#1Neumora Pioneering a New Era of Innovation for Brain Disease September 2023#2Important Disclosures This presentation has been prepared by Neumora on a confidential basis and is made for informational purposes only. Any reproduction or distribution of this presentation, in whole or in part, or the disclosure of any of its contents, without the prior consent of Neumora is prohibited. The information set forth herein does not purport to be complete or to contain all relevant information. Statements contained herein are made as of the date of this presentation unless stated otherwise. This presentation contains certain "forward-looking statements" within the meaning of applicable securities laws. These forward-looking statement include, but are not limited to, those regarding the Neumora's strategy, intellectual property matters, Neumora's clinical development plans and timelines, regulatory matters, and market size and opportunity. 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Certain information contained in this presentation and statements made orally during this presentation relate to or are based on studies, publications and other data obtained from third-party sources as well as our own internal estimates and research. While we believe these third-party sources to be reliable as of the date of this presentation, it has not independently verified, and makes no representation as to the adequacy, fairness, accuracy or completeness of, any information obtained from third-party sources. This presentation is made pursuant to Section 5(d) and/or Rule 163B of the Securities Act of 1933, as amended, and is intended solely for investors that are qualified institutional buyers or certain institutional accredited investors solely for the purposes of familiarizing such investors with Neumora Therapeutics, Inc ("Neumora," "we" or "us") and determining whether such investors might have an interest in a securities offering contemplated by Neumora. No such offering is being made at this time. Any such offering of securities will only be made by means of a registration statement (including a prospectus) filed with the U.S. Securities and Exchange Commission (the "SEC"), after such registration statement becomes effective. No such registration statement has been filed, or become effective, as of the date of this communication. This presentation shall not constitute an offer to sell or the solicitation of an offer to buy these securities, nor shall there be any sale of these securities in any state or jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such state or jurisdiction. Confidential 2#3Offering summary Issuer (Exchange / Ticker): Base offering size: Option to purchase additional shares: Price range: Use of proceeds: Bookrunners: Stabilization agent: Expected pricing date: Lock-up: Neumora Therapeutics, Inc. (Nasdaq / NMRA) 14,710,000 shares (100% primary) 2,206,500 shares (15% of base deal, 100% primary) $16.00-$18.00 per share Neumora Therapeutics anticipates to use the net proceeds of this offering, together with its existing cash, cash equivalents and marketable securities, as follows: approximately $395 million to fund the clinical and preclinical development of our current programs; approximately $30 million to fund research and development activities for additional programs; and the remainder for working capital and other general corporate purposes. J.P. Morgan, BofA Securities, Stifel, Guggenheim Securities, RBC Capital Markets, William Blair ● ● ● J.P. Morgan As early as Thursday, Septem 14th, 2023 180 days for the Company, directors, officers, affiliates and substantially all security holders Confidential 3#4Neumora Our Mission We are focused on redefining neuroscience drug development by bringing forward the next generation of novel therapies that offer improved treatment outcomes and quality of life for patients suffering from brain diseases Confidential 4#5Focused on Building the Leading Global Brain Health Company Built at Scale Raised over $600M to date from leading investors Experienced company builders and leading neuroscience drug developers Leading Pipeline Focus on therapeutic candidates with novel MOAS Improve the efficiency of development and potentially increase the odds of clinical success Advancing seven novel programs