and psychiatric diseases remains significant.

Relatively few therapeutics targeting new mechanisms of action (“MoAs”) have been approved in recent decades, and most patients are not ‘cured’ of these conditions.

Therefore, the need and opportunity for medicines that act upon fundamental biological targets that impact neuronal excitatory/inhibitory balance remain substantial.

Our vision and focus

Our vision is to create sustained, long-term value by advancing a differentiated pipeline of precision, small molecule medicines intended to culminate in a fully integrated neurotherapeutics company with multiple clinical-stage programs and commercial medicines.

We believe the lack of new classes of medicine in neurology and neuropsychiatry represents both an unmet need and a significant opportunity.

Through our research and development (“R&D”) and business development strategies, we have in-licensed and clinically developed potential medicines that may offer first-in-class or best-in-class MoAs.

Our programs are intended to act upon fundamental biological targets associated with neuronal hyperexcitability in a mechanistically precise fashion.

It is our intent to eventually market a franchise of unique medicines that mitigate patient symptoms such as seizures and psychoses, that stem from hyper-excited neurons.

Over time, our efforts have resulted in four clinical-stage drug development programs, including two programs that have advanced to late-stage trials.

Our current clinical programs are indicated for the potential treatment of drug-resistant epilepsies (“DRE”) and psychosis associated with neuronal-synuclein diseases (“NSD”), which includes Parkinson’s disease, and Lewy body dementia (“LBD”).

Several preclinical programs are anticipated to be advanced for other forms of psychosis and mood disorders.

Importantly, we seek to develop medical therapies that are more efficacious and/or have ‘gentler’ profiles for patients, meaning drugs that are intended to deliver preferable safety and tolerability profiles relative to approved drugs.

Improved product profiles in neurology and psychiatry are needed, given that many patients require polypharmacy regimens that create cumulative tolerability issues and drug-drug interactions, significantly impacting quality of life and adherence to therapy.

Our near-term strategy is focused on clinical advancement of potential small molecule medicines to treat specific epilepsies and psychoses that are manifestations of neural excitatory/inhibitory imbalance.

This cohesive scientific focus,

reinforced by our deep professional experience and pipeline of differentiated assets, gives us confidence that we can succeed in our mission.

Additionally, we seek to create stockholder value by creating multiple sources of potential revenue via clinical and commercial milestones from our pipeline, strategic collaborations and partnerships.

Unmet need and opportunity

While seizures and forms of psychosis are some of the earliest maladies documented by humanity, they remain common, and often intractable, medical conditions.

The global epilepsy and psychosis market opportunities reflect massive medical need and economic potential.

Epilepsy and antipsychotic pharmacologic therapies respectively represent approximately $8 billion and $22 billion markets globally and are expected to grow.

Reinforcing the scale of the commercial opportunity is the number and size of recent acquisitions of epilepsy and psychiatric medicines companies, which have been acquired for values ranging from $2.6 billion to $14.6 billion.

Moreover, the regulatory environment appears increasingly amenable to new approaches in epilepsy and psychiatric conditions.

For example, the U.S.

Food and Drug Administration (“FDA”) has encouraged developers to seek “basket labels” for single therapeutic agents that cover more than one underlying disease, such as developmental epileptic encephalopathies (“DEEs”).

For the first time in 50 years, a therapeutic with a novel MoA was approved in schizophrenia in 2024.

The unmet need of people affected by seizures and psychosis is substantial.

Today, managing patient symptoms commonly requires chronic drug therapy, which is not curative, and may not treat the whole disease.

Unmet need in epilepsy

Approximately 50 million people globally live with epilepsy, including an estimated three million adults and half a million children in the United States.

While modern drug discovery efforts have produced more than 30 anti-seizure medications (“ASMs”) over the last 100 years, a substantial number of epilepsy patients continue to experience breakthrough seizures that can cause enduring damage to the brain.

Individuals who suffer from rare forms of epilepsies may experience persistent refractory seizures, with rates ranging from 50% to 90%.

The seizures they suffer can have a devastating impact both upon patients and their families, by triggering permanent motor, cognitive and developmental delays.

Some patients with DEEs experience even greater rates of refractory seizures that are resistant to drug therapy.

With an estimated 70% of epilepsy diagnoses occurring in people younger than 20 years of age, the need to treat seizures early and effectively is critical to mitigate worsening and permanent later-life disabilities.

In the search for seizure control, approximately half of patients take a polypharmacy regimen of five or more ASMs, requiring careful management of drug side effects and interactions.

The large population of patients requiring multiple drug therapies to control seizures, and persistent rates of breakthrough seizures, signal the urgent need for effective new medicines.

For these patients, new mechanisms of action that demonstrate improved efficacy, safety and tolerability profiles are optimal, as they may be more easily incorporated into existing treatment regimens without the fear of drug-to-drug interactions (“DDIs”).

Scientific progress, including the availability of genetic testing, improved radiographic scanning tools, and more accurate means of measuring non-seizure symptoms are illuminating the underpinning seizure disorders.

The great unmet medical need and scientific advancements have set the stage for a potential era of neurotherapeutics, which we believe will be led by ASMs.

The Ovid Strategy

For these patients, MoAs that demonstrate improved efficacy, safety and tolerability profiles are optimal, as they may be more easily incorporated into existing treatment regimens.

Unmet need in psychosis and mood disorders

While Ovid’s potassium chloride cotransporter 2 (“KCC2”) portfolio has potential applications across a range of psychoses and mood disorders, our focus for our first two programs is psychosis among people with NSD and LBD.

These populations share a common pathological link, which is intraneuronal accumulation of alpha synuclein, which leads to neurodegeneration.

Today, there are more than 4.3 million people globally living with psychosis associated with NSD and LBD.

In the United States LBD is the second most common dementia (psychoses affect 80% of the LBD population), affecting 1.5 million Americans (80% of the diagnosed dementia patients), and NSD impacts another one million Americans.

These progressive clinical syndromes are characterized clinically by movement disorders, cognitive impairment, sleep dysregulation, and autonomic instability.

Changes in perception are common, manifesting in visual illusions, misperceptions of visual stimuli and hallucinations, which can create health risks to patients and caregivers.

These conditions lead to high morbidity, mortality and healthcare costs.

Psychosis in these populations is also a high risk factor for hospitalization and nursing home placement.

Atypical antipsychotics are contraindicated for NSD and

LBD as they worsen motor features, their anti-dopaminergic pharmacology is untenable in Parkinson’s disease, and many carry a black box warning for mortality.

The current standard of care for psychosis related to Parkinson’s disease is Nuplazid® (pimavanserin), to which only a small proportion of patients fully respond.

Differentiated potential first-in-class or best-in-class programs

The science underlying the discovery and development of new drugs for the brain has changed fundamentally over the last decade.

We believe that major developments in the understanding of the biology of these diseases means that key areas of unmet need, including many epilepsies and seizure disorders, are now addressable and offer significant medical potential.

Our team has proven expertise in understanding MoAs that underlie seizures and shaping potential therapies to treat rare epilepsies and disorders with seizures.

Specifically, we have built a pipeline focused on treating the extrinsic or intrinsic causes of neuronal hyperexcitability.

This know-how affords us an ability to build Ovid in a manner focused on delivering successive, novel medicines for epilepsies and seizure-related neurological conditions.

Our strategy is to create sustainable, long-term value by advancing an exciting and differentiated pipeline of small molecules that culminates in a fully integrated neurotherapeutics company with multiple commercial medicines and clinical stage programs.

Over time, we intend to seek to expand our current pipeline of predominantly ASMs to include additional franchises of neurology programs via focused clinical development and business development activities.

This corporate strategy is underpinned by specific research and development, financial and business development strategies.

In addition, our Company seeks to protect shareholder value by creating multiple sources of potential revenue via clinical and commercial milestones from our pipeline, strategic collaborations and partnerships.

Our approach to building an epilepsy franchise has already resulted in success, namely the development and subsequent repurchase of our rights to soticlestat by Takeda.

In 2017, we in-licensed a 50% stake in soticlestat for $26.0 million, and further invested $57.0 million in designing and executing soticlestat’s early and mid-stage clinical trials.

In 2021, following encouraging Phase 2 findings, which we delivered six months ahead of schedule, we entered into a Royalty, License and Termination Agreement (“RLT Agreement”) through which we sold back our rights to soticlestat to Takeda.

The RLT Agreement provided us with $196.0 million paid in Q1 2021 and, if soticlestat is approved and successfully commercialized, we are eligible to receive up to $660.0 million in sales and regulatory milestone payments and low double-digits up to 20% of potential net sales-based tiered royalty payments.

The RLT Agreement provides us with a potential stream of non-dilutive capital.

The funds received from this transaction have enabled us to invest in and secure what we believe is a world-leading pipeline during a period when we believe the cost of capital would have been unduly expensive.

In 2023, we sold a 13% stake in the royalty, regulatory and commercial milestone payments that we are eligible to receive under the RLT Agreement to Ligand Pharmaceuticals Incorporated (“Ligand”) for $30.0 million.

Our near-term strategy is focused on building a franchise of potential small molecule medicines to treat certain epilepsies and conditions with seizure symptoms.

In alignment with this focus, in 2023, we made the decision to both out-

license and halt certain non-core activities, including several preclinical genetic medicines programs.

For additional information see the section below under the heading “Genetic Research Programs.” We simultaneously streamlined our organization and reduced headcount related mostly to the genetic programs.

Expert Team and Fit-for-Purpose Infrastructure

We have built a highly specialized, efficient, and focused infrastructure that supports us in our chosen area of neurotherapeutics development.

This infrastructure spans the critical domains of research and development, commercial and market access strategy.

Importantly, it positions us to be a potential partner of choice for leading biopharmaceutical companies who wish to pursue valuable drug candidates and research platforms in neurology.

We have recruited a team of professionals with deep subject-matter expertise in seizures and neurological conditions.

This includes epileptologists, physicians, academic scientists, commercial and biopharmaceutical industry leaders.

In total, we have five individuals with M.D.

degrees and 13 professionals with Ph.D.

degrees specializing in the sciences.

Our operational and commercial leaders have extensive experience fostering market access and sales for leading neurological medicines.

In total, our team’s collective professional experience has involved the successful development or commercial launch of more than 25 CNS medicines, including several epilepsy products.

Our cohesive focus in epilepsies and conditions with seizure symptoms, clear strategy reinforced by our professional experience and pipeline of differentiated assets, gives us confidence we can succeed in our mission.

Research & Development Strategy:

Potential First-In-Class or Best-in-Class Mechanism of Action

Our research and development strategy is focused on designing medicines that can ameliorate neuronal hyperexcitability and return neurons to a state of homeostasis, or “electrophysiological balance.” Many factors can contribute to neuronal hyperexcitability including those extrinsic to the cell such as anatomical abnormalities, trauma, and even infectious disease.

Other factors are intrinsic to the neuron (for example, genetic conditions or the disruption of neuronal metabolism) and others (for example lack of stimulus of the GABA receptor) are caused by imbalances outside the surface of the neuron.

Whatever its origin, imbalance of electrophysiological homeostasis and resultant neuronal hyperexcitability manifests in a range of debilitating neurological conditions, including seizures and epilepsies.

Treatment of epilepsy and seizures today often requires multiple medicines.

Whereas some epilepsy developers expressly focus on one biological target, we believe that until a definitive cure for epilepsy is discovered, multiple MoAs will be needed to successfully treat the heterogeneous causes of seizures.

Accordingly, our pipeline seeks to curate and develop a unique set of compounds that can be effective by itself and/or can provide the necessary intervention to impact multiple mechanisms.

We believe this approach has the potential to provide the basis of a modern differentiated and leading epilepsy franchise.

We believe that major developments in the understanding of the biology of these diseases now make it possible to address key areas of unmet need, including many neurological and psychiatric disorders, offering significant therapeutic potential.

We are specifically cultivating a pipeline of potential first-in-class or potential best-in-class MoAs to treat the underlying causes of neuronal imbalance which can lead to manifestations such as seizures, psychosis, pain and other mood disorders.

Collectively, our differentiated pipeline has produced multiple potential value-creating drug programs.

Several of these therapeutic development programs — OV329, OV350 and OV888 (GV101) — aim to affect signaling and enzymatic pathways and vascular structures that modulate hyperexcitability of neurons.

