Forward-Looking Statements This presentation contains projections for Ovid Therapeutics Inc. ("Ovid") and other forward-looking information. Such projections and information are based on assumptions as to future events t

The Rare Neurological Disorder Company

Corporate Presentation June 9, 2017 Exhibit 99.1

Forward-Looking Statements This

presentation contains projections for Ovid Therapeutics Inc. ("Ovid") and other forward-looking information. Such projections and information are based on assumptions as to future events that are inherently uncertain and

subjective. Ovid, its officers, directors or stockholders make no representations or warranties as to the reasonableness of such assumptions or as to whether the future results will occur as projected. It must be recognized that Ovid is

an early-stage company and that projections of its future performance are necessarily subject to a high degree of uncertainty, that actual results can be expected to vary from the results projected, and that such variances may be material and

adverse. You should and are expected to conduct your own investigation and review of Ovid before determining whether or not to pursue this transaction. Statements made by Ovid in this presentation may contain certain statements that are

forward-looking and involve risks and uncertainties. Words such as "expects," "anticipates," "projects," "estimates," "intends," "plans," "believes," variations of

such words and similar expressions are intended to identify such forward-looking statements. These statements are based on 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 include, but are not

limited to: whether or not any patents issue and the scope of future patent or other intellectual property protection, the risk of third-party challenges to Ovid's intellectual property, the likelihood, timing and scope of any future

collaborations, the initiation, timing, progress and results of our current and future preclinical studies and clinical trials, uncertainties related to drug development results, costs and timelines and regulatory risks. 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. This presentation also contains

estimates and other statistical data made by independent parties and by us relating to market size and growth and other data about our industry. This data involves a number of assumptions and limitations, and you are cautioned not to give undue

weight to such estimates.

To become a leading rare neurological

disorder company Develop innovative therapies addressing disease-relevant pathways to transform the lives of patients and families Built on core pillars of value Rare disorders with a genetic basis & novel MOA Patient-centric approach Scalable

model Compelling growth opportunities Secure early to late stage assets Innovative structures Retain US/EU commercial rights Track record of success Deep expertise in translational science, drug evaluation and orphan clinical drug development

Significant biotech and pharma experience Pipeline of clinical assets Complementary development indications Unmet need and first-in-class MOA OVIDAPPROACH FOCUSED MISSION CLEAR STRATEGY BUSINESS DEVELOPMENT WORLD CLASS TEAM PIPELINE

OURCOMPANY Industry Innovators Jeremy

Levin, DPhil, MB BChir Chairman & CEO Matthew During, MD, DSc Director, Founder, President & CSO Yaron Werber, MD, MBA Chief Business and Financial Officer & Secretary Amit Rakhit, MD, MBA Chief Medical and Portfolio Management Officer

Dirk Haasner, PhD, MPM SVP, Global Regulatory Affairs Claude Nicaise, MD Head, Strategic Orphan Regulatory Affairs Suzanne Wakamoto, SPHR, SHRM-SCP Senior Vice President, Human Resources

-selective GABAA receptor agonist

Angelman Syndrome RESEARCH PRECLINICAL PHASE 1 PHASE 2 PHASE 3 Fragile X Syndrome -selective GABAA receptor agonist -selective GABAA receptor agonist -selective GABAA receptor agonist Oral Adolescent Oral Pediatric Oral Adolescent

Oral Adult OV101 OV101 Undisclosed Indication Intravenous -selective GABAA receptor agonist OV102 *Also known as TAK-935. Co-development program with Takeda Pharmaceutical Company Limited pursuant to a license and collaboration agreement

Epileptic Encephalopathies CH24H inhibitor Oral OV935* Undisclosed Oral Orphan Epilepsy Robust Product Pipeline

Angelman Syndrome Prevalence:

~1/12,000-20,000 No FDA-approved therapies Attractive Market Opportunities OV101 OV935 Dravet Syndrome Incidence: ~1/15,700-20,900 live births No FDA-approved therapies Tuberous Sclerosis Complex Incidence: ~1/6,000 live births Prevalence: ~50,000

in the US Fragile X Syndrome Prevalence: ~1/3,600-4,000 males ~1/4,000-6,000 females No FDA-approved therapies Lennox-Gastaut Syndrome Prevalence: ~30,000 adults & children in the US