Near-Term Catalysts Navacaprant entering Phase 3 pivotal studies in MDD in 3Q23 with readout expected in 2H24 NMRA-511 study in Alzheimer's disease agitation expected to initiate in 1H24 NMRA-266 IND submission expected in 4Q23 Advancing preclinical programs for NMRA- NMDA, NMRA-CK16, NMRA-NLRP3 and NMRA-GCASE Confidential 5#6Led by Experienced Company Builders and Leading Neuroscience Drug Developers Leadership Paul Berns Co-Founder and Executive Chairman ARCH PATSIRS ALLOS" ANACOR Abbott -BASF We crescit abbvie PPD Bristol Myers Squibb Joshua Pinto, Ph.D. Chief Financial Officer CREDIT SUISSE Lilly PIPER SANDLER Michael Gold, MD Chief Medical Officer Lori Houle Chief Quality Officer VIR S Dermira SAREPTA Henry Gosebruch Chief Executive Officer abbvie J.P.Morgan ACELYRINA APTINYX Bill Aurora, Pharm.D. Chief Strategy Officer Dermira Neurocrine MERCK AMGEN Nick Brandon, Ph.D. Chief Scientific Officer MERCK Jnana Pfizer AstraZeneca Raj Manchanda, Ph.D. Chief Technical Operations Officer ANOKION FREQUENCY THERAPEUTICS Biogen Carol Suh Chief Operating Officer and Co-Founder ORBITAL ARCH Sana BOUNDLESS BIO Autobahn Rob Lenz, MD, Ph.D. Head of Research & Development AMGEN Abbott Mary Chamberlain- Tharp, Ph.D. Chief Business Officer abbvie Lilly Amy Sullivan SVP, Human Resources. sobi Takeda Shire Blue Chip Investors A ARCH VENTURE PARTNERS ADGVENTURE ADIA CATALIO MUBADALA SoftBank Vision Fund CAPITAL MANAGEMENT INVUS AMGENⓇ ALEXANDRIA. VENTURE INVESTMENTS LOGOS CAPITAL Exor ALTITUDE Life Science Ventures SURVEYOR F/PRIME Newpath polarispartners Confidential 6#7Advancing Our Neuroscience Pipeline • Targeting novel mechanisms across a broad range of neuropsychiatric and neurodegenerative indications Broad pipeline addressing some of the most prevalent brain health disorders • Scaling pipeline through internal discovery efforts and business development activities ● ● Multiple clinical trial initiations planned in 2023/2024 Strong IP with worldwide rights to all programs Pipeline Indications: 60M Total addressable U.S. population 1,2,3 7 Development programs PROGRAM Target/Mechanism Neuropsychiatry Programs Navacaprant (NMRA-140) KOR Antagonist NMRA-511 V1aR Antagonist NMRA-266 M4R Modulator NMRA-CK18 CK18 Inhibitor INDICATION US Prevalence NMRA-NLRP3 NLRP3 Inhibitor NMRA-GCASE GCASE Activator Major Depressive Disorder 21M Bipolar Depression 7M Agitation in Alzheimer's Disease 6M NMRA-NMDA NMDA Modulator Neurodegeneration Programs Schizophrenia 3M Schizophrenia 3M ALS/Alzheimer's Disease 25K/6M Parkinson's Disease 1M Parkinson's Disease 1M 1) National Institute of Mental Health, 2021. 2) National Alliance of Mental Illness, 2017. 3) Figure includes total adressable U.S. population across all neurophsychiatric and neurodegenerative indications Preclinical Phase 1 Phase 2 Phase 3 ANTICIPATED PROGRAM MILESTONES . Initiate KOASTAL-1 (3Q23), KOASTAL-2 (1Q24), KOASTAL-3 (4Q23) and KOASTAL-LT (2H23) Studies Topline data from KOASTAL-1 (2H24) Initiate clinical study in bipolar depression (1H24) Initiate clinical study in Alzheimer's disease agitation (1H24) File IND with the FDA (4Q23) Continue to advance preclinical development Continue to advance preclinical development Continue to advance preclinical development Continue to advance preclinical development Confidential 7#8Navacaprant: KOR Antagonism has Potential for Broad Neuropsychiatric Impact Potential to be first novel mechanism approved in MDD in decades Pharmacologic Profile Selective kappa opioid receptor (KOR) antagonist Greater than 300-fold selectivity of KOR over mu opioid receptor (MOR) and supports 90% receptor occupancy coverage Pathophysiology The KOR/dynorphin system is a well-characterized pathway known to modulate depression, anhedonia, and anxiety - Exposure to stress leads to elevated expression of the KOR ligand dynorphin, resulting in depressive and anxiety-related symptoms Blocking this action via KOR antagonists has antidepressant- and anxiolytic-like effects In animal models, KOR agonists induce depressive and anxiogenic behaviors (including drug-seeking behaviors), whereas KOR antagonists exert antidepressant and anxiolytic effects In humans, KOR agonists induce dysphoric, anxiogenic, and depressive effects Drug Profile Oral, once-daily, 80 mg dose Strong Biological Rationale