Ovid Therapeutics Cowen and Company 39th Annual Health Care Conference March 11, 2019 Exhibit 99.1

Disclaimers and Forward-Looking Statements This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Words such as "may," "will," "expect," "plan," "anticipate" and similar expressions (as well as other words or expressions referencing future events or circumstances) are intended to identify forward-looking statements. Forward-looking statements contained in this presentation include statements about the progress, timing, clinical development and scope of clinical trials and the reporting of clinical data for the Company’s product candidates; the potential clinical benefit of the Company’s product candidates; the timing and outcome of discussions with regulatory authorities; the success of any partnering opportunities; and the use of 24HC as a biomarker for target engagement. Each of these forward-looking statements involves risks and uncertainties. These statements are based on the Company’s current expectations and projections made by management and are not guarantees of future performance. Therefore, actual events, outcomes and results may differ materially from what is expressed or forecast in such forward-looking statements. Factors that may cause actual results to differ materially from these forward-looking statements are discussed in the Company’s filings with the U.S. Securities and Exchange Commission, including the "Risk Factors" sections contained therein. Except as otherwise required under federal securities laws, we do not have any intention or obligation to update or revise any forward-looking statements, whether as a result of new information, future events, changes in assumptions or otherwise.

Ovid Highlights: Building a Leading Company in Neurology Ovid is focused on developing novel medicines for patients with rare CNS disorders Phase 2 and Phase 3 clinical development stage programs OV101: Phase 3 pivotal study of OV101 in Angelman Syndrome (NEPTUNE study, start 2H’19) OV101: Phase 2 ongoing study in Fragile X (ROCKET study, data 2H’19) OV935: Phase 2 studies for rare epilepsy types, including: Dravet, LGS, Dup15q Syndrome and CDKL5 Deficiency (ELEKTRA, ARCADE, ENDYMION) Well capitalized to execute on our plan; multiple near-term milestones expected Leadership team with deep experience developing drugs and building companies

Focused Product Pipeline in Neurodevelopment and Epilepsies * Also known as TAK-935. Co-development program with Takeda Pharmaceutical Company Limited pursuant to a license and collaboration agreement. RESEARCH PRECLINICAL PHASE 1 PHASE 2 PHASE 3 δ-selective GABAA receptor agonist Angelman Syndrome OV101 δ-selective GABAA receptor agonist Fragile X Syndrome OV101 OV329 GABA aminotransferase inhibitor Treatment-resistant Epilepsy OV935* Developmental and Epileptic Encephalopathies CH24H inhibitor CDKL5 deficiency disorder & Dup15q syndrome CH24H inhibitor Dravet syndrome & Lennox-Gastaut syndrome Angelman Syndrome: Orphan Drug & Fast Track Designations Fragile X Syndrome: Orphan Drug & Fast Track Designations DEE: Orphan Drug Designations for LGS and Dravet Syndrome Plan to start pivotal Ph 3 NEPTUNE in 2H19

Focus on Rare Neurology with Ongoing Programs in Neurodevelopment Disorders and Epilepsy Types Glutamatergic Pathways (Excitatory) GABAergic Pathways (Inhibitory) Rare Neurology Angelman syndrome Fragile X syndrome Epilepsies Dravet syndrome CDKL5 Deficiency Disorder Neurodevelopment Lennox-Gastaut Dup 15q

OV101 Potential First-in-Class Therapeutic for Angelman & Fragile X Syndromes

OV101, a First-in-Class Extrasynaptic δ-Selective GABAA Receptor Agonist OV101 is differentiated from other GABAA modulators Chemical structure conformationally rigid leading to greater specificity at binding pocket Active when endogenous GABA levels are low or absent Selectively targets extrasynaptic δ-subunit-containing GABAA receptors to restore tonic inhibition1 OV101 potentiates tonic inhibition at low nM concentrations2,3 Important in differentiating ‘signal’ to ‘noise’ in a variety of disorders such as AS (Angelman Syndrome), FXS (Fragile X Syndrome) 1. Egawa K et al. Sci Transl Med. 2012;4:163ra157. 2. Meera P et al. J Neurophysiol. 2011;106:2057-2064. 3. Belelli D et al. J Neurosci. 2005;25:11513-11520.