Through our scientific expertise and strategic business development, we have performed translational research and in-licensed compounds to build a robust development pipeline of potential medicines, including:

• OV329, a highly potent next-generation GABA-aminotransferase inhibitor (“GABA-AT”).

OV329 is intended to deliver preferable seizure reduction, safety profile and dosing relative to prior medicines in the class, which have known safety challenges.

OV329 is an oral therapy intended to optimally regulate GAB

• A, the inhibitory neurotransmitter.

OV329 is nearing completion of a Phase 1 study that is evaluating safety, tolerability, and pharmacokinetics (“PK”), as well as evaluating biomarkers that offer insight into target engagement, pharmacodynamic (“PD”), and clinical effects.

To date safety data of OV329 in healthy subjects has been well-tolerated with no serious adverse events reported.

Initial biomarker data from the most recent multiple-ascending dose cohort suggest encouraging directional signs of target engagement and clinical effects as measured by MRS and TMS.

These indicate signs of increased GABAergic activity consistent with the intended mechanism of action by inhibiting GABA-aminotransferase.

• KCC2 library is a portfolio of potential first-in-class direct activators of potassium chloride cotransporter2.

KCC2 is a fundamental biological target, solely expressed in the CNS, that enables synaptic inhibition.

KCC2 dysregulation has been implicated in a broad range of neuropathologies.

We are actively advancing up to four unique drug development programs that emerged from our KCC2 direct activator library containing more than 100 molecules.

These include OV350 (intravenous injection), OV4071 (oral and intramuscular injection), OV4041 (oral) and another undisclosed molecule.

Each program has potential distinct therapeutic and potency characteristics as demonstrated in varying phenotypic screens and animal disease models, reflecting multiple therapeutic opportunities and optionality for co-development.

The portfolio is being evaluated for a range of therapeutic indications, that have symptoms associated with psychoses or mood disorders.

◦ OV350, a first-in-human KCC2 direct activator.

OV350 is the most advanced program in the KCC2 library and is expected to be the first direct activator dosed in humans.

We filed for regulatory approval and initiated a Phase 1 study of OV350 among healthy volunteers in Australia.

We intend to study the safety, tolerability and PK of this potential first-in-class program, which will deliver important insights to the oral KCC2 program.

Both OV350 and OV4071 are intended for the potential treatment of psychosis associated with NSD and LBD.

• OV888 (GV101), a highly selective inhibitor of rho-associated coiled-coil containing protein kinase 2 (“ROCK2”).

OV888 (GV101) is a potential first-in-class medicine to treat cerebral cavernous malformations (“CCM”), a condition in which seizures are a common symptom.

OV888 (GV101) has completed two Phase 1 double-blind, multiple-ascending dose trials with no serious adverse events reported.

OV888 (GV101) was tested at doses of 100 mg, 200 mg and 600 mg and was well-tolerated at all doses.

Headaches were the most common adverse event, reported in 23% of participants, which resolved in all patients.

Signs of target engagement and a PD response were detected using biomarkers of IL-17 and IL-21 at the intended clinical dose.

OV888 (GV101) is ready to be dosed in a Phase 2 study in patients with CCM, but we have paused initiation to evaluate emerging data from competitor and academic studies in CCM.

Collectively, these development programs are expected to generate a range of value-creating milestones for investors in the near- and mid-term.

R&D strategy:

Differentiated MoAs to precisely target the causes of neural hyperexcitability

Our R&D strategy is dedicated to designing medicines that can ameliorate excessive neuronal excitation and return neurons to a state of homeostasis, or electrophysiological “balance.” Many factors can contribute to neuronal hyperexcitability including those that are intrinsic or extrinsic to the cell.

Extrinsic factors can include an imbalance or dysfunction of neurotransmitters, traumas, and infections.

Other factors are intrinsic to the neuron (e.g., genetic conditions or the disruption of neuronal metabolism).

Whatever its origin, electrophysiological imbalance and resultant neuronal hyperexcitability manifests in a range of debilitating symptoms, including seizures and psychiatric symptoms such as psychosis, pain, behavioral, mood disorders and more.

Such symptoms are prevalent and debilitating across a range of diagnoses, including:

epilepsies, neurodegenerative diseases and neurodevelopmental disorders.

Therefore, drugging targets that lead to excessive neural excitation may have widespread therapeutic utility.

While some drug development companies focus exclusively on a single biological target or MoA, we believe that multiple MoAs will be necessary to effectively treat the heterogeneous causes of hyperexcitability.

Accordingly, our pipeline seeks to curate and develop a unique set of molecules that can be effective as monotherapies and within the context of polypharmacy regimens.

We believe this approach will create a differentiated and leading epilepsy and psychosis franchise.

Core tenets of our approach include a focus on:

• Small molecule compounds.

Ovid’s pipeline is comprised of small molecule programs that can potentially be delivered as a pill, injection, or intravenously.

Recent advances in synthetic methodology, formulation technology, generative artificial intelligence and biology target research have unlocked more opportunities for innovative and creative medicines.

The compounds we seek to develop are brain-permeable and are designed to modulate specific biological targets.

We seek to take advantage of the versatility small molecules have to offer in terms of manufacturing, chemistry, and dosing to potentially deliver novel and next-generation medicines that will make meaningful improvements in the lives of patients.

• Unique biological targets implicated in neuronal regulation.

There is compelling evidence that the novel targets we pursue directly or indirectly modulate hyperexcitability.

These targets are associated with regulating inherent intracellular excitatory/inhibitory balance within neurons.

• Differentiated potential first-in-class or best-in-class mechanisms of action.

We cultivate a pipeline of potential first-in-class or potential best-in-class MoAs to intercept and mitigate the underlying cause of seizures or brain disease.

Collectively, our differentiated pipeline has produced four active potential value-creating drug programs.

Several of these therapeutic development programs (soticlestat, OV888 (GV101) and OV329) seek to affect metabolic, signaling, and enzymatic pathways to modulate extrinsic causes of hyperexcitability, thereby restoring neural balance.

In essence, they seek to change the environment surrounding the neuron.

Our KCC2 mechanisms of action act on the intrinsic excitability of the neuron.

• Sentinel indication clinical development.

Our drug development approach generally pursues rare, resistant conditions as initial “sentinel” indications.

Pursuing rare acute conditions can enable us to demonstrate the rapid proof-of-concept (“POC”) for our compounds, while additionally exploring efficient regulatory pathways and

Case studies of the life-cycle management for prior ASMs suggest that demonstration of refractory seizure reduction is often indicative of therapeutic effect in more common and tractable seizure types.

Similarly, many ASMs were later proven to have clinical efficacy in other neurological conditions.

Simply put, effective therapeutic outcomes in highly pharmaco-resistant indications often bodes well for treating broader neuropathologies.

Ovid’s pipeline consists of small molecule programs that can potentially be delivered orally, by subcutaneous or intramuscular injection, or intravenously.

The compounds we seek to develop are mechanistically designed to activate or modulate specific biological targets.

We plan to take advantage of the versatility small molecules have to offer in terms of manufacturing, chemistry and dosing, with the ultimate goal of delivering medicines that can be easily taken by patients for chronic conditions.

• Target validation and indication selection.

Our therapeutic development programs focus on precise MoAs for biological targets that are confirmed to be relevant in excessive neural excitation with established relevance to hyperexcitability through in vitro and in vivo animal models.

Prior to advancing our drug candidates from nonclinical evaluation into clinical trials, we apply a systematic approach to de-risk molecules using emerging tools, phenotypic screens and animal disease biology models.

Additionally, we prioritize targets that are either uniquely (1) expressed in the CNS, such as KCC2 co-transporters, or are (2) over-expressed in a pathological state, such as GABA-AT and ROCK2.

• Prioritization of the total drug profile.

We strive to develop drug candidates that deliver therapeutic efficacy while maintaining safe and well-tolerated side effect profiles.

As noted above, for neurology patients and clinicians who must regularly manage side effects associated with polypharmacy regimens, it is preferable to have medicines that are well tolerated and exhibit few DDIs.

In addition, we strive to impact the broader symptomatology of disease, including for example, the measurement of behavior and communication change.

As the field of ASM advances, we believe connections may be established between the root cause of hyperexcitability and other neurological conditions affecting larger populations.

These include neuropsychiatric and neuro degenerative disorders and pain.

However, our strategy focuses initially on evaluating our investigational medicines for pathways and targets impacting rare brain conditions.

If effective in rare disease, our intent is to explore expanding on that success to broader conditions of the brain for which the MoA may hold therapeutic relevance.

Accordingly, in the future, we expect to be able to extend our knowledge and drug programs to other neurological conditions.

This approach is supported by research indicating that more than ten ASMs are used in treatment of other (non-epilepsy) neurological diseases today.

Scientifically Driven

We take a scientifically driven approach to identify promising drug candidates for our pipeline.

We are building our portfolio based on the existence of known biological rationales that are associated with targets, and which can be evaluated using validated biomarkers and/or clear endpoints, for study in clinical trials.

As we advance our drug candidates through nonclinical and clinical evaluation, we apply a systematic approach for de-risking compounds using emerging tools, animal models and trial designs.

This paradigm is continuously informed and refined with emerging scientific and clinical insights to strengthen and de-risk development for prospective programs and trials.

Specifically, our approach is driven by the following scientific principles:

• Pursuit of validated and emerging targets.

We are building a pipeline of therapeutic development programs representing distinct MoAs, including validated and emerging biological targets in epilepsy and neurovascular disorders such as CCMs.

We seek to target biological pathways or genes for which POC has already been established via in vitro or animal models.

Additionally, we prioritize targets that are either uniquely (1) expressed in the CNS, such as:

CH24 and KCC2 co-transporters or (2) over-expressed in a pathological state, such as ROCK and GABA-AT.

• Blood brain barrier (“BBB”) penetration.

The brain is one of the most difficult organs in the body to treat, in part due to the challenge of penetrating the BBB.

Ovid’s drug development programs include potential small molecule therapies that demonstrate penetration of the BBB.

• Clinically translatable preclinical models .

Recent advances in genetics enable us to employ predictive in vitro and in vivo genetic models of specific brain diseases.

We believe these predictive models will allow us to evaluate and observe a drug candidate’s potential activity prior to initiation of human trials.

Applying these models, we believe we will be able to select the most relevant indication and seizure endpoints for our studies and increase the potential for clinical success.

• Clear primary endpoints and scales .

We primarily focus on disorders that are characterized by epilepsy-related symptoms and seizures.

Many seizure types afford clear observable endpoints and biomarkers that help capture and measure evidence of the clinical impact of our drug candidates.

Our team of development experts has extensive experience designing scales to measure other symptoms that are common among seizure-disorders, such as cognitive declines, movement deficiencies and behavioral manifestations.

These skills support our desire and ability to develop medicines that may provide a clinical benefit across multiple aspects of patient health.

• Trial design enables early observation of proof-of-concept.

By employing surrogate biomarkers and endpoints that are highly relevant and designed to detect meaningful clinical benefits, we anticipate that many of our studies may provide early POC in clinical development, thereby directing the use of our capital to projects with higher probability of later-stage success.

• Motivated and accessible patient populations.

We are targeting our programs for disorders with motivated and accessible patient populations.

We believe that the patients and caregivers affected by epilepsies and brain disorders have increasing access to diagnostics and genetic testing.

Additionally, many are avid users of social media, through which they learn new insights about their conditions and share relevant information and experiences.

We conduct patient disease community outreach and activities on digital platforms to efficiently identify new patients for our clinical trials, raise disease awareness and help connect with patients and caregivers.

Pipeline Enhanced by Academic Collaborations and Disciplined Business Development

To support our strategy we continue to enhance and expand our pipeline via two complementary efforts:

(1) internal research and development efforts in collaboration with external leaders in the field and academic collaborators;

and (2) business development activities to partner assets that have promising potential in and outside our chosen therapeutic areas.

Ovid conducts focused internal drug discovery, which helps us maintain lower costs for laboratory facilities.

We identify compounds with what we believe is untapped value sitting in other organizations’ pipelines and look to in-license or enter into collaborative agreements to secure such assets and advance clinical development.

This strategy directs our efforts where we excel at creating value, which is specifically shaping translational and clinical-stage development in our therapeutic area.