KOR/dynorph in are important regulators of stress- induced alterations in reward processing, mood states and cognition Strong IP Protection Expect exclusivity through 2041, based on composition of matter protection and estimated patent term extension Dynorphin is released -O in response to stress and activates KOR When KOR is activated, these neurotransmitters are modulated Dopamine GABA KOR Antagonist of KOR Gi . Serotonin Dysregulation of these neurotransmitters can lead to changes in circuits involved in: . Depression. Anhedonia • Anxiety Cognitive impairment NMRA-140 Neuron Glutamate Endogenous pathways Obstructed in disease Drug impact Confidential 8#9Navacaprant: Phase 2a Trial Design Amended by Neumora after Acquisition of BlackThorn Amendments included expanding enrollment criteria to allow patients with moderate-to-severe MDD Inherited from BlackThorn ● Screening & Randomization 1-4 weeks ● Baseline Navacaprant 80 mg QD, n=102 Placebo QD, n=102 Randomized, Double-Blind Treatment WK Key Efficacy - WK 8 4 Assessments Initial Study Inclusion (pre-Neumora) Enrollment focused on mild-to-moderate patients (baseline HAMD-17 range 14-22) Target enrollment of 120 (20 sites) Efficacy assessments at week 4 and week 8 Safety Follow-Up 4 weeks WK 12 MDD Severity Criteria HAMD-17 > 24 HAMD-17 > 23 MADRS > 25 HAMD-17 > 20 Lumateperone MADRS > 24 Phase 3 trials posted to clinicaltrials.gov after Jan 1, 2020, and have been completed or currently enrolling, excludes trials without disclosed criteria Neumora Amended to Fit With MDD Studies Product Candidate SAGE-217 PRAX-114 Aticaprant MD-120 Neumora Amendments to Optimize Trial Increased HAMD-17 inclusion to focus on moderate-to-severe patients (baseline HAMD-17 range 22-30) Increased target enrollment to 204 (40 sites) ● ● 1) Patients with a baseline HAMD-17 total score that received at least one dose of study drug and had at least one post-baseline HAMD-17 assessment 2) Baseline HAMD-17 score >22 Study Endpoints Primary Endpoint: • A from Baseline to WK 8 on the HAMD-17 (depression) NMRA Prespecified Subgroup Analysis of Primary Endpoint • A from Baseline to WK 8 on the HAMD-17 ≥22 at baseline Secondary Endpoints: % of HAMD-17 responders (≥50%) • A from Baseline in SHAPS (anhedonia) • A from Baseline in HAM-A (anxiety) Final Efficacy Population: N=171 patients¹ N=100 moderate-to-severe MDD² ● ● Confidential 9#10Navacaprant: Established Proof-of-Concept for Treatment of Depression and Anhedonia in Patients with Moderate-to-Severe MDD Change From Baseline HAMD-17, LS Mean (SE) 0 -2 CO -10 -12 Week 0 HAMD-17 Week 4 -5.5 -8.5 ALSM = -3.0 P = 0.015 Week 8 -7.1 -9.9 ALSM = -2.8 P = 0.037 Improvement Change From Baseline SHAPS, LS Mean (SE) - Placebo - Navacaprant Note: Graphs depict prespecified statistical sensitivity analysis for moderate-to-severe patients (n=100; baseline HAMD-17 > 22) 0 -2 -4 6 -8 -10 -12 Week 0 SHAPS Week 4 -4.0 -6.4 ALSM = -2.4 P = 0.071 Week 8 -4.4 -9.2 ALSM = -4.8 P = 0.0006 Improvement Confidential 10#11Navacaprant: Demonstrated Efficacy Across Broad Range of Treatment Outcome Measures in Moderate-to-Severe Population Depressive Symptom Improvement HAMD-17 Total Score Change from Baseline HAMD-17 Response Rate % 250% Reduction in HAMD-17 from Baseline Remission HAMD-17 Score ≤7 HAMD-6 Score (Core Symptoms) Change from Baseline in HAMD-6 CGI-I % of Patients with Very Much / Much Improvement CGI-S Change from Baseline Anhedonia Symptom Improvement SHAPS Total Score Change from Baseline Anxiety Symptom Improvement HAM-A Total Score Change from Baseline Functional Improvement SDS Total Score Change from Baseline Note: Prespecified statistical sensitivity analysis for moderate-to-severe patients (HAMD-17 > 22) Week 4 Difference (p-value) -3.0 (0.015) 21.4% (0.010) 14.9% (0.014) -2.4 (<0.001) 12.4% (0.178) ΝΑ -2.4 (0.071) -2.4 (0.035) -2.5 (0.146) Week 8 Difference (p-value) -2.8 (0.037) 25.9% (0.007) 20.3% (0.005) -1.9 (0.013) 19.0% (0.056) -0.5 (0.041) -4.8 (<0.001) -1.6 (0.197) -4.0 (0.013) Confidential 11#12Navacaprant: Well Tolerated with Lower TEAE Incidence Rate Compared to Placebo ● ● ● Navacaprant was well tolerated and demonstrated lower TEAE incidence rate compared to placebo: - Overall discontinuation rates were higher on placebo compared to navacaprant (29% navacaprant and 