2015 2016 2017+ In-licensed OV101 from

Lundbeck Recruited experienced team Completed ~$75m series B financing Initiated manufacturing validation & fill/finish activities Submitted IND for adult AS Phase 2 STARS trial & adolescent AS/FXS Phase 1 PK trial with OV101 Granted Method

of Use for OV101 Granted Orphan Drug Designation for OV101 for the treatment of AS Validated API & completed fill/finish activities Announced global collaboration with Takeda for OV935 Initiated Phase 2 OV101 STARS trial Initiated Phase 1 OV101

PK trial Completed initial public offering Initiate Phase 1b/2a trial with OV935 in epileptic encephalopathies Phase 1 OV101 PK trial data (H2:17) Topline Phase 2 OV101 STARS trial data (2018) Our Accomplishments & Key Milestones NEAR-TERM

INITIATIVES Continue strategic business development activities 2017+

OV101 Potentially First-in-Class

Therapeutic for Angelman & Fragile X Syndromes

Potent, -selective, extrasynaptic

GABAA receptor agonist Validated by clinical data in >4,000 adults with insomnia (approximately 950 patient-years of exposure) Demonstrated ability to restore tonic inhibition and address several key manifestations of AS/FXS Phase 2 STARS trial

recruiting adult AS patients Phase 1 PK trial recruiting adolescents with AS/FXS Preclinical toxicology ongoing to support pediatric studies Portfolio of global polymorph patents to expire in 2025-'28 Two U.S. patents for methods of treating

AS issued in 2016; due to expire in 2035 Orphan drug designation for OV101 for the treatment of AS granted in 2016 MECHANISM OF ACTION DEVELOPMENT PLAN PRECLINICAL DATA INTELLECTUAL PROPERTY INDICATIONS OV101 SEGA For Angelman and Fragile X

Target Neurodevelopment Disorders:

Genetics and Clinical Manifestation Angelman Syndrome Monogenetic trinucleotide repeat disorder in the FMR1 gene Intellectual disability, behavior and language impairments Anxiety and repetitive behaviors No FDA-approved therapies available Current

options limited to physical, communication, behavior and symptomatic therapy Fragile X Syndrome Monogenetic disorder that silences UBE3A gene Developmental delay Impaired motor coordination, seizures/abnormal EEG Sleep and severe speech impairments

Anxiety No FDA-approved therapies available Current options limited to symptomatic and anti-seizure therapies

TONIC INHIBITION CURRENTS Key

mechanism in deciphering excitatory & inhibitory neurological signals correctly Mediated by the -subunit containing GABAA receptors located extrasynaptically Impaired tonic inhibition linked to Angelman and Fragile X syndromes Restoring

tonic inhibition improves common symptoms in animal models Tonic Inhibition is Disrupted in Neurological Disorders Tonic Inhibition 1Olmos-Serrano et al. J. Neurosci. 2010 2Egawa et al. Sci. Trans. Med. 2012 Healthy Fragile X Syndrome (Fmr1 KO)1

100 M Gabazine 100 M Gabazine Healthy Angelman Syndrome (Ube3am-/p+)2

Fragile X Syndrome (FXS) FMRP

Deficiency2 Reduced expression of GAD65/67 Decreased GABA synthesis Decreased GABA release 1Ubiquitin protein ligase E3A (UBE3A) 2Fragile X Mental Retardation Protein (FMRP) Reduced GABA Levels Lead to Loss of Tonic Inhibition in AS and FXS Models

Angelman Syndrome (AS) UBE3A Deficiency1 GAT1 does not get tagged' Increased GAT1 Increased GABA reuptake Decreased Extrasynaptic GABA Levels Decreased Tonic Inhibition