Our preclinical and toxicology work seeks to screen for and respectively avert drug or dose dependent effects, such as sedation or drug-drug interactions, that could impact patient tolerability.

Business development strategy:

Pipeline built through disciplined business development and enhanced through academic collaborations

Ovid has primarily built our pipeline through strategic business development.

We identify molecules with untapped potential value and seek to in-license or enter into collaborative agreements to secure such assets and advance clinical development.

This strategy directs our efforts where we excel in creating value, shaping translational and clinical stage development.

An integral part of our process is establishing collaborations with academic research centers to support translational expertise for our programs, including the Stephen Moss Lab of Neuropharmacology at Tufts University.

The multiple programs in our diversified pipeline create optionality to pursue disciplined business development to expand our opportunities.

The multiple programs in our diversified pipeline provide optionality to pursue out-bound business development to expand our opportunities.

As the pipeline progresses, we may endeavor to partner the development of our compounds in non-core indications or extend regional market rights outside the United States.

1 unchanged sentence

Collectively, our senior management has transacted hundreds of in-licensing deals and collaborations.

Patient-Focused

Ovid is developing product candidates that we hope will create new possibilities and more good days for people living with rare epilepsies and brain conditions.

For example, we believe that our therapeutic candidates may be able to meaningfully reduce harmful seizures, mitigate burdensome symptoms, and potentially slow down the underlying progression of disease.

Patient communities are critical to informing every aspect of our approach.

Each disorder for which we are developing potential neurotherapeutics is a condition that carries serious risk of morbidity and requires extensive and specialized involvement from the patients’ families, caregivers, physicians and from patient advocacy groups.

Our strategy is enhanced by the following patient-focused principles:

• pursue under-addressed rare conditions that can be evaluated via scaled clinical trials;

• develop close relationships with patient communities, caregivers, families, disease foundations and key opinion leaders, to better understand the history of these disorders, raise awareness, identify patients and facilitate enrollment of clinical trials;

• identify clinically meaningful endpoints, including seizures, symptoms, and cognitive and behavioral scales that are based on input from the patient communities and their physicians and caregivers;

• develop digital capabilities to be deeply informed and engaged with the patient communities we serve.

We continue to enhance and expand our pipeline via two complementary efforts:

(1) internal R&D efforts in collaboration with external leaders in the field and academic collaborators;

and (2) business development activities to partner with collaborators that have promising programs or assets in our chosen therapeutic areas.

Clinical Development Approach

We take a scientifically driven and evidence-based approach to translation and clinical development of our programs.

We are building our portfolio based on the existence of known biological rationales that are associated with

targets, and which can be evaluated using validated biomarkers and clear endpoints that are meaningful to patients, clinicians and regulators.

Our early clinical development efforts focus on time and cost-efficient trials that address key questions critical to de-risking future development.

Our approach is driven by the following scientific principles:

• Clinically translatable preclinical models inform indication selection .

Recent advances in genetics and artificial intelligence enable us to employ predictive in vitro and in vivo models of specific brain diseases and symptoms.

We believe these predictive disease biology models will allow us to evaluate and observe a drug candidate’s potential phenotypic and therapeutic activity prior to initiation of human trials.

• Sentinel indications.

Our drug development approach generally pursues rare, resistant conditions as initial “sentinel” indications.

Pursuing rare, resistant conditions can enable us to demonstrate rapid proof-of-concept (“POC”) for our compounds while potentially exploring efficient regulatory pathways and incentives.

Similarly, many ASMs were later proven to have clinical efficacy in other neurological conditions.

• Biomarker strategies for early PD and clinical insight.

Whenever possible we integrate biomarker strategies beginning early in translational and clinical development to help identify whether our programs are achieving target engagement and having a PD effect on clinical parameters that are relevant to disease processes and manifestations.

Such biomarkers can help identify whether we are achieving biologically active doses to inform patient studies.

Using such biomarkers may provide early POC in clinical development and, in turn, guide capital allocation toward projects with a higher probability of later stage success.

• Meaningful endpoints and scales.

We focus on clear, observable endpoints that are meaningful to patients, caregivers, clinicians and regulators.

Our clinical development experts have extensive experience identifying and using validated scales and designing scales to measure symptoms that are common among seizure- and psychiatric disorders, such as cognitive declines, movement deficiencies, hallucinations and behavioral manifestations.

These skills support our ability to develop medicines that may provide clinical benefit across multiple aspects of patient health.

• Motivated and accessible patient populations.

We seek to develop medicines for disorders with motivated and accessible patient populations.

Patients and caregivers affected by intractable brain disorders have increasing access to diagnostics and genetic testing.

Additionally, many are social media users, through which they learn new insights about their conditions and share relevant information and experiences.

We conduct patient disease community outreach and activities to inform our clinical design, educate patients about trial opportunities and support efficient study enrollment.

Fit-for-purpose infrastructure

We have built a highly specialized, efficient, and focused infrastructure that supports our chosen area of neurotherapeutics development.

This infrastructure spans the critical domains of R&D and market access strategy.

The scale and design of the organization reflects the needs of our pipeline programs and our status as a publicly-traded company.

We have recruited a team of 23 professionals, many with deep subject matter expertise in seizures and neurological conditions.

This includes physicians, academic scientists, and commercial and biopharmaceutical industry leaders.

We have two individuals with M.D.

degrees and seven professionals with Ph.D.

degrees specializing in the sciences.

Our operational leaders have extensive experience developing, formulating, manufacturing, regulatory controls and implementing market access strategies for leading neurological medicines.

In total, our team’s collective professional experience has resulted in the successful development or commercial launch of more than 25 medicines, including many CNS products.

Over time, we have built upon our core strength in the clinical development of medicines for anti-seizure and genetic neurodevelopmental conditions and expanded into adjacent therapeutic areas of drug development in the CNS where strong mechanistic evidence exists.

Financial strategy

We are focused on delivering long-term value for shareholders.

Our financial strategy seeks to apply our capital in a focused manner to advance a differentiated pipeline of neurotherapeutics, which we believe may generate multiple value-creating milestones from data and ultimately, commercial sales.

Management believes that we have sufficient cash on hand to fund Ovid's operations into the first half of 2026.

To achieve this cash runway, in October 2023, we sold 13% of our interest in the milestones and royalties that we are eligible

to receive from soticlestat's potential approval and commercialization to Ligand for $30.0 million.

We retain 87% interest in soticlestat's regulatory and commercial milestones and royalties on sales if the drug is successfully approved and commercialized by Takeda.

These future payments may contribute to funding our operations and business development activities.

For additional information, see the description of the Ligand Agreement below under the heading “License and Collaboration Agreements – 2023 Ligand Pharmaceuticals Milestones and Royalties Monetization.”

We are focused on delivering long-term value for stockholders.

Our financial strategy applies our capital in a focused manner to advance a differentiated pipeline of neurotherapeutics, which we believe will generate multiple value-creating data-driven milestones and ultimately commercial sales.

Management believes that we currently have sufficient cash on hand to fund our operations into the second half of 2026.

See “ Item 7.

Management’s Discussion and Analysis of Financial Condition and Results of Operations—Liquidity and Capital Resources ” for more information.

Ovid pipeline

Our efforts have already brought drug candidates from POC into human clinical trials.

Today, we are one of the few companies that has researched and developed three distinct MoAs to target seizures and one of the only clinical development programs to evaluate a highly selective ROCK2 inhibitor for neurological disease.

We believe this pipeline of potential first-in-class or potential best-in-class mechanisms differentiates us and provides the basis of an attractive franchise of potential small molecule neurotherapeutics.

The following table (Figure 1) sets forth our drug candidate programs and their development status, MoA, and anticipated near-term milestones:

Our efforts have already brought drug candidates from POC into late-stage patient clinical trials.

Today, we are one of the few companies that has researched and developed three distinct MoAs to target seizures and we believe we are the only company that has a portfolio of direct activators of KCC2.

We believe this pipeline of potential first-in-class or best-in-class mechanisms differentiates us and provides the foundation for a productive franchise of potential small molecule neurotherapeutics for epilepsies, psychoses and other mood disorders.

The following table (Figure 1) sets forth our drug candidate programs and their development status, their respective MoAs, and anticipated near-term milestones.

In the event we are unable to raise capital or enter into partnerships or co-development opportunities as and when needed, we will be required to delay, reduce the scope of or eliminate research and development programs.

Ovid Therapeutics Pipeline

Eligible for Non-Dilutive Capital from Takeda Pharmaceuticals

We retain significant financial interest in soticlestat, a novel CH24 inhibitor for the potential treatment of patients with resistant epilepsies, following our role in its successful early and mid-stage development program.

We believe soticlestat has the potential to become a first-in-class medicine targeting the metabolism of cholesterol in the brain.

It has been shown to gradually reduce inflammation in the brain as well as indirectly acting on the N-methyl D-aspartate pathway.

We believe that this dual mechanism plays an important role in modulating excitatory signals involved in epilepsy, and thereby suppressing seizures.

Soticlestat is currently being studied by Takeda in two global, pivotal Phase 3 trials for people living with Lennox-Gastaut syndrome (“LGS”) and Dravet syndrome (“DS”).

Takeda has stated two pivotal Phase 3 clinical trials studying soticlestat as a treatment for Lennox-Gastaut syndrome and Dravet syndrome completed enrollment, and it anticipates topline data readout by September 2024.

Takeda has stated that it anticipates filing soticlestat for regulatory approval in its fiscal year 2024 (April 2024 – March 2025).

If soticlestat receives regulatory approval and is commercialized, under the RLT Agreement, we are eligible to receive regulatory and commercial milestones payments of up to $660.0 million, in addition to potential net sales based tiered royalties of up to 20%.

In 2023, we sold a 13% stake in the royalty, regulatory and commercial milestone payments that we are eligible to receive under the RLT Agreement to Ligand for $30.0 million.

Royalty payments are eligible on net sales across all regions and all future indications.

The future milestones payments do not include an initial upfront payment that we received from Takeda in March 2021 of $196.0 million.

Background on Takeda Royalty, License & Termination Agreement

The soticlestat development program began in January 2017 as a license and collaboration agreement between us and Takeda for rare epilepsies.

Under this original agreement, Ovid held a 50% ownership stake in soticlestat and Takeda retained the remaining 50%.

Following a successful Phase 2 development program led by us, in March 2021, we entered into the RLT Agreement.

Under the terms of the RLT Agreement, we terminated our original collaboration agreement with Takeda, and Takeda subsequently secured an exclusive license and intellectual property rights to repurchase our 50% share in soticlestat.

In exchange, we received an upfront payment of $196.0 million.

In addition, if soticlestat achieves regulatory approval, and is successfully commercialized, we are eligible to receive up to an additional $660.0 million in regulatory and commercial milestone payments and potential tiered royalties on net sales of soticlestat at percentages ranging from the low double-digits up to 20%, subject to standard reductions in certain circumstances.

Royalties are payable on a country-by-country and product-by-product basis during the period beginning on the date of the first commercial sale of such product and ending on the expiration of patent rights in such country.

As a result of this agreement, Takeda secured all the global rights to develop and commercialize soticlestat for the treatment of developmental and epileptic encephalopathies, including DS and LGS.

In addition, Takeda has assumed responsibility for all development and commercialization costs associated with soticlestat.

We have no ongoing costs or obligations.

OV888 (GV101) – A highly selective ROCK2 inhibitor

In May 2023, we invested in and entered a collaboration with Graviton Bioscience Corporation (“Graviton”) to develop a portfolio of highly selective inhibitors of ROCK2 for the treatment of rare neurological conditions.

The collaboration includes the development of lead program OV888 (GV101), which is a small molecule ROCK2 inhibitor that is currently completing a Phase 1, double-blind multiple-ascending dose trial.

The trial is progressing on track, a higher dose has been added and no serious adverse events have been reported.

For additional information, see the description of the Graviton collaboration agreement below under the heading “License and Collaboration Agreements – 2023 In-licensing and Collaboration Agreement with Graviton Bioscience Corporation.”

OV888 (GV101) is a potent, BBB penetrant inhibitor that is highly selective for ROCK2.

ROCK2 is expressed abundantly in skeletal muscles and in the brain and is believed to primarily function to regulate intracellular cytoskeletal organization.

We believe that the ROCK2 signaling pathway may be hyperactivated in multiple neurological diseases, including disorders involving vascular structures and nerve myelination diseases that can result in seizures, spasms and a variety of other symptoms.