37% placebo) - Incidence rates of TEAEs were 35% (navacaprant) and 44% (placebo) Discontinuation rates related to TEAEs were higher on placebo compared to navacaprant (1% navacaprant and 12% placebo) The most common (>2%) TEAES in the navacaprant group were mild to moderate in severity Navacaprant was not associated with common side effects of current antidepressant therapies - such as weight gain or sexual dysfunction No evidence of suicidal behavior was identified as assessed the Columbia Suicide Severity Rating Scale Preferred Terms TEAES Incidence (>2% in either treatment group) Placebo n=102 n (%) 5 (4.9) 3 (2.9) 1 (1.0) 3 (2.9) 1 (1.0) Headache COVID-19 Nausea Diarrhea Upper respiratory tract infection Navacaprant n=102 n (%) 5 (4.9) 4 (3.9) 5 (4.9) 2 (2.0) 3 (2.9) Confidential 12#13Pivotal Studies Designed to Evaluate Potential Benefits of Navacaprant Monotherapy in MDD KOASTAL KOASTAL-1: Planned 3Q23 Initiation Placebo-controlled, double-blind RCT evaluating efficacy and safety of navacaprant monotherapy in patients with moderate-to- severe MDD KOASTAL-2: Planned 1Q24 Initiation Placebo-controlled, double-blind RCT evaluating efficacy and safety of navacaprant monotherapy in patients with moderate-to- severe MDD KOASTAL-3: Planned 4Q23 Initiation Placebo-controlled, double-blind RCT evaluating efficacy and safety of navacaprant monotherapy in patients with moderate-to- severe MDD KOASTAL-LT: Planned 2H23 Initiation Open-label extension trial evaluating long- term safety of navacaprant monotherapy in patients with moderate-to-severe MDD Pivotal Efficacy Studies H Screening (up to 4 weeks) Inclusion Criteria: Primary Endpoint: Key Secondary Endpoint: Randomization . (1:1) KOASTAL-1, KOASTAL-2, KOASTAL-3 Summary Baseline WK 1 Navacaprant 80 mg QD Randomized, Double-Blind Treatment WK 2 Adults ages 18-65 diagnosed with MDD MADRS ≥ 25 at baseline A from baseline to Week 6 in MADRS total score Placebo QD A from baseline to Week 6 in SHAPS total score WK 4 Key Efficacy Assessments Other Secondary Endpoints Include: Key Exploratory Endpoints*: ● ● . WK 6 Opportunity to enroll in OLE A from baseline to each timepoint in CGI-S and CGI-I A from baseline to each timepoint in PHQ-9 A from baseline to each timepoint in HAM-A A from baseline to each timepoint in SDS A from baseline to each timepoint in the EQ-5D 5L A from baseline to each timepoint in the WPAI-GH *Safety Assessments include Change in Sexual Functioning Questionnaire (CSFQ-14) CGI-I = Clinical Global Impression-Improvement scale; CGI-S = Clinical Global Impression-Severity scale; EQ-5D 5L = EuroQol-5D 5L; HAM-A = Hamilton Anxiety Rating Scale; MADRS = Montgomery-Åsberg Depression Rating Scale; MDD = major depressive disorder; PHQ-9 = Patient Health Questionnaire-9; QD = once daily; SDS Sheehan Disability Scale; SHAPS = Snaith-Hamilton Pleasure Scale; wk = week; WPAI-GH = Work Productivity and Activity Impairment Questionnaire - General Health. Confidential 13#14Navacaprant: Differentiated Profile Relative to Approved Agents Drives Physician Preference Novel Mechanism Dosing Side Effect Profile Efficacy Degree of preference: High Medium Low Provider Preference Approved Agents Navacaprant Rationale Most KOLs find the ability to target multiple neurological circuits as a key strength of the KORA mechanism and mention anhedonia as a suitable target population. "...This is a viable target receptor; there is a classic column of serotonergic and dopaminergic effects you find in other meds... GABAergic is interesting because it will address anxiety. Glutamatergic can address cognitive impairment, which is also helpful..." Psychiatrist, Academic Center, Europe Once daily dosing of navacaprant provides a competitive advantage relative to recently approved agents which could lead to higher compliance. "... Once daily dosing with no titration is definitely a positive, it's really preferred...a lot of patients forget the second dose, and it's great that it's with or without food..." Psychiatrist, Private Practice #2, U.S. Selectivity profile of navacaprant will enable optimal receptor occupancy that supports a potentially beneficial efficacy/tolerability profile over other approved agents. "... It's very attractive that this profile does not have issues with sexual dysfunction and weight gain, as this