Tonic Inhibition is Central to Angelman & Fragile X Syndrome Pathophysiology Loss of tonic inhibition leads to dysregulation of neuronal circuit excitability Synaptic GABAA receptors mediate phasic inhibition Extrasynaptic δ-subunit-containing GABAA receptors mediate tonic inhibition Mouse models of AS and FXS have reduced extrasynaptic GABAA signaling resulting in loss of tonic inhibition UBE3A silencing in mouse models results in a phenotype similar to AS in humans including motor, learning and behavioral deficits2 Mouse models of FXS (Fmr1-/-) exhibit a behavioral and cognitive phenotype similar to human disease Restoring Tonic Inhibition in these models improves core symptoms1,2,3 1Olmos-Serrano et al., J. Neurosci. 2010 2Egawa et al., Sci. Trans. Med. 2012 3Olmos-Serrano et al., Dev Neurosci. 2011 Healthy Fragile X Syndrome (Fmr1 KO)1 100µM Gabazine 100µM Gabazine Healthy Angelman Syndrome (Ube3am-/p+)2 Tonic Inhibitory Currents are Reduced in FXS and AS

Data Suggest a Prolonged Pharmacodynamic Effect of OV101, Despite its Similar Pharmacokinetic Profile to Other GABAA Agonists Statistical analysis of planar gradiometer configured *magnetoencephalographic (MEG) data OV101 (n=10) Source: Neuropharmacology 88 (2015), D. Nutt et al 60mins 160mins Zolpidem (n=12) 60mins 160mins Red = relatively more power following the drug Blue = relatively less MEG* data of OV101 results in sustained increase in delta, theta, alpha, and beta frequencies Zolpidem and OV101 have similar PK profiles…but OV101 has longer lasting effects (PD profile)

OV101: Scientific Rationale in Two Serious Rare Disorders Well Defined Genetic Disorders High unmet medical need No approved therapies in US, EU, or ROW; treatment is limited to supportive care Lifelong disorders that present early in childhood Fragile X Syndrome Caused by CGG expansion in FMR1 gene Significant anxiety, behavior challenges, and cognitive impairment Most common inherited form of intellectual disability Prevalence**: ~1/3,600-4,000 males ~1/4,000-6,000 females Males with FXS are more severely affected than females Angelman Syndrome Loss of functional UBE3A protein due to defect of UBE3A gene on maternal chromosome 15 Decreased extrasynaptic GABA levels lead to decreased tonic inhibition and resulting downstream clinical phenotype Global disruption in behavior, motor, sleep and cognitive functions Prevalence in general population*: 1 in 12,000 to 20,000 people . Sources: *NORD, NIH website, Genetics Home Reference and NCBI . ** National Fragile X Foundation

Angelman Syndrome: Clinical Characteristics Average age of diagnosis is 21 Months Requires life-long care Life span typically normal Source: Angelman Syndrome Foundation website Physical / Motor Wide-based, unstable gait Protruding tongue Suck / swallow disorders Frequent drooling Other fine and gross motor impairments Medical / Sleep CNS: Seizures, Strabismus Sleep: Abnormal sleep-wake cycles GI: Constipation Behavior / Cognitive Significant developmental delay Severe language impairment (e.g. need external communication support) Hyperactivity Short attention span

STARS was First Industry-Sponsored Clinical Trial in Angelman Syndrome * Excluding, poorly controlled seizure activity, concomitant use of minocycline, levodopa, zolpidem, zaleplon, eszopiclone, ramelteon, or cannabinoid derivatives or any other investigational agent, device, and/or procedure. BID=twice a day; BL=baseline; QD=every day. Key Inclusion Criteria: Age 13 - 49 years, inclusive 12 sites in US, 1 site in Israel Confirmed molecular diagnosis of Angelman syndrome Stable regimen of concomitant medications* Primary Outcome Measure: Safety and tolerability of OV101 vs placebo Exploratory Outcome Measures: Efficacy measures of OV101 vs placebo Placebo (placebo morning, placebo night) OV101 BID (10 mg morning, 15 mg evening) OV101 QD (placebo morning, 15 mg evening) -2 0 6 12 Screening Baseline & Randomize (1:1:1) Assessment Points (weeks)