Despite this link, there has been limited clinical development of ROCK2 inhibitors due to challenges penetrating the BBB and the inherent challenge of avoiding inhibition of rho-associated coiled-coil-containing protein kinase 1, which can have unwanted side effects.

The initial indication for OV888 (GV101) is anticipated to be CCM for which there is strong mechanistic evidence for inhibiting ROCK2 (see Figure 2 below).

CCMs are one of the most common intracranial vascular malformation in humans, presenting as mulberry-shaped abnormal blood vessels with thin, leaky walls located in the brain and or spinal cord.

It is thought CCMs affect approximately 1:250 individuals.

At diagnosis, the majority of CCM patients present symptomatically with hemorrhage, focal neurologic deficit and/or seizures, which reflect areas of core competency for our development acumen.

To date, preclinical and human safety studies evaluating OV888 (GV101) have shown it has a favorable toxicology profile with no serious adverse events reported.

We anticipate initiating the Phase 2 program for OV888 (GV101) in the second half of 2024.

Throughout OV888's (GV101) clinical development, we intend to harness the expertise held by the team at Graviton, who previously pioneered the development of Rezurock, the first approved ROCK2 inhibitor for graft vs.

host disease.

Believed mechanism of action for OV888 (GV101) in CCM

Ovid has a Phase 2-ready ROCK2 inhibitor, OV888 (GV101), in collaboration with Graviton Bioscience.

This program was cleared by regulators toinitiate Phase 2 but is currently paused while Ovid monitors the outcome of regulatory interactions by competitors.

OV329 - A next-generation GABA-AT inhibitor

OV329 is an investigational, next-generation GABA-AT inhibitor that we are developing for the treatment of adult and pediatric epilepsy disorders.

OV329 represents a potential best-in-class GABA-AT inhibitor and was designed to supplant vigabatrin, which is an approved therapeutic in the United States and European Union for the treatment of infantile spasms.

Vigabatrin has demonstrated substantial seizure reduction, which led to sales of more than $300 million by Lundbeck in the United States alone.

However, vigabatrin's clinical and commercial use has been limited by lack of a therapeutic window.

Specifically, vigabatrin has generated deleterious ocular effects in some patients, including retinal degradation and irreversible vision loss that led to significant post-market restrictions and monitoring.

We believe OV329 to be an improved GABA-AT inhibitor with a different chemical structure, potency and inhibition profile than vigabatrin.

We have observed OV329 to deliver increased potency and efficiency in the target binding site and has been shown in our preclinical research to be more than 200-fold more potent.

We are actively studying two formulations of OV329:

(1) an oral formulation for chronic seizures, which is currently in a Phase 1 trial and 2) an intravenous formulation for acute seizures, which is being readied for an IND (or an equivalent regulatory application) expected in late 2024.

We believe that OV329 has the potential to be therapeutic in refractory and drug-resistant epilepsies such as seizures associated with tuberous sclerosis and refractory status epilepticus (“SE”).

OV329 is a clinical-stage, next-generation GABA-AT inhibitor that we are developing for the treatment of adult and pediatric drug-resistant epilepsies.

OV329 represents a potential best-in-class GABA-AT inhibitor and was designed to supplant vigabatrin (“VGB”), which is an approved therapeutic globally for the treatment of infantile spasms.

VGB was a first-generation medicine that demonstrated substantial seizure reduction, however, its clinical and commercial use was limited by lack of a therapeutic window.

Specifically, VGB was proven to generate deleterious and irreversible ocular effects in some patients, including retinal degradation and irreversible vision loss that led to significant post-market restrictions and monitoring.

We believe OV329 to be an improved GABA-AT inhibitor with a different chemical structure, potency, binding, PK and PD profile as compared to VGB.

OV329 has been shown to deliver increased potency and efficacy in the target binding site.

In preclinical research it was demonstrated to be 100-fold more potent than VGB.

We are actively studying an oral pill of OV329 in a Phase 1 trial that has multiple biomarkers to measure clinical effect and target engagement, in addition to evaluating safety, tolerability and PK.

We believe that OV329 has the potential to be a therapeutic option for adult and pediatric drug-resistant epilepsies, including several DEEs.

A benefit of our OV329 program is that it acts upon a validated drug target for seizures.

1 unchanged sentence

OV329 leads to increased concentrations of GABA by inhibiting its metabolism.

Given that epilepsy is characterized by excessive neuronal excitation, the increased levels of GABA may suppress this excitatory signaling and may reduce seizures.

OV329 oral formulation

Based upon preclinical data supporting OV329, we believe that the oral formulation has the potential to provide (in comparison to vigabatrin) preferred (lower) dosing.

We believe that these preclinical data suggests that OV329 could allow for seizure reduction efficacy and improved tolerability in comparison to existing therapeutics.

To support this profile, seven animal seizure models presented at medical conferences in 2022 and 2023 demonstrate the seizure reduction potential of OV329 (see Figure 3 below).

These findings in both chronic and acute seizure models provide additional confidence about the therapeutic potential of OV329 in humans.

Seven preclinical animal models reaffirm OV329 seizure reduction activity, including resistant seizure models

To further differentiate OV329’s potential profile from vigabatrin, our preclinical efforts sought to extensively characterize its safety and tolerability, including any potential ocular effects.

We have demonstrated that the tissue clearance of OV329 is rapid, leading us to believe that the accumulation in the back of the eye may be less likely than vigabatrin, which has a longer half- life.

The pharmaco-dynamic profile of OV329 is also highly differentiated from vigabatrin.

Preclinical research has shown that OV329 induces phasic (synaptic) and tonic (extrasynaptic) inhibition of GABA-AT.

This produced more GABA in the synapse and environmental milieu, potentially contributing to prolonged inhibitory effects.

Additionally, we applied a clinically translatable rodent model of albino Sprague-Dawley rats to determine if any ocular changes could be observed associated with the predicted therapeutic doses of OV329 and vigabatrin, as compared to placebo.

This rodent model is an accepted proxy by the U.S.

Food and Drug Administration (“FDA”) for the ocular effects seen in humans treated with vigabatrin.

Given that epilepsy is characterized by excessive neuronal excitation, the increased levels of GABA may suppress this excitatory signaling and thus reduce seizures.

OV329 profile

Based upon preclinical data supporting OV329, we believe it has the potential to provide (in comparison to VGB) greater seizure reduction efficacy and improved tolerability and safety profiles without sedation, and lower dosing in comparison to existing therapeutics.

To support OV329’s anti-convulsant profile, nine animal seizure models have demonstrated its seizure reducing effects (see Figure 2 below).

These findings from both chronic and acute seizure models provide additional confidence about the therapeutic potential of OV329 in humans.

The PD profile of OV329 is differentiated from VGB.

Preclinical research has shown that OV329 induces phasic (synaptic) and tonic (extra-synaptic) inhibition of GABA-AT.

This produced more GABA in the synapse and environmental milieu, potentially contributing to more durable inhibitory effects.

Nine preclinical animal models reaffirm OV329 seizure reduction activity, including resistant seizure models

OV329 safety profile

To date, OV329 has exhibited acceptable tolerability in humans in our Phase 1 study.

There have been no drug-associated serious adverse events reported and minor and transient adverse events, such as headache.

Additionally, to characterize OV329’s potential safety profile relative to VGB, our preclinical efforts sought to extensively study safety and tolerability, including any potential ocular changes.

We are cleared to study OV329 in humans with daily dosing for 28 days.

Toxicology that enables our Phase 2 program is expected to be completed by third quarter 2025.

We have demonstrated that the tissue clearance of OV329 is rapid, which when coupled with its potency and irreversible binding, leads us to believe that the accumulation in the back of the eye does not occur as it does with VGB, which has a longer half-life.

In 2024, we presented results at the American Epilepsy Society meeting of a head-to-head animal study evaluating whether OV329 could be found to accumulate in mouse retinas and brains, as has been previously shown to occur with VGB.

The preferential accumulation of VGB in the eye is thought to be a contributing factor in VGB’s ocular toxicity.

The findings (summarized in Figure 3 below), found that OV329 cleared and remained undetectable in the retinas, eyes, and brains of mice after 48 hours of continuous exposure via a sub-cutaneous osmotic pump, suggesting a lack of accumulation.

In contrast, ocular accumulation of VGB was confirmed within this period.

These results replicate previously published findings that indicate VGB preferentially and rapidly accumulates within mouse tissue and plasma, including retina, visual cortex, and brain at sub-therapeutic doses (70 mg/kg).

In contrast, a therapeutic dose of OV329 in animals (5 mg/kg) did not show signs of ocular accumulation in the same study design.

OV329 clears brain and eye tissue rapidly and does not accumulate like VGB

1 Tsai, J., et al.

Evaluation of the Potential Accumulation of OV329 in the Brain, Retina, and Eye Following Continuous Infusion .

presented at the 2024 Epilepsy Pipeline Conference

These results complement previously presented studies which showed that therapeutic doses of OV329 (3 mg/kg) did not result in retinal tissue pathology at 45 days in Sprague-Dawley rats, an animal model that investigates structural and functional ocular toxicity (see Figure 4).

In contrast, VGB did show retinal cell degradation at the therapeutic dose in animals of 300 mg/kg at 45 days.

We applied a clinically translatable rodent model of albino Sprague-Dawley rats to determine if any ocular changes could be observed associated with the predicted therapeutic doses of OV329 and VGB, as compared to placebo.

This rodent model is an accepted proxy by the FDA for the ocular effects seen in humans treated with VGB.

Figure 4 (below) demonstrates the results of our research.

After 45 days of dosing with the therapeutic dose of vigabatrin and an expected therapeutic dose of OV329 (3 mg/kg), the model showed no ocular effect in animals taking OV329, whereas disruption in retinal cells was seen in animals taking the therapeutic dose of vigabatrin (300 mg/kg).

After 45 days of dosing with the therapeutic dose of VGB and an expected therapeutic dose of OV329 (3 mg/kg), the model showed no ocular effect in animals taking OV329, whereas disruption in retinal cells was seen in animals taking the therapeutic dose of VGB (300 mg/kg).

In this short-term model, OV329’s ocular profile appears similar to placebo, and no disruption to the retina was seen at the anticipated therapeutic dose.

These models must be confirmed in human studies, though they lead us to believe that OV329 may offer significant seizure reduction benefit with a therapeutic window not provided by vigabatrin.

These models must be confirmed in human studies, though they lead us to believe that OV329 may offer significant seizure reduction benefit with a therapeutic window not provided by VGB.

No ocular changes seen in rodents treated with expected therapeutic dose of OV329 (3 mg/kg)

In late 2022, our IND for OV329 was cleared by the FDA and subsequently, we initiated a Phase 1 trial.

That study is currently ongoing at the Nucleus Network at Alfred Hospital in Australia and is expected to complete in the second half of 2024.

Human studies and biomarker strategy

Our Phase 1 trial of OV329 is currently ongoing with CMAX Clinical Research in Adelaide, Australia, with topline data expected in the third quarter of 2025.

The trial is being conducted in two parts, including:

a single-ascending dose and a multiple-ascending dose portion.

Endpoints will evaluate the pharmacokinetic profile, safety, tolerability and target engagement associated with escalating doses of OV329 in healthy volunteers.

Two surrogate biomarkers will be applied in the study, including:

(1) transcranial magnetic stimulation (“TMS”) will be measured and is a corollary for clinical efficacy and (2) magnetic resonance spectrometry (“MRS”) will be used to measure target engagement.

Previous studies have reported MRS measurement of GABA concentration levels increase following treatment with GABA-AT inhibitors, which has been shown to correlate with seizure reduction efficacy in existing GABA-AT inhibitor programs.

If OV329 proves to effectively engage the target and exhibits a tolerable safety profile in the Phase 1 study, these metrics may inform mid-to-late-stage development of the program.

Upon results from the Phase 1 program, we anticipate OV329 could be further studied for the treatment of seizures associated with tuberous sclerosis complex, infantile spasms and other epilepsies associated with focal onset seizures.

If the safety and efficacy profile of OV329 is positive, we will also consider lifecycle management strategies in broader epilepsy indications.

OV329 Intravenous Formulation

We are actively formulating and conducting IND-enabling studies for an intravenous use of OV329, which would be intended for the treatment of acute seizures, such as refractory status epilepticus (“RSE”).