can be a huge problem with the standard of care especially in younger patients..." Psychiatrist, Crossover Health, U.S. Navacaprant efficacy is distinguished by treating core symptoms of depression, anhedonia and anxiety. "... This is very promising... the medication apparently has a very good effect on anhedonia which is a core component of depression...so I could see it having widespread use, especially because it is generally a safe treatment..." Psychiatrist, Private Hospital, Europe Most providers prefer navacaprant compared to approved agents due to navacaprant's novel mechanism, superior dosing and side effect profile. Some providers would still use recently launched novel agents in patients who are unwilling to wait two or more weeks for onset. Independent market research, interviews, and analysis conducted by L.E.K. Consulting, March 2023. Confidential 14#15Navacaprant: MDD Market in U.S. Provides Potential Large Blockbuster Opportunity for Differentiated Product with Novel Mechanism of Action MDD Market Represents Large Patient Opportunity 21M Patients Diagnosed in U.S. 50% not on therapy 11M Patients Pharmacologically Treated 1st line 47% 5.2M patients 2nd line 26% 2.8M patients Upside drivers 3rd line 16% 1.8M patients 4th line 11% Navacaprant adjustments: Adoption, Competition, Market Access, Compliance 3-5% Net Penetration (330-550K patients treated) Safer agent drives treatment seeking 1.2M patients Patients fast fail 1st line Neuropsychology Pricing Catalogues GTN discount Rexulti Vraylar Nuplazid Auvelity WAC (per month) $1,419 $1,378 Safer agent drives compliance $4,565 $1,080 -36% Pharmacy Director, Anthem BCBS OH -32% -20% "...is a combo of two products that exist; I would expect a pretty steep discount, for example 50-60% is going to be what it takes ... [navacaprant] is a lower discount since it is a unique MOA...' Executive, Magellan -50% "... 15-25% or up to 30% are reasonable discounts [for navacaprant] a few years after launch, given it's a new MoA as an antidepressant, that's a big benefit..." Inflation adjusted pricing Confidential 15#16Potential for Broad Applicability of Navacaprant Beyond MDD Includes Bipolar Depression Strong Rationale for Efficacy in Bipolar Depression (BPD): ● ● ● Evidence from the navacaprant Phase 2 study and the NIMH- sponsored FASTMAS demonstrate the utility of KOR pharmacology for depression and anhedonia symptoms Anhedonia is a highly prevalent and clinically relevant symptom in BPD, and there is a growing body of research in the pathophysiologic underpinnings of anhedonia in BPD Given that navacaprant studies have demonstrated meaningful improvements in anhedonia symptoms in patients with moderate-to-severe MDD, we believe it may also be effective in treating anhedonia related to BPD The primary endpoint for evaluating efficacy in bipolar depression is MADRS Currently approved therapies (e.g., atypical antipsychotics) have significant limitations Signal-seeking study in patients with BPD enables decision- making on advancing navacaprant to proceed to pivotal program in BPD Stage 1: Signal Seeking Randomization (1:1) Baseline Navacaprant QD Placebo QD Evaluate Effect Size to Inform Next Step Robust Effect Size: Advance Program to Pivotal Studies or Proof of Concept Supportive Effect Size: Advance Program to Proof of Concept Marginal Effect Observed: Stop Program in BPD and consider other LCM opps Stage 2: Proof of Concept (Randomized Double-Blinded Treatment) Confidential 16#17NMRA-511: V1aR Antagonist Broad Potential Across Neuropsychiatric Disorders Pharmacology Antagonist of vasopressin 1a receptor (V1aR), with high selectivity over V1b, V2 (greater than 3,000-fold) and oxytocin receptors (approximately 300-fold) Vasopressin plays a role in the regulation of aggression, affiliation, stress and anxiety response Indication Agitation in Alzheimer's disease Status Conducting Phase 1 Multiple Ascending Dose (MAD) study in human healthy volunteers Drug Profile Oral, once-daily Strong IP Protection Expect exclusivity through 2042+, based on composition of matter protection and estimated patent term extension Strong Biologic Activity Demonstrated NMRA-511 reduced measures of anxiety in an NHP preclinical model, with a corresponding EEG signature in Phase 1 V1aR EXPRESSION HPC-O CeA- ECM -Lateral