STARS Trial: OV101 Achieved Primary Endpoint of Safety and Tolerability and Demonstrated Statistical Significance in Exploratory Endpoints Primary Endpoint (Safety/Tolerability): OV101 was well-tolerated with a favorable risk profile Majority of AEs were mild Exploratory Endpoints (Efficacy): Global symptoms: Clinical Global Impressions- Improvement (CGI-I) Combined OV101 treatment groups vs placebo (p=0.0103) driven by QD group (p=0.0006); BID not significant (NS) Symptom Specific (QD arm): Sleep: Improvements on Latency to sleep onset which is important symptom in AS Motor: Improvements on overall and gross motor function, mobility, stride velocity/cadence, and daily activity Global Improvement Sleep Motor

CGI-I (Clinical Global Impression-Improvement) the Right Endpoint for Studying Patients with Angelman Syndrome Patients Rated on a Likert 7-Point Scale* 1 = very much improved 2 = much improved 3 = minimally improved 4 = no change 5 = minimally worse 6 = much worse 7 = very much worse Validated measure used in neurology and psychiatry trials Clinician Assessed Changes of even 1 point in the scale represent a clinically meaningful change for this patient population Co-primary endpoint in several FDA-approved and ongoing clinical trial programs including: Nuplazid (Psychosis), Intuniv (ADHD) Captures the improvement in the totality of a patient’s symptoms Each patient represents his/her own control providing sensitivity and validity in measuring change in a highly heterogenous disorder Neurodevelopmental conditions like AS are highly heterogeneous Individual patients with AS have varying degrees of impairment with sleep, communication, behavior, motor, or seizures * Scores are assessed from baseline, defined as initiation of treatment.

Data support rationale for OV101 15 mg QD as an apparent efficacious dose in AS Based on Patients’ Scores at Week 12, Two-Thirds Experienced Clinically-Meaningful Improvement and Nearly One-Third Had Much Improvement *Mean CGI-I Symptoms Overall Score at Week 12 (MMRM) *LS mean difference [Drug-Placebo] (95% CI) was -0.78 (-1.22, -0.35) with OV101 QD and -0.21 (-.064, .022) with OV101 BID Source: AACAP Poster 2018 Patients in each CGI-I score category (%) CGI-I Symptoms Overall at Week 12 Blue bars highlight scores of patients with improvement (2,3) p=0.0006 p=0.3446 Difference Vs Placebo*

STARS Phase 2 Trial in Angelman Syndrome: Summary and Conclusions Source: Ovid press release dated December 6, 2018 STARS achieved primary endpoint of safety and tolerability Exploratory efficacy with improvements in global function and relevant symptom domains in QD dosing arm vs placebo Global: Statistically significant improvement in CGI-I Sleep: Reduction in sleep onset latency and improvement in clinical impressions of overall sleep; observed reduction in latency to sleep onset may be indicative of target engagement Motor: Noted changes (post hoc) in relevant assessments of gait, activities of daily living Behavior: Among those who had CGI- improvements, associated parental narratives report improvements in communication, behavior but no changes seen on traditional assessment scales (ABC, ADAMS) QD Dosing appears to be efficacious dose Actigraphy and clinical data suggest induction of tolerance with BID dose exposure leading to the observed reduced efficacy in the BID group Consistent with the known pharmacology of other CNS drugs (e.g. SSRIs, benzodiazepines) where tolerance develops at higher dosages

OV101’s Development in Angelman Syndrome – Pivotal Phase 3 and Next Steps Pivotal Phase 3 NEPTUNE trial Design based on End-of Phase 2 Meeting with the FDA Single 12-week, two-arm, randomized, double-blind, placebo-controlled trial Once-daily (weight-based) dose Approximately 60 patients aged 4 to 12 years Primary endpoint of CGI-I score at week 12 Secondary endpoints: Sleep measures and Vineland-3 developmental scale (adaptive behavior) Trial initiation pending FDA Type C meeting agreement on protocol and supporting materials Enrollment expected to begin in 2H:19 ELARA Open-Label Extension study for people with AS who previously completed an OV101 trial Recruitment initiated with FPI in Feb 2019 Source: Ovid press release dated December 6, 2018 FPI: First Patient In