It is thought that approximately 35,000 Americans experience RSE.

RSE is defined as a medical emergency where patients experiencing seizures of five minutes of duration or longer do not respond to first or second-line therapies.

Status epilepticus (“SE”) and RSE can lead to enduring brain damage and increased rates of mortality.

While there is no intravenous formulation of vigabatrin for acute use, some investigator led studies have shown that the application of this GABA-AT inhibitor via a nasal-gastric tube has produced strong results that have led to the cessation of status epilepticus.

Drawing on these findings, Ovid intends to submit an IND (or an equivalent regulatory application) for the IV formulation of OV39 in late 2024 and advance it in human studies for potential use in refractory SE.

Portfolio of KCC2 Transporter Direct Activators, Including OV350

We in-licensed a large portfolio of compounds from AstraZeneca AB (“AstraZeneca”) in December 2021 that are direct activators of a biological target expressed exclusively in the CNS:

We believe this portfolio represents the only small molecule program in the biopharmaceutical industry that directly activates the KCC2 transporter.

KCC2 is a channel that regulates chloride homeostasis in neurons, and thereby is potentially important in the control of neuronal excitability and seizures.

The portfolio includes a lead compound, OV350, and several other compounds that we believe are suitable for pharmaceutical development.

We intend to analyze multiple candidates from the KCC2 portfolio for development in epilepsy as well as other possible neurological conditions associated with behavior, neuropathic pain or neurodegeneration.

Since several compounds within the portfolio appear to be amenable for multiple formulations, the broad KCC2 program may provide Ovid with the ability to partner compounds for neurology indications outside our core competencies.

In vivo proof-of-concept studies in animals have established that restoring KCC2 activity leads to reduced seizure sensitivity and seizure-induced mortality.

In one preclinical model, designed to mimic the acute seizure state of SE, OV350 terminated status and restored the efficacy of diazepam in SE seizures, whereas diazepam treatment alone failed to halt the seizures (see Figure 5 below).

Preclinical mechanistic studies have also demonstrated that OV350 was well-tolerated and did not induce sedation.

These findings must now be studied and demonstrated in humans.

OV350 Terminates Benzodiazepine Resistant Status Epilepticus

In 2023, we evaluated several compounds in the KCC2 portfolio and began optimizing the lead candidate, OV350, for possible intravenous and oral administration formulations.

Dual formulations are optimal for patients who are treated acutely in the hospital and need chronic dosing to maintain outcomes in an out-patient setting.

To support human studies, we initiated a range of disease model experiments in seizure and psychosis models.

As noted above, we believe that the anticonvulsant properties of OV350 are compelling in preclinical SE models.

Additionally, two different animal models that are a proxy for human psychosis suggest that OV350 has a profile akin to atypical antipsychotics, though, it does not appear to carry the undesirable tolerability issues common in medicines for mental health conditions.

Such a profile may represent an exciting profile for future psychosis medicines.

Further research and IND-enabling studies are ongoing.

We expect to submit the first IND from the KCC2 program by the end of 2024.

OV350 Demonstrates Antipsychotic Effects in Schizophrenia Model

Endpoints will evaluate the PK profile, safety, tolerability and target engagement associated with escalating doses of OV329 in healthy volunteers.

Two surrogate biomarkers are being applied in the study, including:

(1) transcranial magnetic stimulation (“TMS”), which is being measured as a corollary for clinical biological effect and (2) magnetic resonance spectrometry (“MRS”), which will be used to measure target engagement.

Initial biomarker data from the most recently completed multiple-ascending dose cohort suggests encouraging directional signs of target engagement and clinical effects as measured by the above stated biomarkers.

These findings indicate signs of increased GABAergic activity consistent with the intended mechanism of action by inhibiting GABA-aminotransferase.

Previous studies have reported that MRS measurement of GABA concentration levels increase following treatment with GABA-AT inhibitors, which has been shown to correlate with seizure reduction efficacy in existing GABA-AT inhibitor programs.

These metrics coupled with safety, data and pharmacokinetic data may inform mid- to late-stage development of the program.

Upon results from the Phase 1 program, we anticipate OV329 could be further studied for the potential treatment of drug-resistant epilepsies, including adult epilepsies and DEEs.

OV350 and KCC2 direct activator portfolio

In late 2021, we in-licensed a portfolio of more than 100 molecules from AstraZeneca AB (“AstraZeneca”), which are direct activators of the KCC2.

Since that time, we have extensively characterized the library for bioavailability, formulation amenability and therapeutic potential.

As a result, we now have four unique programs that we intend to successively progress into human clinical studies.

These include OV350, OV4071 and OV4041 and another undisclosed program.

Based upon our phenotype screens, disease model studies, and published evidence, we believe this portfolio offers broad therapeutic potential in a range of potential brain conditions and symptoms including psychosis, other behavior and mood disorders, and seizures.

This may include neurodegenerative and neurodevelopmental diseases that exhibit the above mentioned symptoms.

Given the broad therapeutic relevance of KCC2 in many brain disorders, it is our desire to unlock the full value of KCC2 for shareholders and patients.

We will explore doing so through our own development efforts and via potential development partners.

A fundamental target in the CNS

KCC2 is a fundamental biological target expressed exclusively in the CNS and is central to maintaining synaptic inhibition.

Hundreds of publications link KCC2 dysregulation directly or indirectly to various medical conditions and symptoms associated with excessive neural excitation.

KCC2 is an ion co-transporter that regulates chloride extrusion in neurons.

A functioning chloride gradient is essential to GABA being inhibitory in neural synapses.

By directly activating KCC2, our development programs seek to restore GABAergic inhibition and bring hyper-excited neurons into homeostasis.

We believe that our KCC2 portfolio represents the only small molecule library within the broad biopharmaceutical industry that directly activates this unique ion co-transporter.

Other companies have tried to activate KCC2.

To our knowledge none, apart from us, have been successful, though some companies may potentiate the co-transporter, which will likely have different clinical effects.

KCC2 direct activator library

Our KCC2 direct activator portfolio includes four programs in active characterization and development, which we believe are suitable for pharmaceutical development.

We have characterized and translated multiple candidates from the KCC2 portfolio for development in epilepsy as well as other possible neurological conditions associated with psychiatric, neurodegeneration and neurodevelopmental disorders.

Phenotypic screens and confirmatory animal disease models suggest that our programs, including:

OV350, OV4071 and OV4041, have potential therapeutic properties associated with anti-psychosis, anxiolytic and anticonvulsant response.

We have also determined that the unique molecules in the library are amenable to a range of formulations, including intravenous, oral and intramuscular injections.

For the next three to four years, we anticipate filing regulatory submissions for human trials annually for successive programs emerging from our KCC2 portfolio.

As noted above, these programs represent opportunities for in-house development or co-development and out-licensing.

The library of early-stage small molecules that target the KCC2 transporter, including OV350, are included in a pending composition-of-matter application that was filed globally and, if issued, will expire in 2041 excluding any potential regulatory extensions.

Genetic Research Programs

The majority of our development activities are dedicated to small molecule programs.

However, we believe that genetic medicine will play an important role in the long-term future of treating genetic epilepsies and neurological disorders.

Accordingly, we engage in appropriately scaled, early-stage research programs with certain collaborators, including Gensaic, Inc., formerly M13 Therapeutics, Inc.

(“Gensaic”), a next-generation gene therapy developer.

Phage-Based Scaffolds:

Gensaic Research Collaboration

In August 2022, we entered into an investment in and research collaboration with Gensaic (the “Gensaic Collaboration Agreement”), a private biotech company that is developing gene therapies.

Specifically, Gensaic is applying phage-display science that uses M13 phages as platforms to deliver genetic sequences.

Though still in its nascence, we believe phage-based scaffolds may offer significant advantages for the delivery of genes, as compared to the current platform alternatives of adeno-associated viral (“AAV”) vectors.

This collaboration is a part of a low cost and long-term strategy to potentially enable unique treatment modalities in genetic disorders with a potentially unique and proprietary, low-cost alternative to current therapies.

AAV gene therapies are not optimal for treating neurological conditions.

Specifically, AAV gene therapies have limited cloning capacity, which restricts their use for delivering large genetic cargo.

Additionally, they are immuno-reactive, have poor BBB permeability, and provide relatively poor tropism to target cells.

In contrast, we believe phages offer the potential to:

deliver larger genes (up to 20kb);

be engineered to cross the BBB and deliver cargo to specific cell types;

avert the immune system response to enable redosing;

and be produced in a more cost-effective manner.

As a result, we believe phage-based gene therapy has an improved potential for the treatment of genetic epilepsies and neurological diseases.

We can pursue up to three targets in collaboration with Gensaic, which are not yet disclosed.

Genetic Programs:

OV350, OV4071 and OV4041

Prior to our strategic pipeline review in 2022, we had developed a series of early candidates for antisense oligonucleotide (“ASO”) and RNAi medicines as part of our collaborations with Columbia University and the University of Connecticut.

These research programs included:

OV815, which was in development for the treatment of mutations associated with KIF1A-associated neurological disorder (KAND);

HNRNPH2 (also known as Bain Syndrome), which was a potential treatment for an X linked gene predominantly occurring in females;

and OV882, a potential disease-modifying gene therapy for Angelman syndrome that used short hairpin RNA to deliver a vector that reduced expression of UBE3A-antisense and restores UBE3A expression.

At year-end 2023, we determined to pause these programs to prioritize our expanding clinical footprint in small molecule programs.

We will continue to seek collaborations or out-licensing opportunities for these programs.

In the first quarter of 2025, OV350 IV initiated first-in-human studies, which will assess class safety, tolerability and exploratory biomarkers for clinical change via quantitative EEG.

We expect to announce topline results in the fourth quarter of 2025.

It is our intent to develop OV350 as well as OV4071 and OV4041, oral programs that behave similarly in phenotypical screens, for the treatment of psychosis in people with NSD and LBD.

As noted above, these conditions have deep unmet patient need and are underserved by the current standard of care.

Furthermore, in vivo proof-of-concept studies have established that restoring KCC2 activity reduced psychotic behaviors in animals (see Figure 5 below).

Preclinical mechanistic studies have also demonstrated that OV350, OV4071 and OV4041 were well-tolerated and did not induce sedation.

OV350 demonstrates antipsychotic effects in schizophrenia model

OV888 (GV101) – A highly selective ROCK2 inhibitor

The collaboration includes the development of lead program OV888 (GV101), which is a small molecule ROCK2 inhibitor in clinical stage studies.

OV888 (GV101) is a potent blood-brain-barrier (“BBB”) penetrant inhibitor that is highly selective for ROCK2.

ROCK2 is expressed abundantly in skeletal muscles and in the brain and is believed to primarily function to regulate intracellular cytoskeletal organization.

We believe that the ROCK2 signaling pathway may be hyperactive in multiple neurological diseases, including disorders involving vascular structures and nerve myelination diseases that can result in seizures, spasms and a variety of other symptoms.

Despite this link, there has been limited clinical development of ROCK2 inhibitors due to challenges penetrating the BBB and the inherent challenge of avoiding inhibition of rho-associated coiled-coil containing protein kinase 1, which can present unwanted side effects.

The initial indication for OV888 (GV101) is desired to be CCM, for which there is strong mechanistic evidence for inhibiting ROCK2, though this program is currently on pause pending regulatory feedback on another competitive clinical-stage development program for CCM.

CCM is one of the most common intracranial vascular malformations in humans, presenting as mulberry-shaped abnormal blood vessels with thin, leaky walls located in the brain and/or spinal cord.

It is thought CCM affects approximately 1 in 250 individuals.

At diagnosis, the majority of CCM patients present symptomatically with hemorrhage, focal neurologic deficit and/or seizures, which reflect areas of core competency for our development acumen.

As noted above, preclinical and human safety studies evaluating OV888 (GV101) demonstrated that it has a favorable toxicology profile with no serious adverse events reported.

We will evaluate next steps and additional studies with OV888 pending review of emerging data from competitor and academic studies in CCM.

License and Collaboration Agreements

2023 Ligand Pharmaceuticals Milestones and Royalties Monetization

In October 2023, we sold Ligand a 13% stake in the royalties and milestones owed to Ovid related to the potential approval and commercialization of soticlestat (the “Ligand Agreement”).