Neuron cytoplasm septum Expressed in multiple brain regions -BNST -A/LHy V1aR Gq/11 Endogenous pathways Enhanced in disease Drug impact Antagonist of V1aR PLC signaling cascade IP₁ DAG NMRA-511 The vasopressin system acting through V1aR modulates anxiety and threat-related behaviors, aggression and social-emotional processing Increased intracellular Ca2+ PKC PKC activation and translocation to membrane Confidential 17#18NMRA-511 Demonstrates Relevant Pharmacodynamics with the Potential to Address Anxiety Disorders In a human threat test study completed in marmosets, NMRA-511 demonstrated activity in brain circuits that regulate mood and anxiety. An additional EEG study demonstrated that the pharmacodynamic effects of NMRA-511 translated to humans. Change from Baseline (V²) Marmoset Vehicle NMRA-511 Vehicle *p<0.05 vs vehicle mean +/- SD NMRA-511 theta alpha Change from Baseline (uV²) 0.3- 0.2- 0.1- 0.0- -0.1- -0.2 Placebo NMRA-511 Human T Placebo NMRA-511 *p<0.1 vs placebo mean +/- SD theta alpha Interim assessment using effect size in adaptive signal-seeking study provides opportunity to make an informed decision on advancing NMRA-511 program most efficiently Stage 1: Signal Seeking Randomization (1:1) Baseline NMRA-511 QD Placebo QD Evaluate Effect Size to Inform Next Step Robust Effect Size: Advance Program to Pivotal Studies or Proof of Concept Supportive Effect Size: Advance Program to Proof of Concept Marginal Effect Observed: Stop Program 1) Wallace TL. et al, NMRA-511, a novel vasopressin 1a (V1a) receptor antagonist reduces threat behaviors in marmosets and alters EEG power spectra similarly in marmosets and humans. Presented at the American College of Neuropsychopharmacology 2022 Annual Congress. Stage 2: Proof of Concept (Randomized Double-Blinded Treatment) Confidential 18#19NMRA-266: Potentially Differentiated M4R PAM for Schizophrenia Pharmacology Designed as a highly selective positive allosteric modulator (PAM) for the M4 muscarinic receptor for antipsychotic-like efficacy with the potential for improved safety profile with an oral once-daily dosing profile Indication Schizophrenia Epidemiology Estimated 3 million patients in the U.S. with schizophrenia¹ Status Plan to submit IND to FDA in 4Q 2023 Drug Profile Oral, once-daily Strong IP Protection Expect exclusivity through 2042+, based on composition of matter protection and estimated patent term extension 1) Wander, C. Am J Manag Care. 2020;26:S62-S68. Emerging Clinical Activity Muscarinic receptor-targeting compounds have demonstrated potential as an approach to treating schizophrenia Endogenous pathways Enhanced in disease Drug impact Pre-synaptic neuron Synaptic cleft STRIATAL DOPAMINE HYPERACTIVITY Dopaminet receptor In SZ, hyperactivity of striatal dopamine and cortical glutamate contribute to disease pathology O- Dopamine Neurotransmitter Overactive dopamine pathways ACh DA M4R Glu NMRA-M4R Positive allosteric modulator of the M4 muscarinic receptor CORTICOSTRIATAL GLUTAMATE HYPERACTIVITY Glutamate-O Glutamatergic receptor Overactive glutamate pathways Confidential 19#20Profile of NMRA-266 is Comparable to Other M4R Programs M4 EC50 (CAMP) Human t₁/2 Brain:Plasma ratio Selectivity at other M subtypes (EC50) Bioavailability Molecular weight Emraclidine¹ 12 nM M1,3,5> 9-12 h 1:1 ;> 10 μΜ, Μ, 5.8 μΜ Unknown 390.4 KarXT2-4 52 nM 4-5 h 1:10 M₁ 0.3 nM, M₂ 92.5 nM, M3 5 nM <1% due to extensive first pass metabolism 281.4 (xanomeline) NMRA-2665 32 nM Pending Phase 1 Study 1:1[1] Μ1,3,5 > 10 μΜ, Μ, 6.8 μΜ 1. CERE Company data; 2. Heinrich, J.N., et al. Pharmacological comparisons of muscarininc ligands: Historical versus more recent muscarinic M1-preferring agonists. Eur. J. Pharmacology. 605, 53-6(2009). 3. Mirza, Naheed R., et. al., NS drug reviews9, no.2 (2003): 159-186 4. Medina, Aharon, et. al., Hypertension 29, no.3 (1997):828-834. 5. Neumora Company data Note: Data on this slide is presented for illustrative purposes only and the data for emraclidine and KarXT were not derived from Neumora clinical trials or preclinical studies. 