OV101: Scientific Rationale in Two Serious Rare Disorders Well Defined Genetic Disorders High unmet medical need No approved therapies in US, EU, or ROW; treatment is limited to supportive care Lifelong disorders that present early in childhood Fragile X Syndrome Caused by CGG expansion in FMR1 gene Significant anxiety, behavior challenges, and cognitive impairment Most common inherited form of intellectual disability Prevalence**: ~1/3,600-4,000 males ~1/4,000-6,000 females Males with FXS are more severely affected than females Angelman Syndrome Loss of functional UBE3A protein due to defect of UBE3A gene on maternal chromosome 15 Decreased extrasynaptic GABA levels lead to decreased tonic inhibition and resulting downstream clinical phenotype Global disruption in behavior, motor, sleep and cognitive functions Prevalence in general population*: 1 in 12,000 to 20,000 people . Sources: *NORD, NIH website, Genetics Home Reference and NCBI ** National Fragile X Foundation

Fragile X Syndrome: Clinical Characteristics Average age of diagnosis Males: 35 – 37 months Females: 41.6 months 29% of FXS families have 2 or more children with FXS Life span typically normal Williams et al., 2006 Physical Large prominent ears, prominent jaw & forehead Hyperflexible joints Classic gaze aversion Medical CNS: Seizures (15%); Strabismus (30%) ENT: Otitis, sinusitis CV: Mitral valve prolapse GI: Reflux, Sleep apnea, Loose stools Behavior Attention deficit (80% of males) Hyperactivity (65% of males) Anxiety (70% of males) Self-injurious Aggressiveness

OV101 in Fragile X Syndrome: Phase 2 Clinical Trials Underway Orphan Drug and Fast Track designations Primary Objective: Assess safety and tolerability of OV101 over 12 weeks of treatment across 3 daily dosing regimens Patient Population (n=30): Adult and adolescent males with diagnosis of FXS Ages: 13-22 years Timeline: Data expected in 2H’19 Endpoints: Primary – incidence of AEs. Secondary – changes in behavior (ABC scales) Status: Recruiting Primary objective: Cohort, non-drug study to assess suitability of scales to measure behavior, sleep, and functioning in individuals with Fragile X syndrome 0

Phase 2 ROCKET Trial in Patients with Fragile X Syndrome 1 OV101 Treatment Arm (5mg QD) OV101 Treatment Arm (5mg TID) OV101 Treatment Arm (5mg BID) Screening Baseline & Randomize (1:1:1) Week 12 Timeline Key Endpoints Trial Initiated: Q3:18 Topline Data Expected: 2H: 19 Primary Endpoint: Incidence of AEs Secondary Endpoint: Changes in behavior (ABC scales)

OV935 New Approach to Potentially Treat Rare Developmental and Epileptic Encephalopathies

Refractory seizures do not respond to medicines that exert anti-seizure effect through same target or MOA as marketed AEDs Approximately 100,000 - 200,000 US Population with Rare Seizure Disorders* Illustrative purposes only 1 out of 3 PATIENTS Small number achieve seizure freedom with addition of 1 or more AEDs 1 out of 2 PATIENTS ALL EPILEPSY PATIENTS Current marketed AEDs act through four main mechanisms: 1. Modulation of voltage-gated ion channels 2. Enhancement of GABA-mediated inhibition 3. Interactions with elements of the synaptic release machinery 4. Blockage of ionotropic glutamate receptors Seizure free with one AED Refractory seizures despite available medications Novel Mechanism of Actions are Needed to Treat Refractory Seizures Source: *Orphanet

Focus of Broad OV935 Development Program: Severe Developmental and Epileptic Encephalopathies Dravet 80% have mutation in SCN1A gene US prevalence: ~1;15,000 – 1:21,000 Few treatment options Lennox- Gastaut Some patients have SCN2A mutations US prevalence: ~1:10,000 <10% controlled by existing medications CDKL5 (CDD) Mutation of cyclin- dependent kinase- like 5 gene on X chromosome US prevalence: ~1:40,000–1:60,000, increasing with genetic testing No approved targeted treatments Dup15q Caused by duplications of chromosome 15q11.2-q131.1 US incidence: ~1:30,000 No approved targeted treatments Frequent and prolonged treatment-resistant seizures Most patients uncontrolled even on multiple AEDs

CH24H is a brain-specific enzyme for cholesterol catabolism 24HC is a clinically monitorable plasma marker that appears to correlate with active target engagement OV935: Mechanism of Action OV935 T In Plasma In Brain *CH24H, cholesterol 24‑hydroxylase ; 24HC, 24S-hydroxycholesterol CH24H Pathway is Unique to the Brain – 24HC is a Measurable Marker in Plasma*