In return, we received a $30.0 million payment, less certain reimbursable expenses.

We retained 87% of our interest in soticlestat's potential royalties and milestones.

In the event that soticlestat is not approved and commercialized, we have no continuing debt or other obligations to Ligand.

In-licensing and Collaboration Agreement with Graviton Bioscience Corporation (2023)

In April 2023, we entered into a Collaboration and License Agreement with Graviton, a privately held early-stage drug development company specializing in therapeutics that inhibit ROCK2.

Under the terms of the agreement, we purchased shares of Graviton's preferred stock for $10.0 million and secured rights to develop their lead program OV888 (GV101) as well as a portfolio of ROCK2 inhibitors in mutually agreed upon rare CNS indications, excluding amyotrophic lateral sclerosis.

Under the terms of the agreement, we purchased shares of Graviton’s preferred stock for $10.0 million and secured rights to develop their lead program OV888

(GV101) as well as a portfolio of ROCK2 inhibitors in mutually agreed-upon rare CNS indications, excluding amyotrophic lateral sclerosis.

The agreement provides us with worldwide rights, excluding China, Hong Kong, Macau and Taiwan.

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Graviton retains rights to licensed products in all fields of study outside of rare brain disorders.

We will evaluate next steps and additional studies with OV888 pending review of emerging data from competitor and academic studies in CCM.

Research Collaboration and Equity Investment in Gensaic (2022)

Under the terms of an equity agreement we entered into as an investor in Gensaic, we invested a total of $5.1 million in exchange for convertible preferred stock in Gensaic.

We also entered into a collaboration agreement with Gensaic (the “Gensaic Collaboration Agreement”) to potentially develop up to three genetic medicines for neurological indications of interest to us, harnessing Gensaic’s proprietary phage-derived particle platform.

Under the terms of an equity agreement, we invested a total of $5.1 million in exchange for convertible preferred stock in Gensaic, Inc.

Jeremy Levin, our Chairman and CEO, is a director of Gensaic.

Gensaic retains full rights to its platform technology.

We will have commercial rights to license and develop any resulting phage-derived gene therapies that emerge from this collaboration subject to agreed-upon terms.

We will have commercial rights to license and develop any resulting therapies and delivery technologies that emerge from this collaboration subject to agreed-upon terms.

We also retained rights to invest in future equity financing rounds.

2022 Out-License Agreement with Marinus Pharmaceuticals

In March 2022, we entered into an exclusive patent license agreement with Marinus, (“Marinus License Agreement” ) .

Under the Marinus License Agreement, we granted Marinus an exclusive, non-transferable (except as expressly provided therein), royalty-bearing right and license under certain Ovid patents relating to ganaxolone to develop, make, have made, commercialize, promote, distribute, sell, offer for sale and import licensed products in the territory (which consists of the United States, the European Economic Area, United Kingdom and Switzerland) for the treatment of CDKL5 deficiency disorders.

Royalties Associated with Marinus Out-License Agreement (2022)

In March 2022, we entered into an exclusive patent license agreement with Marinus Pharmaceuticals, Inc.

(“Marinus”) (“Marinus License Agreement”).

Following the date of regulatory approval by the FDA of the first licensed product in the territory, which was received on March 18, 2022, Marinus issued, at the Company’s option, 123,255 shares of Marinus common stock, par value $0.001 per share.

The Marinus License Agreement also provides for payment of royalties from Marinus to us in single digits on net sales of each such licensed product sold.

2022 License and Option Agreement with Healx

In January 2025, Marinus was acquired by Immedica Pharma, S.A.

Healx License and Option Agreement (2022)

In February 2022, we entered into an exclusive license option agreement (“Healx Agreement”) with Healx, Ltd (“Healx”).

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In February 2023, we amended the Healx Agreement to extend the option period by three months.

At the end of the option period, Healx has the option to secure rights to an exclusive license under our relevant intellectual property rights, in exchange for an additional payment of $2.0 million (“Option Fee”), development and commercial milestone payments, and low to mid-tier double digit royalties.

At the end of the option period, Healx had the option to secure rights to an exclusive license under our relevant intellectual property rights, in exchange for an additional payment of $2.0 million (“Option Fee”), development and commercial milestone payments, and low to mid-tier double digit royalties.

Royalties are payable on a country-by-country and product-by-product basis during the period beginning on the date of the first commercial sale of such product in such country and ending on the later to occur of the expiration of patent rights covering the product in such country and a specified anniversary of such first commercial sale.

In June 2023, the Healx Agreement was further amended to:

(i) grant Healx a development license;

(ii) grant a commercial license upon payment of the Option Fee to us;

and (iii) restructure the timing of the Option Fee payable to us.

In June 2023, the Healx Agreement was further amended to (i) grant Healx a development license, (ii) grant a commercial license upon payment of the Option Fee to us, and (iii) restructure the timing of the Option Fee payable to us.

Healx assumed all responsibility for and costs of development of gaboxadol in June 2023.

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In exchange for an upfront payment of $5.0 million in cash and $7.3 million in shares of our common stock to AstraZeneca, we are responsible for using commercially reasonable efforts to carry out all future development and commercialization of KCC2 transporter activators in epilepsies and potentially other neuropathic conditions.

We are obligated to pay AstraZeneca potential clinical development milestones of up to $8.0 million, regulatory milestones of up to $45.0 million and total commercial milestones of up to $150.0 million, as well as tiered royalty payments ranging from the single-digits up to ten percent on net sales.

the single digits up to ten percent on net sales.

At the time of proof of clinical efficacy, AstraZeneca will have the right of first negotiation to opt in to co-develop and co-commercialize KCC2 transporter activators with Ovid.

The license option will continue until the expiration of all relevant royalty terms.

2016 Northwestern License for OV329

Northwestern University License for OV329 (2016)

In December 2016, we entered into a license agreement (“Northwestern Agreement”) with Northwestern University (“Northwestern”), pursuant to which Northwestern granted us an exclusive, worldwide license to patent rights in certain inventions (“Northwestern Patent Rights”) which relate to a specific compound (OV329) and related methods of use for such compound, along with certain know-how related to the practice of the inventions claimed in the Northwestern Patent Rights.

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We are responsible for all ongoing costs of filing, prosecuting and maintaining the Northwestern Patent Rights, but we also have the right to control such activities using our own patent counsel.

In consideration for the rights granted to us under the Northwestern agreement, we are required to pay to Northwestern up to an aggregate of $5.3 million upon the achievement of certain development and regulatory milestones for the first product covered by the Northwestern Patents, and, upon commercialization of any such products, will be required to pay to Northwestern a tiered royalty on net sales of such products by the Company, its affiliates or sublicensees, at percentages in the low to mid-single-digits, subject to standard reductions and offsets.

In consideration for the rights granted to us under the Northwestern Agreement, we are required to pay to Northwestern up to an aggregate of $5.3 million upon the achievement of certain development and regulatory milestones for the first product covered by the Northwestern Patent Rights, and, upon commercialization of any such products, will be required to pay to Northwestern a tiered royalty on net sales of such products by Ovid, its affiliates or sublicensees, at percentages in the low to mid-single-digits, subject to standard reductions and offsets.

Our royalty obligations continue on a product-by-product and country-by-country basis until the later of the expiration of the last-to-expire valid claim in a licensed patent covering the applicable product in such country and ten years following the first commercial sale of such product in such country.

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License Agreement with H.

In March 2015, we entered into a license agreement with Lundbeck, which we subsequently amended in May 2019, and July 2020 (collectively, the “Lundbeck Agreement”).

Lundbeck A/S (2015)

In March 2015, we entered into a license agreement with H.

Lundbeck A/S (“Lundbeck”), which we subsequently amended in May 2019, and July 2020 (collectively, the “Lundbeck Agreement”).

As part of the Lundbeck Agreement, we obtained from Lundbeck an exclusive (subject to certain reserved non-commercial rights), worldwide license to develop, manufacture and commercialize OV101, also known as gaboxadol.

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Under the terms of the Amended Lundbeck Agreement, if Healx exercises its option, we will owe Lundbeck an equal share of all milestone and royalty payments received from Healx, if we choose not to exercise the Ovid Opt-In Right.

If we choose to exercise the Ovid Opt-In Right, to co-develop and co-commercialize the program with Healx, we will owe an equal share of the net profit share to Lundbeck.

If we choose to exercise the Ovid Opt-In Right to co-develop and co-commercialize the program with Healx, we will owe an equal proportion of the net profit share to Lundbeck.

Sales and Marketing

Given our stage of development, we have not yet established a commercial organization or distribution capabilities.

Given our stage of development, we have not yet established a commercial infrastructure or distribution capabilities.

However, we do have internal market access and commercial strategy capabilities that inform our pipeline strategy and execution.

As our pipeline assets move into the clinic in the future, we intend to build focused capabilities to commercialize our programs focused on epilepsies and seizure-related disorders.

As our pipeline assets advances in the clinic, we intend to build focused capabilities to commercialize our programs.

In markets for which commercialization may be less capital efficient for us, we may selectively pursue strategic collaborations with third parties in order to maximize the commercial potential of our drug candidates.

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However, certain members of our management have broad experience in manufacturing, which we believe may provide a competitive advantage.

We believe Zogenix, Inc.

(acquired by UCB in 2022), Jazz Pharmaceuticals plc (acquired by UCB in 2022), Sage Therapeutics, Inc., Marinus Pharmaceuticals, Inc., Mallinckrodt plc, SK Biopharmaceuticals Inc., Epygenix Therapeutics, Inc., Stoke Therapeutics, Inc.

and Xenon Pharmaceuticals, Inc.

are our most direct competitors with respect to soticlestat, OV329 and OV350.

The field of epilepsy and psychiatric medicines is highly fragmented.

There is no one direct competitor, though there are others in the field of epilepsy who market to similar indications as we may explore.

Those include:

UCB, Jazz Pharmaceuticals plc, Sage Therapeutics, Inc., SK Biopharmaceuticals Inc., Harmony Biosciences, and Xenon Pharmaceuticals, Inc.

These are our most direct competitors with respect to OV329.

Our OV350 program is intended for the treatment of psychosis in people with NSD and LBD.

The only existing medicine indicated for NSD is marketed by Acadia Pharmaceuticals Inc.

We are aware of one other company seeking to develop KCC2 potentiators, which is Axonis Therapeutics, Inc.

As it relates to OV888 (GV101), we believe Neurelis Inc.

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The primary competitive factors that will affect the commercial success of any drug candidate for which we may receive marketing approval include efficacy, safety and tolerability profile, dosing convenience, price, coverage and reimbursement.

Many of our existing or potential competitors have substantially greater financial, technical and human resources than we do and significantly greater experience in the discovery and development of drug candidates, as well as in obtaining regulatory approvals of those drug candidates in the United States and in foreign countries.

Our current and potential future competitors also have significantly more experience commercializing drugs that have been approved for marketing.

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Moreover, many jurisdictions, including the United States, permit third parties to challenge issued patents in administrative proceedings, which may result in further narrowing or even cancellation of patent claims.

Moreover, we cannot provide any assurance that any patents will be issued from our pending or any future applications or that any potentially issued patents will adequately protect our intellectual property.

We cannot provide assurance that any patents will be issued from our pending or any future applications or that any potentially issued patents will adequately protect our intellectual property.

We have exclusively licensed a portfolio of issued U.S.

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OV329’s composition of matter patent expires in 2036, excluding regulatory extensions.

We have also filed, and own, multiple patent families directed to the synthesis of OV329 and methods of treatment with OV329.

We have also filed, and own, multiple patent families involving the synthesis of OV329 and methods of treatment with OV329.

OV888 (GV101) was licensed from Graviton.

The composition of matter patent for OV88 expires in October 2038 excluding any potential regulatory extensions.

The composition of matter patent for OV888 (GV101) expires in 2038 excluding any potential regulatory extensions.

Graviton has also filed patents on methods of use with OV888 (GV101).

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The molecules are included in a pending composition-of-matter application that was filed globally and, if issued, will expire in 2041, excluding any potential regulatory extensions.

We have also filed, and own, multiple patent families directed to methods of treatment with KCC2 molecules, including OV350.

In addition, we have a library of proprietary genetic sequences that target UBE3A, KIF1A, HNRNPH2, and PDP2RD.