67% (predicted) 412.5 Confidential 20#21NMRA-NMDA: Novel Approach for the Treatment of Schizophrenia Pharmacology NMDA receptor hypofunction is a leading hypothesis for the cause of schizophrenia. NMDA positive allosteric modulators (PAMS) can selectively enhance physiological NMDAR function, decrease network hypersynchrony observed in schizophrenia and improve symptoms. Indication Schizophrenia Epidemiology Estimated ~3 million patients in the U.S. with schizophrenia¹ Status Undergoing IND-enabling activities Drug Profile Oral, once-daily Strong IP Protection Expect exclusivity through 2044+, based on composition of matter protection plus potential for patent term extension Strong Biological Rationale Glutamate is the major excitatory neurotransmitter in the brain and dysregulation is believed to be a key driver of schizophrenia Principal neuron Synaptic cleft Post-synaptic neuron SZ PATHOLOGY O GABA Understimulated GABA pathways Pre-synaptic neuron O-Glutamate Hypofunctional NMDAR In SZ, hypofunctional NMDARS cause excitatory/inhibitory imbalance - NMRA-NMDA PAM NMDA receptor- dependent signaling Positive allosteric modulator of NMDAR Dopamine receptor Endogenous pathways Obstructed in disease Drug impact O- Dopamine Overstimulated dopamine pathways Confidential 21#22NMRA-CK18 for Amyotrophic Lateral Sclerosis Pharmacology - Focused on inhibiting the protein casein kinase-16 (CK18) to reduce levels of the pathological form of TDP-43 and slow disease progression in ALS - CK16 also regulates tau biology which may enable indication expansion Epidemiology -5,000 people diagnosed in U.S. each year and ~16,000 patients in U.S. live with ALS at a given time¹ Status Discovery stage; identified compounds demonstrating CK10 selectivity, nanomolar potency, and properties consistent with favorable CNS penetration Strong IP Protection Expect exclusivity through 2043+, based on composition of matter protection plus potential for patent term extension 1) CDC.gov, 2018. Strong Biological Rationale CK18 phosphorylates TDP-43, a key driver of TDP-43-driven pathology in ALS ALS PATHOLOGY Motor neuron Cytoplasm Nucleus CK18 O-ATP TDP-43 NMRA- CK18 Inhibits CK18 to reduce levels of pathological TDP-43 Phosphorylation TDP-43 aggregation can promote neurodegeneration Toxic TDP-43 aggregates Endogenous pathways. Enhanced in disease Drug impact Confidential 22#23Precision strategy for NMRA-CK18 in Amyotrophic Lateral Sclerosis (ALS) incorporates drug specific properties to define potential best responders AALS data set Incorporating machine learning mediated ALS patient clustering from the Answer ALS (AALS) data set with NMRA-CK10 transcriptomic drug signature enriches for subpopulations distinct patient populations Unsupervised clustering of the AALS data set shows patient heterogeneity with little distinction MVAE Unsupervised MVAE Clustering 45 14 Distance 11 Unsupervised Cluster Proximity to NMRA-CK10 drug signature *MVAE: Multimodal Variational Autoencoder NMRA-CK10 induced gene expression change Grouped by biological function Supervised clustering with the NMRA-CK18 drug signature and enhances precision identifying distinct patient groups within the ALS patient population ▬▬▬▬▬▬ CK10 substrate genes 1-statistic (compound effect) AALS data set MVAE 01 DO D.D Knowledge-Based MVAE Clustering 0.5 Characterizing more homogeneous patient populations has the potential to enable more targeted, biomarker driven clinical development plans 10 15 Knowledge Based Cluster M Confidential 20 Distance Proximity to NMRA-CK10 drug signature C 23#24NMRA-NLRP3 for Parkinson's Disease Pharmacology Focused on inhibiting the NLRP3 inflammasome to modulate the immune response in neurodegeneration Indication Parkinson's disease (PD) Epidemiology ~1 million people in the U.S. have PD¹ Status Discovery stage; identified small molecule series showing potency, on-target selectivity & CNS penetrance 1) Yang et al. NPJ Parkinsons Dis. 2020; 6: 15. Strong Biological Rationale NLRP3 inflammasome is activated in microglia in response to disease linked proteins such as a-synuclein,, leading to proinflammatory signaling in neurodegeneration diseases ECM Microglia Toxic a-synuclein aggregates Dysfunctional mitochondria NMRA- NLRP3 mitoROS Inhibits NLRP3 NLRP3 NLRP3 inflammasome complex formation PD PATHOLOGY Neurodegeneration O IL-1B Cleavage Pro-inflammatory cytokine release (e.g., IL-13) Pro IL-13 Endogenous pathways Enhanced in disease <-/● Drug impact Confidential 24#25NMRA-GCase for Parkinson's Disease Pharmacology Focused on elevating