Highly potent, orally administered, inhibitor of brain specific cholesterol 24-hydroxylase Composition-of-matter patents through 2032, without regulatory extensions and Orphan Drug designations for Dravet and Lennox-Gastaut syndromes Novel mechanism of action and acts through pathways that are not targets of other anti-epileptic drugs (AEDs) Survival benefit in transgenic epilepsy models1 Anti-inflammatory and glial modulatory activity contributing to disease modification in animal models Neuroprotection from glutamate toxicity2 Potential for 24 Hydroxycholesterol to act as a plasma biomarker3,4 1 Nishi, T et al. Inhibition of Cholesterol 24-hyrdroxylase Improves the Survival of a Mouse Model… Society for Neuroscience, poster, Nov 2018 2 Hasegawa S, et al. Cholesterol 24-hydroxylase Inhibition is a Novel Pharmacological Mechanism That Exerts Neuroprotective Effects… Society for Neuroscience, poster, Nov 2018 3Ma s t N, et a l. J Biol Chem. 2017 4Sodero AO, et a l. EMBO J. 2012. OV935: First in Class Inhibitor of CH24H

Key endpoints Primary endpoint Safety and tolerability Secondary and exploratory endpoints Pharmacokinetics (PK) parameters 24S-Hydroxycholesterol (24HC) plasma levels Change in seizure frequency from baseline Trial design Two-part trial* Part 1: Titration Titration (20 days): OV935 100/200 mg BID Treatment (10 days): OV935 300 mg BID Part 2: Open label  Titration (10 Days): OV935 200/300 mg BID Treatment (50 Days): OV935 300 mg BID OV935 Phase 1b/2a Clinical Trial Design OV935 BID Placebo BID Part 1 Double-blind Tx (30 days) Part 2 Open-label Tx (60 days) Follow-up (30 days) Safety and PK assessments Safety, PK, and exploratory assessments OV935 BID End of trial Screening/baseline Randomization Key inclusion criteria Inclusion Adult patients ages 18-65 years Established diagnosis of DEE At least one bilateral motor seizure in baseline period * Eleven US Sites

* Diazepam excluded; generally taken as needed and not as a scheduled medication † All patients prescribed concomitant AEDs Diagnoses Total (N=18) Lennox-Gastaut Syndrome 6 Epileptic Encephalopathy†† 6 Partial Seizures with Secondarily Generalization 1 Frontal Lobe Epilepsy 1 Tuberous Sclerosis Complex 1 Cerebral Dysgenesis 1 Hypothalamic Hamartoma 1 Dravet Syndrome 1 Patients with concomitant AEDs at baseline† Placebo (n=4) OV935 (n=14) Total (N=18) 1 2 - 2 2 - 3 3 3 - 5 5 4+ 2 6 8 † † Epilepsies Not Otherwise Specified AEDs Taken by ≥ 3 Patients Clobazam Clonazepam Lacosamide Lamotrigine Lorazepam Zonisamide Perampanel Phase 1b/2a Trial Results: Heterogeneous Patient Population – Multiple Concomitant AEDs Typical for DEE Median baseline seizure frequency per 28 days OV935 higher baseline seizure frequency vs placebo Source: Ovid press release on December 17, 2018

Primary endpoints: Safety and Tolerability OV935 had a favorable safety profile and generally well tolerated; most AEs were mild PK OV935 plasma levels were dose proportional Seizure Frequency 61% reduction in median seizure frequency observed at Day 92 (end of Treatment Period, excluding patients on perampanel) Observed interaction effect with concomitant perampanel use Two of 11 patients became seizure-free during the last 28 days of treatment (to Day 92) 24HC Reduction of 24HC with OV935 treatment associated with decrease in seizure frequency over time Supports continued investigation of 24HC as a potential biomarker of target engagement Secondary and exploratory endpoints: PK, Seizure frequency, 24HC Source: Ovid press release on December 17, 2018 Phase 1b/2a Trial Results: OV935 Was Generally Well Tolerated With a Favorable Safety and Tolerability Profile—Majority of AEs Were Mild