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Furthermore, we rely upon trade secrets and know-how and continuing technological innovation to develop and maintain our competitive position.

We seek to protect our proprietary information, in part, using confidentiality agreements with our employees and consultants and any potential commercial partners and collaborators and invention assignment agreements with our employees.

We seek to protect our proprietary information, in part, using confidentiality agreements with our employees and consultants and any potential commercial partners and collaborators, as well as invention assignment agreements with our employees.

We also have or intend to implement confidentiality agreements or invention assignment agreements with our selected consultants and any potential commercial partners.

These agreements are designed to protect our proprietary information and, in the case of the invention assignment agreements, to grant us ownership of technologies that are developed through a relationship with a third party.

These agreements may be breached, and we may not have adequate remedies for any breach.

These agreements may be breached, and we may not have adequate remedies for any such breach.

In addition, our trade secrets may otherwise become known or be independently discovered by competitors.

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In the United States, the FDA regulates drugs under the Federal Food, Drug, and Cosmetic Act ( “ FDCA ” ) and its implementing regulations.

The process of obtaining regulatory approvals and the subsequent compliance with applicable

federal, state, local and foreign statutes and regulations requires the expenditure of substantial time and financial resources.

The process of obtaining regulatory approvals and the subsequent compliance with applicable federal, state, local and foreign statutes and regulations requires the expenditure of substantial time and financial resources.

Failure to comply with the applicable U.S.

requirements at any time during the product development process, approval process or after approval, may subject an applicant to a variety of administrative or judicial sanctions, such as the FDA’s refusal to approve pending New Drug Applications ( “ NDAs ” ) or Biologics License Applications ( “ BLAs ” ), withdrawal of an approval, imposition of a clinical hold, issuance of warning letters, product recalls, product seizures, total or partial suspension of production or distribution, injunctions, fines, refusals of government contracts, restitution, disgorgement or civil or criminal penalties.

requirements at any time during the product development process, approval process or after approval, may subject an applicant to a variety of administrative or judicial sanctions, such as the FDA’s

refusal to approve pending New Drug Applications ( “ NDAs ” ) or Biologics License Applications ( “ BLAs ” ), withdrawal of an approval, imposition of a clinical hold, issuance of warning letters, product recalls, product seizures, total or partial suspension of production or distribution, injunctions, fines, refusals of government contracts, restitution, disgorgement or civil or criminal penalties.

The process required by the FDA before a drug product may be marketed in the United States generally involves the following:

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Preclinical studies include laboratory evaluation of product chemistry, toxicity and formulation, as well as animal studies to assess potential safety and efficacy.

An IND sponsor must submit the results of the preclinical tests, together with manufacturing information, analytical data and any available clinical data or literature, among other things, to the FDA as part of an IND.

An IND sponsor must submit the results of the preclinical studies, together with manufacturing information, analytical data and any available clinical data or literature, among other things, to the FDA as part of an IND.

Some preclinical testing may continue even after the IND is submitted.

An IND automatically becomes effective 30 days after receipt by the FDA, unless before that time the FDA raises concerns or questions related to one or more proposed clinical trials and places the clinical trial on a clinical hold.

In such a case, the IND sponsor and the FDA must resolve any outstanding concerns before the clinical trial can begin.

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In addition, an IRB at each institution participating in the clinical trial must review and approve the plan for any clinical trial before it commences at that institution.

Information about certain clinical trials must be submitted within specific timeframes to the National Institutes of Health ( “ NIH ” ) for public dissemination on their www.clinicaltrials.gov website.

Information about certain clinical trials must be submitted within specific timeframes to the National Institutes of Health ( “ NIH ” ) for public dissemination on their website www.clinicaltrials.gov.

Human clinical trials are typically conducted in three sequential phases, which may overlap or be combined:

• Phase 1 clinical trial:

The drug is initially introduced into healthy human volunteers or patients with the target disease or condition and tested for safety, dosage tolerance, absorption, metabolism, distribution, excretion and, if possible, to gain an early indication of its effectiveness.

The drug is initially introduced into healthy human volunteers or patients with the targeted disease or condition and tested for safety, dosage tolerance, absorption, metabolism, distribution, excretion and, if possible, to gain an early indication of its effectiveness.

• Phase 2 clinical trial:

The drug is administered to a limited patient population to identify possible adverse effects and safety risks, to preliminarily evaluate the efficacy of the product for specific targeted diseases and to determine dosage tolerance and optimal dosage.

The drug is administered to a limited patient population to identify possible adverse effects and safety risks, to preliminarily evaluate the efficacy of the product for specific targeted diseases or conditions and to determine dosage tolerance and optimal dosage.

• Phase 3 clinical trial:

The drug is administered to an expanded patient population, generally at geographically dispersed clinical trial sites, in well-controlled clinical trials to generate enough data to statistically evaluate the efficacy and safety of the product for approval, to establish the overall risk-benefit profile of the product and to provide adequate information for the labeling of the product.

Progress reports detailing the results of the clinical trials must be submitted at least annually to the FDA and more frequently if serious adverse events occur.

Progress reports detailing the results of the clinical trials must be submitted at least annually to the FDA, and more frequently if serious adverse events are observed.

Each of Phase 1, Phase 2 and Phase 3 clinical trials may not be completed successfully within any specified period, or at all.

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Under the Prescription Drug User Fee Act ( “ PDUFA ” ) guidelines that are currently in effect, the FDA has a goal of ten months from the date of “filing” of a standard NDA for a new molecular entity to review and act on the submission.

This review typically takes twelve months from the date the NDA is submitted to FDA because the FDA has approximately two months to make a “filing” decision.

This review typically takes twelve months from the date the NDA is submitted to the FDA because the FDA has approximately two months to make a “filing” decision.

The FDA conducts a preliminary review of all NDAs within the first 60 days after submission, before accepting them for filing, to determine whether they are sufficiently complete to permit substantive review.

The FDA may request additional information rather than accept an NDA for filing.

The FDA may request additional information rather than accepting an NDA for filing.

In this event, the application must be resubmitted with the additional information.

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The FDA also may require submission of a risk evaluation and mitigation strategy ( “ REMS ” ) plan to ensure that the benefits of the drug outweigh its risks.

The REMS plan could include medication guides, physician communication plans, assessment plans, or elements to assure safe use, such as restricted distribution methods, patient registries, or other risk minimization tools.

A REMS plan could include medication guides, physician communication plans, assessment plans, or elements to assure safe use, such as restricted distribution methods, patient registries or other risk minimization tools.

The FDA may refer an application for a novel drug to an advisory committee.

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If a product that has orphan drug designation subsequently receives the first FDA approval for the disease for which it has such designation, the product is entitled to orphan product exclusivity, which means that the FDA may not approve any other applications, including a full NDA or BLA, or an abbreviated NDA (“ANDA”) or biosimilar application, to market a drug or biologic with the same active moiety for the same indication for seven years, except in limited circumstances, such as a showing of clinical superiority to the product with orphan drug exclusivity.

Orphan drug exclusivity does not prevent FDA from approving a different drug or biologic for the same disease or condition, or the same drug or biologic for a different disease or condition.

Orphan drug exclusivity does not prevent the FDA from approving a different drug or biologic for the same disease or condition, or the same drug or biologic for a different disease or condition.

Among the other benefits of orphan drug designation are tax credits for certain research and a waiver of the application user fee.

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For example, the FDA may require post-marketing testing, including Phase 4 clinical trials and surveillance to further assess and monitor the product’s safety and effectiveness after commercialization.

In addition, drug manufacturers and other entities involved in the manufacture and distribution of approved drugs are required to register their establishments with the FDA and state agencies and are subject to periodic unannounced inspections by the FDA and these state agencies for compliance with cGMP requirements.

Changes to the manufacturing process are strictly regulated and often require prior FDA approval before being implemented.

In addition, drug manufacturers and other entities involved in the manufacture and distribution of approved drugs are required to register their establishments with the FDA and state agencies and are subject to periodic unannounced inspections by the FDA and state agencies for compliance with cGMP requirements.

Changes to the manufacturing process

are strictly regulated and often require prior FDA approval before being implemented.

FDA regulations also require investigation and correction of any deviations from cGMP requirements and impose reporting and documentation requirements upon the sponsor and any third-party manufacturers that the sponsor may decide to use.

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Each payor determines whether or not it will provide coverage for a therapy, what amount it will pay the manufacturer for the therapy, and on what tier of its formulary it will be placed.

The position on a payor’s list of covered drugs, or formulary, generally determines the co-payment that a patient will need to make to obtain the therapy and can strongly influence the adoption of such therapy by patients and physicians.

Adoption of price controls and cost-containment measures, and adoption of more restrictive policies in jurisdictions with existing controls and measures, could further limit our net revenue and results.

The position on a payor’s list of covered drugs, or formulary, generally determines the copayment that a patient will need to make to obtain the therapy and can strongly influence the adoption of such therapy by patients and physicians.

Decreases in third-party reimbursement for our drug candidates or a decision by a third-party payor to not cover our drug candidates could reduce physician usage of our drug candidates, once approved, and have a material adverse effect on our sales, results of operations and financial condition.

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Other Healthcare Laws

Because of our current and future arrangements with healthcare professionals, principal investigators, consultants, customers and third-party payors, we will also be subject to healthcare regulation and enforcement by the federal government and the state and foreign governments in which we will conduct our business, including our clinical research, proposed sales, marketing and educational programs.

Because of our current and future arrangements with healthcare professionals, principal investigators, consultants, customers and third-party payors, we will also be subject to healthcare regulation and enforcement by the federal government and the state and foreign governments in which we will conduct our business, including clinical research, proposed sales, marketing and educational programs.

laws that may affect our ability to operate, among others, include:

the federal Health Insurance Portability and Accountability Act of 1996 ( “ HIPPA ” ), as amended by the Health Information Technology for Economic and Clinical Health Act ( “ HITECH ” ), which governs the conduct of “covered entities,” including certain healthcare providers, health plans, and healthcare clearinghouses, as well as their respective “business associates,” including their covered subcontractors, that create, receive, maintain or transmit individually identifiable health information for or on behalf of a covered entity, with respect to certain electronic healthcare transactions and protecting the security and privacy of protected health information;

the Health Insurance Portability and Accountability Act of 1996 (“HIPAA”), as amended by the Health Information Technology for Economic and Clinical Health Act (“HITECH”), which created federal criminal statutes that prohibit, among other things, knowingly and willfully executing a scheme to defraud any healthcare benefit program, including private third-party payors and knowing and willfully falsifying, concealing or covering up a material fact or making any materially false, fictitious or fraudulent statement in connection with the delivery of or payment for healthcare benefits, items or services, and governs the conduct of “covered entities,” including certain healthcare providers, health plans and healthcare clearinghouses, as well as their respective “business associates,” including their covered subcontractors, that create, receive, maintain or transmit individually identifiable health information for or on behalf of a covered entity, with respect to certain electronic healthcare transactions and protecting the security and privacy of protected health information;

certain state laws governing the privacy and security of health information in certain circumstances, some of which are more stringent than HIPAA and many of which differ from each other in significant ways and may not have the same effect, thus complicating compliance efforts;

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Department of Health and Human Services (“HHS”) information related to payments and other transfers of value to physicians (defined to include doctors, dentists, optometrists, podiatrists and chiropractors), certain other healthcare professionals (such as physician assistants and nurse practitioners) and teaching hospitals, and ownership and investment interests held by physicians and their immediate family members.

In addition, many states have similar laws and regulations, such as anti-kickback and false claims laws that may be broader in scope and may apply regardless of payor, in addition to items and services reimbursed under Medicaid and other state programs.

Additionally, to the extent that our product is sold in a foreign country, we may be subject to similar foreign laws.

Failure to comply with these laws, where applicable, can result in the imposition of significant penalties, including civil, criminal, and administrative penalties, damages, disgorgement, monetary fines, possible exclusion from participation in Medicare, Medicaid and other federal healthcare programs, imprisonment, and integrity oversight and reporting obligations.

Failure to comply with these laws, where applicable, can result in the imposition of significant penalties, including civil, criminal, and administrative penalties;

damages, disgorgement, monetary fines, exclusion from participation in Medicare, Medicaid and other federal or state healthcare programs, imprisonment, and integrity oversight and reporting obligations.