-containing extrasynaptic

GABAA receptor OV101 (Gaboxadol) Distinct Pharmacological Profile We believe OV101 provides differentiated profile over current options Triggers tonic inhibitory signaling Potentiates tonic inhibition at nM concentrations4,5 Activity in the presence

of low GABA concentrations Provides pharmacologic compensation for decreased tonic inhibition in AS/FXS mouse models1,2,3 1Olmos-Serrano et al. J. Neurosci. 2010; 2Egawa et al. Sci. Trans. Med. 2012; 3Olmos-Serrano et al. Dev. Neuro. 2011; 4Meera et

al., J Neurophysiol. 2011; 5 Belelli et al., J. Neurosci.2005

AS OV101 Restored Tonic Inhibition

& Improved Motor Behavior in AS Mouse Model Animal model for AS developed1: UBE3A gene-knockout mouse model Replicates impaired motor function of Angelman Syndrome In AS mouse model, OV1011: Restored tonic inhibition in cerebellar cells Improved

gait and balance on rotarod Decreased clasping reflex 1Egawa et al., Sci. Trans. Med. 2012 Elevated rate of neuronal firing Restored rate of neuronal firing AS AS + OV101 Baseline rate of neuronal firing Control UBE3A deficient Control

FXS OV101 Restored Tonic Inhibition

& Improved Motor Behavior in FXS Mouse Model Fmr1 gene knockout mouse model of FXS: Electrophysiological studies show loss of tonic inhibition in the amygdala Mice are hyperactive, show increased sensitivity to "audiogenic" seizures,

and reduced performance on learning and memory tasks In FXS mouse model, OV1011: Restored tonic inhibition in the amygdala Improved hyperactivity Partially normalized response to startling sounds Improved pre-pulse inhibition (signal-to-noise ratio)

1Olmos-Serrano et al. Dev. Neuro. 2011 Distance (m) * * * * Hyperactivity Fragile X Mouse Velocity (mm/s) *p<0.05 FMR1 KO Wild type Wild type FMR1 KO

SAFETY Lundbeck & Merck

developed gaboxadol for primary insomnia through Phase 3 trials Gaboxadol improved sleep architecture with minimal next day residual effects Over 4,000 adults treated in clinical trials (approximately 950 patient-years of exposure) Well-tolerated in

Phase 2 and 3 insomnia trials Activity was observed on several sleep metrics versus placebo and relative to active control (Ambien) Most common adverse events were headache, nausea, vomiting, somnolence and dizziness Low rate of SAEs observed OV101:

1.3% (2 weeks) and 3.0% (12 months) vs placebo: 0% and 1.0%, over same timeframe Commercial decision not to file NDA after Phase 3 trials were completed in 2007 Overall clinical profile did not support further development OV101 Established Safety

OV101 Clinical Development in

Angelman and Fragile X Syndromes Phase 2 Adult Angelman Syndrome Clinical Trial: A Randomized, Double-Blind, Safety and Efficacy Trial of OV101 Inclusion N=75, age 18-49 years Diagnosis of AS Exclusion Poorly controlled seizures Concomitant disease

that would limit participation Baseline Week 12 Randomization Placebo twice daily OV101 twice daily OV101 once daily 15 mg night, 10 mg day 15 mg night Primary endpoint Incidence of adverse events Exploratory endpoints Clinical Global Impression,

Motor Function, Sleep, Behavior, Quality of Life Phase 1 PK Trial in Adolescent Subjects with AS/FXS n=12 Age: 13-17 years Single dose, open label, PK trial Designed to select dosing for future trials

OV935 Our Approach to Rare Epileptic

Epileptic Encephalopathies Target

rare epileptic disorders typically diagnosed in childhood Commence in adults with a focus to move to adolescent and pediatric patients Potent (nM), highly selective, cholesterol 24-hydroxylase inhibitor (CH24H) Anti-seizure activity across several

epileptic animal models 24HC potentiates NMDA signaling Initiate a Phase 1b/2a trial in patients with Epileptic Encephalopathies including, Dravet syndrome, Lennox-Gastaut syndrome, and Tuberous Sclerosis Complex in 2017 Portfolio of issued U.S. and

international patents directed to composition-of-matter expiring in 2032 MECHANISM OF ACTION DEVELOPMENT PLAN PRECLINICAL DATA INTELLECTUAL PROPERTY INDICATIONS OV935 Novel CH24H Inhibitor for Epileptic Encephalopathies

No FDA-approved therapies available

Seizures tend to be refractory to traditional anti-epileptic treatments 80% have mutated SCN1A gene 1-4% of childhood epilepsies Seizures do not respond well to approved anti-epileptic treatments Some individuals have de novo mutations, including