Plasma 24HC concentration assessed at baseline, pre-dose at Days 11-85, and Day 121 (~30 days following the end of the Treatment) Plasma 24HC (ng/mL) On OV935 in both Part 1 and Part 2 On Placebo and who cross-over to OV935 after Day 31 4 13 4 12 4 7 4 OV935 plasma levels confirm PK/PD modeling and dosing OV935 treatment reduced 24HC plasma levels OV935 PK Plasma levels are dose-proportional 24HC plasma levels Dose- and time-dependent reduction trend observed Following washout, plasma 24HC recovered to pre-treatment levels 8 4 6 4 7 4 8 Phase 1b/2a Trial Results: OV935 Reduced Plasma 24HC vs Placebo – 24HC Potential Biomarker of Target Engagement Part 1 OV935 vs placebo groups Part 2 All on OV935 End of Trial Off treatment Time (Study days) Source: Ovid press release on December 17, 2018

24% 28% 45% 0% 20% 40% 60% 80% 100% Reduction Median Reduction from Baseline in Total Seizures* per 28 Days (FSA, Part 2, including patients on perampanel) 69 85 Time (Study Days) 92 n=16 n=14 n=14 37% 41% 61% 0% 20% 40% 60% 80% 100% Reduction Time (Study Days) Median Reduction from Baseline in Total Seizures* per 28 Days (FSA, Part 2, excluding patients on perampanel) 69 85 92 n=13 n=11 n=11 *The total seizures are based on a period of 28 days on and prior to a specific study day; the first dose day is Study Day 1 Phase 1b/2a Exploratory Analysis: OV935 Reduced Seizure Frequency Over Time in Part 2 *Data represent per protocol analyses; ITT group (n=18) demonstrated median reduction in total seizures of 36% at Day 85. Two patients withdrew in Part 1 (weakness (n=1); difficulty with walking/worsening lethargy (n=1)) and two patients withdrew in Part 2 (seizure cluster (n=2)). Source: Ovid press release on December 17, 2018

Percent change in seizure frequency vs plasma 24HC in Part 2 treatment period Correlation Coefficient (p-value) Day Pearson Spearman Day 85 (n=6) 0.7747 (0.0704) 0.6957 (0.1248) Day 92 (n=6) 0.7962 (0.0581) 0.9856 (0.0003) Time 24 HC Seizure Day 11 Day 11 Day 2 - 11 Day 31 Day 31 Day 22 - 31 Day 85 Day 85 Day 58 - 85 Day 92 Day 85 Day 65 - 92 24HC plasma level (ng/mL) *Day 31: outlier at 358.2% /2.1 ng/mL Phase 1b/2a Exploratory Analysis: Change in Seizure Frequency vs. Plasma 24HC – Excluding Patients on Placebo and Perampanel Source: Ovid press release on December 17, 2018

Dup15q syndrome CDKL5 syndrome Lennox-Gastaut syndrome Dravet syndrome ARCADE: Phase 2 Open-label pilot trial ~30 pediatric patients ELEKTRA: Phase 2 Double-blind, placebo-controlled trial 126 pediatric patients Primary endpoint: Safety and tolerability Phase 1b/2a Adult patients Primary endpoint: Percent change seizure frequency ENDYMION Open-label extension (OLE) trial DEE Primary endpoint: Percent change seizure frequency Current OV935 Clinical Development Program for DEE

Financial Highlights As of December 31, 2018 (1) $72.5 million in cash, cash equivalents and short-term investments ~40.1 million shares of common stock outstanding (1) Pro forma for the net proceeds, before expenses, from an equity financing in February 2019.

*Also known as TAK-935. Co-development program with Takeda Pharmaceutical Company Limited pursuant to a license and collaboration agreement 2019 Business Priorities and Milestones Angelman Syndrome OV101 Fragile X Syndrome OV101 DEE & Rare Epilepsies OV935* Finalize Phase 3 NEPTUNE protocol and submit to FDA (1H:19) Initiate NEPTUNE clinical trial (2H:19) Continue enrollment in ELARA Complete enrollment in Phase 2 ROCKET trial Announce Phase 2 ROCKET trial data (2H:19) Announce SKY ROCKET trial data (2H:19) Submit Phase 1b/2a results to medical meeting (1H:19) Complete enrollment in ARCADE (2H:19) Continue enrollment in ELEKTRA Continue ENDYMION enrollment Corporate Evaluate partnering opportunities that could accelerate development of OV101

Ovid Therapeutics: Our Inspiration to Succeed