Healthcare Reform

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For example, implementation of the Patient Protection and Affordable Care Act, as amended by the Health Care and Education Reconciliation Act, collectively the Affordable Care Act ( “ PPACA ” ), has substantially changed healthcare financing and delivery by both governmental and private insurers, and significantly impacted the pharmaceutical industry.

The PPACA, among other things, established an annual, nondeductible fee on any entity that manufactures or imports certain specified branded prescription drugs and biologic agents, revised the methodology by which rebates owed by manufacturers to the state and federal government for covered outpatient drugs under the Medicaid Drug Rebate Program are calculated, increased the minimum Medicaid rebates owed by most manufacturers under the Medicaid Drug Rebate Program, extended the Medicaid Drug Rebate program to utilization of prescriptions of individuals enrolled in Medicaid managed care organizations, provided incentives to programs that increase the federal government’s comparative effectiveness research and created a licensure frame work for follow-on biologic products.

The PPACA, among other things, established an annual, nondeductible fee for any entity that manufactures or imports certain specified branded prescription drugs and biologic agents, revised the methodology by which rebates owed by manufacturers to the state and federal governments for covered outpatient drugs under the Medicaid Drug Rebate Program are calculated, increased the minimum Medicaid rebates owed by most manufacturers under the Medicaid Drug Rebate Program, extended the Medicaid Drug Rebate program to utilization of prescriptions of individuals enrolled in Medicaid managed care organizations, provided incentives to programs that increase the federal government’s comparative effectiveness research and created a licensure framework for follow-on biologic products.

Since its enactment there have been executive, judicial and congressional challenges to certain aspects of the PPACA.

For example, on June 17, 2021, the U.S.

Supreme Court dismissed a challenge on procedural grounds that argued the PPACA is unconstitutional in its entirety because the “individual mandate” was repealed by Congress.

Further, on August 16, 2022, President Biden signed the

Inflation Reduction Act of 2022 ( “ IRA ” ) into law, which among other things, extends enhanced subsidies for individuals purchasing health insurance coverage in PPACA marketplaces through plan year 2025.

The IRA also eliminates the “donut hole” under the Medicare Part D program beginning in 2025 by significantly lowering the beneficiary maximum out-of-pocket cost and creating a new manufacturer discount program.

It is possible that the PPACA will be subject to judicial or Congressional challenges in the future.

It is unclear how any such challenges and the healthcare reform measures of the Biden administration will impact the PPACA.

On August 16, 2022, the Inflation Reduction Act of 2022 ( “ IRA ” ) was signed into law, which among other things, extended enhanced subsidies for individuals purchasing health insurance coverage in PPACA marketplaces through plan year 2025.

The IRA also eliminated the “donut hole” under the Medicare Part D program beginning in 2025 by significantly lowering the beneficiary maximum out-of-pocket cost and creating a new manufacturer discount program.

It is possible that the PPACA

will be subject to judicial or congressional challenges in the future.

It is unclear how any such challenges and the healthcare reform measures of the current administration will impact the PPACA and our business.

In addition, other legislative changes have been proposed and adopted since the PPACA was enacted.

In August 2011, then President Obama signed into law the Budget Control Act of 2011, which, among other things, created the Joint Select Committee on Deficit Reduction to recommend to Congress proposals for spending reductions.

In August 2011, the Budget Control Act of 2011 was signed into law, which, among other things, created the Joint Select Committee on Deficit Reduction to recommend to Congress proposals for spending reductions.

The Joint Select Committee did not achieve a targeted deficit reduction of at least $1.2 trillion for the years 2013 through 2021, triggering the legislation’s automatic reduction to several government programs.

This includes reductions to Medicare payments to providers of 2% per fiscal year, which went into effect in April 2013 and, due to subsequent legislative amendments, including the BBA, will remain in effect until 2032 unless additional congressional action is taken.

Additionally, in January 2013, then President Obama signed into law the American Taxpayer Relief Act of 2012, which, among other things, reduced Medicare payments to several providers and increased the statute of limitations period for the government to recover overpayments to providers from three to five years.

Congress is also considering additional health reform measures.

Further, there has been heightened governmental scrutiny over the manner in which manufacturers set prices for their marketed products.

For example, there have been presidential executive orders, Congressional inquiries and proposed and enacted federal and state legislation designed to, among other things, bring more transparency to drug pricing, review the relationship between pricing and manufacturer patient programs, and reform government program reimbursement methodologies for drug products.

For example, in July 2021, the Biden administration released an executive order, “Promoting Competition in the American Economy,” with multiple provisions aimed at prescription drugs.

In response to Biden’s executive order, on September 9, 2021, HHS released a Comprehensive Plan for Addressing High Drug Prices that outlines principles for drug pricing reform and sets out a variety of potential legislative policies that Congress could pursue as well as potential administrative actions HHS can take to advance these principles.

Further, the IRA, among other things (i) directs HHS to negotiate the price of certain high-expenditure, single-source drugs and biologics covered under Medicare and (ii) imposes rebates under Medicare Part B and Medicare Part D to penalize price increases that outpace inflation.

These provisions started to take effect in fiscal year 2023 and will continue to take effect progressively thereafter, although may be subject to legal challenges.

On August 29, 2023, HHS announced the list of the first ten drugs that will be subject to price negotiations, although the Medicare drug price negotiation program is currently subject to legal challenges.

It is currently unclear how the IRA will be implemented but is likely to have a significant impact on the pharmaceutical industry.

In response to the Biden administration’s October 2022 executive order, on February 14, 2023, HHS released a report outlining three new models for testing by the CMS Innovation Center which will be evaluated on their ability to lower the cost of drugs, promote accessibility, and improve quality of care.

It is unclear whether the models will be utilized in any health reform measures in the future.

Further, on December 7, 2023, the Biden administration announced an initiative to control the price of prescription drugs through the use of march-in rights under the Bayh-Dole Act.

Further, there has been heightened governmental scrutiny recently over the manner in which drug manufacturers set prices for their marketed products, which have resulted in several presidential executive orders, congressional inquiries and proposed and enacted federal and state legislation designed to, among other things, bring more transparency to product pricing, review the relationship between pricing and manufacturer patient programs, and reform government program reimbursement methodologies for drug products.

At the federal level, the IRA, among other things, (i) directs the U.S.

Department of Health and Human Services (“HHS”) to negotiate the price of certain high-expenditure, single-source drugs that have been on the market for at least 7 years and biologics that have been on the market for at least 11 years covered under Medicare (the “Medicare Drug Price Negotiation Program”), and (ii) imposes rebates under Medicare Part B and Medicare Part D to penalize price increases that outpace inflation.

These provisions began to take effect progressively starting in fiscal year 2023.

On August 15, 2024, HHS announced the agreed-upon price of the first ten drugs that were subject to price negotiations, although the Medicare Drug Price Negotiation Program is currently subject to legal challenges.

On January 17, 2025, HHS selected fifteen additional products covered under Part D for price negotiation in 2025.

Each year thereafter more Part B and Part D products will become subject to the Medicare Drug Price Negotiation Program.

Further, on December 7, 2023, an initiative to control the price of prescription drugs through the use of march-in rights under the Bayh-Dole Act was announced.

On December 8, 2023, the National Institute of Standards and Technology published for comment a Draft Interagency Guidance Framework for Considering the Exercise of March-In Rights which for the first time includes the price of a product as one factor an agency can use when deciding to exercise march-in rights.

While march-in rights have not previously been exercised, it is uncertain if that will continue under the new framework.

Additionally, in the United States and some foreign jurisdictions there have been, and continue to be, several legislative and regulatory changes and proposed reforms of the healthcare system in an effort to contain costs, improve quality, and expand access to care, particularly in light of the recent U.S.

presidential and congressional elections.

These reform initiatives may, among other things, result in modifications to the aforementioned laws and/or the implementation of new laws affecting the healthcare industry.

Human Capital Management

Our employees are dedicated to our mission of developing and delivering medicines that create new possibilities and more good days for people living with epilepsies and brain conditions.

As of December 31, 2023, we had 40 full-time employees, the majority of whom were primarily engaged in research and development activities, including five individuals with M.D.

degrees and 13 professionals with Ph.D.

As of December 31, 2024, we had 23 full-time employees, the majority of whom were primarily engaged in research and development activities, including two individuals with M.D.

degrees and seven professionals with Ph.D.

degrees specializing in the sciences.

Many of these professionals have extensive epilepsy and neurology experience.

In total, within our management team, we have colleagues who worked to shape the development or commercialization of a number of important marketed neurology and ASMs, including:

In total, within our management team, we have colleagues who worked to shape the development or commercialization of a number of important marketed neurology drugs and ASMs, including:

Ztalmy, Fintepla, Brineura, Gilenya, Tysabri and Tecfidera.

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We emphasize a number of measures and objectives in managing our human capital assets, including, among others:

employee engagement, development and training, talent acquisition and retention, employee wellness, diversity, inclusion, and compensation, benefits and equity.

employee engagement, development and training, talent acquisition and retention, employee wellness, diversity and inclusion, and compensation, benefits and equity.

We believe that developing a diverse and inclusive culture is central to continuing to attract and retain the top talent necessary to deliver on our growth strategy.

As such, we are investing in a work environment in which our employees feel inspired, included and enjoy a strong sense of belonging.

This includes a focus on extending our diversity,

equity, inclusion and belonging (“DEIB”) initiatives across our entire workforce, with specific employee engagement via the DEIB Committee.

Approximately half of our employees are female, as are one-third of our board of directors.

Approximately half of our organization is multicultural.

We value our employees’ insatiable curiosity to translate scientific discoveries into innovative medicines and their courage and perseverance to overcome obstacles and operate with a sense of purpose and urgency on behalf of patients.

Grounded in these guiding principles, we believe we have developed a collaborative environment where our colleagues feel respected, valued, and can contribute to their fullest potential.

We value our employees’ curiosity to translate scientific discoveries into innovative medicines and their courage and perseverance to overcome obstacles and operate with a sense of purpose and urgency on behalf of patients.

Grounded in these guiding principles, we believe we have developed a collaborative and highly engaged environment where our colleagues feel respected and valued, and can contribute to their fullest potential.

We have equity incentive plans that are designed to attract, retain and motivate selected employees, consultants and directors through the granting of equity-based compensation awards and cash-based compensation awards, in order to increase stockholder value and the success of our company by motivating such individuals to perform to the best of their abilities and achieve our objectives.

In addition, our governance is overseen by an independent and diverse Board of Directors who provide and complement our expertise to help oversee the strategy and performance of our Company.

Among our Board of Directors, five out of six members are independent.

In addition, our governance is overseen by an independent and diverse Board of Directors who provide and complement our expertise to oversee the strategy and performance of our company.

Among our Board of Directors, four out of five members are independent.

Collectively, our Board of Directors provides insight and expertise in areas of importance to the performance and growth of our enterprise, including experience as:

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financial, transactional and oversight experience at public companies;

proven biopharmaceutical and neuroscience experience;

proven biopharmaceutical experience;

research and regulatory acumen in drug development;

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We lease the space for our principal executive offices, which are located at 441 Ninth Avenue, 14th Floor, New York, New York.

In June 2022, we formally instituted our hybrid work policies.

In 2022, we executed what we believe was a smooth transition to a hybrid work environment while ensuring that ample resources, support and flexibility were available to our employees.

Our headquarter office facilities in New York, New York have received LEED Platinum certification.

In 2022, we formally instituted hybrid work policies.

Our office facilities have received LEED Platinum certification.

Corporate and Other Information

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Our corporate website address is www.ovidrx.com.

Information contained on or accessible through our website is not a part of this Annual Report, and the inclusion of our website address in this Annual Report is an inactive textual reference only.

Information contained on or accessible through our website is not a part of this Annual Report on Form 10-K, and the inclusion of our website address in this Annual Report is an inactive textual reference only.

We file electronically with the Securities and Exchange Commission (“SEC”) our annual reports on Form 10-K, quarterly reports on Form 10-Q, current reports on Form 8-K and amendments to those reports filed or furnished pursuant to Section 13(a) or 15(d) of the Exchange Act.

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Compared sentence by sentence after normalising whitespace, quotation marks, case and digits, so re-formatting and restated figures do not read as changed language. Wording changes appear as one removal and one addition. The current filing and the prior one are authoritative.

What changed 10-K

Item 1. Business