SCN2A gene 60-90% develop seizures during lifetime Seizures are refractory to traditional anti-epileptic treatments Most cases caused by de novo mutation of TSC1 or TSC2 genes Epileptic Encephalopathies: A Significant Unmet Need Typically diagnosed

early in life Electrographic EEG paroxysmal activity Seizures that are usually multi-form and intractable Cognitive, behavioral and neurological deficits Premature death Dravet Syndrome Lennox Gastaut Syndrome Tuberous Sclerosis Complex

Tissue Slice Slice Tissue CH24H

knock-out Wild type Potential first-in-class CH24H inhibitor, a target for epilepsy Highly selective and potent (nM) Favorable pharmacology CH24H predominantly expressed in brain & has a central role in cholesterol homeostasis Preclinical data

demonstrated that inhibition of brain CH24H reduces glutamatergic signaling via NMDA receptors 1,2,3 Increased excitatory signaling and activation of NMDA receptors has been implicated in a number of neurological disorders, including epilepsy CH24H

Enzyme Inhibition by OV935 Brain Liver Lipoproteins 24-hydroxycholesterol (24HC) Bile Cholesterol Reduced NMDA Receptor Potentiation Decreased Excitatory Signaling Decreased 24HC Levels OV935 An Innovative Approach to Epilepsy 1Sun et al. J

Neurophys. 2016; 2Lisenbardt et al. Neuroph, 2014; 3 Paul et al. J. Neuro, 2013 P<0.05 * 24S-HC Level (ng/ml) ** ** P<0.001 24HC decreased in the absence of CH24H (CYP46A1-/-) NMDA activity decreased in the absence of CH24H (CYP46A1-/-)

OV935 Anti-Epileptic Effects are

Consistent Across Preclinical Models Fring's audiogenic seizure model SCN1A knock-in model of Dravet Syndrome APP/PS1 transgenic mouse model Mouse model of TMEV infection Pentylenetetrazol (PTZ) Kindling model Reduction in audiogenic seizures

Increased temperature threshold for hyperthermia-induced seizures Prolonged overall survival Reduction in seizure severity and duration Reduced PTZ-induced seizure progression MODEL OBSERVED OV935 ACTIVITY

OV935 Shows Encouraging Activity in

Acute Seizure Induction Models Fring's audiogenic seizure model OV935 treatment resulted in a dose-dependent reduction in seizures * p < 0.05 ** p < 0.01 *** p < 0.001 SCN1A+/- knock-in mouse model of Dravet Syndrome

OV935 increased temperature threshold for hyperthermia-induced seizures CRF - Control Food The data has been obtained by RIKEN Brain Science Institute, Neurogenetics laboratory (Lab head; Kazuhiro Yamakawa). Details of the study will be

published by RIKEN 40 42 44 41 43 45 39 OV935 OV935 CRF CRF Scn1a(+/-) Male Scn1a(+/-) Female Febrile seizure threshold ( C)

P < 0.05 P < 0.05 OV935 Shows

Activity in Spontaneous Seizure Models Mouse viral encephalitis (TMEV) inflammation-induced seizure model OV935 reduced total number of seizures and number of stage 4/5 seizures APP/PS1 transgenic mouse model show electrographic seizures, increases

seizure frequency, and mortality OV935 treatment significantly prolonged overall survival in APP/PS1 Model DAYS

TOTAL SEIZURE BURDEN OV935 Delayed

Seizure Development in the PTZ-induced Kindling Mouse Model Mice dosed daily with OV935 demonstrated a significant delay in seizure development Control OV935 10 9 8 7 6 5 4 3 2 1 0 Cumulative seizure score p < 0.01 **

Design Phase 1, randomized, double

blind, placebo controlled, single ascending dose Subjects 48 Dosage 15-1,350mg QD Design Phase 1, randomized, double-blind, placebo controlled, multiple ascending dose Subjects 40 Dosage 100-600mg QD, and 300mg BID; 14 days Design Open-label,

non-randomized Subjects 11 Dosage 50-600mg QD Design Phase 1, randomized, open-label, single dose trial Subjects 9 Dosage 300mg (tab.) QD; 300mg (sol.) QD Safety and tolerability Safety and tolerability Brain CH24H enzyme occupancy using PET

Relative bioavailability (tablet vs. solution); effect of food Four Phase 1 Trials Completed 86 Healthy Subjects Dosed Single doses of up to 1,350mg of OV935 were well tolerated In 14-day MAD trial, doses of 100mg, 300mg and 400mg QD were well