activity of the GCase enzyme, which is encoded by the GBA1 gene, and may help to degrade toxic a-synuclein aggregates Indication Parkinson's disease (PD) Epidemiology ~10% of PD patients have GBA mutations, the single largest genetic risk factor for PD¹ Additionally, loss of GCase activity is found in sporadic PD brains² Status Discovery stage; identified small molecule series of activators through a high-throughput screen Selected hits activate WT and mutant enzymes with similar potency Strong Biological Rationale GCase deficiencies lead to lysosomal dysfunction and the accumulation of alpha-synuclein, a hallmark of PD PD PATHOLOGY Dopaminergic neuron Dysfunctional lysosome GCase Increased lysosome function a-synuclein degradation Endogenous pathways Obstructed in disease Enhanced in disease Drug impact Elevates GCase activity In PD, mutant Gcase results in accumulation of a-synuclein 1) Avenali et al. Front. Aging Neurosci., 21 April 2020. 2) Gegg, ME, Schapira, AHV, The role of glucocerebrosidase in Parkinson disease pathogenesis. FEBS J. 2018 Oct;285(19):3591- 3603. doi: 10.1111/febs.14393. Epub 2018 Feb 19. PMID: 29385658. NMRA- GCase Cytoplasm Toxic a-synuclein aggregates ECM Lewy bodies Confidential 25#26Neumora's Precision Medicine Approach Can Be Leveraged to Maximize the Value of Our Programs Challenge: Match Right Drug to the Right Patient ● ● ● How do we gain further confidence in a selected target? How do we identify indications for a given target? How do we identify likely responders / treatment non- responders? Neumora's Precision Toolbox Proprietary analytical capabilities with one petabyte of data onboarded Molecular, Translational, and Clinical Tools (e.g., genomics, proteomics, EEG, Imaging, Digital, Clinical measures) Multimodal Methods (e.g., Al/ML, analytic capabilities) Longitudinal, Multi-modal patient datasets (MDD, schizophrenia, anxiety, ALS, PD, AD) Maximize Value: Improve Probability of Success & Expand Indications ● Gain confidence in target and/or indication • Characterize more homogeneous, targeted patient populations Inform inclusion / exclusion criteria Increase indication expansion opportunities ● • Identify placebo responders • Identify biomarkers ● Neumora applies precision medicine approaches to our programs on an as needed basis in a fit for purpose manner Confidential 26#27Building a Company with the Scale and Scope to Address the Brain Disease Crisis for Patients Company Built at Scale with Differentiated Approach Pipeline of Novel Mechanisms ● ● ● ● ● ● ● ● ● Raised >$600M to date from leading investors and collaborators, including Series B close in Oct. 2022 Led by experienced company builders and leading neuroscience drug developers Precision approach leveraging unique data sciences capability underlying development strategy Strong capital position to support growth with compelling use of proceeds story for proposed offering Strategy supported by long-dated composition of matter patents for each of our programs, into 2041+ Portfolio of seven clinical and preclinical programs targeting novel mechanisms of action, with large therapeutic and commercial potential creating rich set of catalysts Lead program, navacaprant (KOR antagonist) demonstrated positive Phase 2 clinical data and is currently in Phase 3 trials with topline data expected in 2H 2024 Mid-stage clinical program, NMRA-511 (V1aR antagonist) expected to enter AD agitation studies in 1H 2024 IND submission planned for NMRA-266 (M4 PAM) in the fourth quarter of 2023 Deep preclinical pipeline with near-IND assets focused on Parkinson's, ALS and other indications Confidential 27#28Neumora is Poised to Become the Leader in Brain Health with Multiple Catalysts Expected Through 2025 to Drive Value Built at Scale Raised >$600M to date from leading investors with a team of expert company builders and neuroscience drug developers 2023 Navacaprant Initiate KOASTAL-1 Study (3Q23) Initiate KOASTAL-3 Study (4Q23) Initiate KOASTAL-LT (2H23) ● ● NMRA-266 ● IND submission (4Q23) Leading Pipeline Advancing seven programs with NCE therapeutic candidates with novel MOAS in areas of significant unmet need 2024 Navacaprant Initiate KOASTAL-2 Study (1Q24) Topline data readout from KOASTAL-1 study (2H24) Initiate clinical study in bipolar depression (1H24) NMRA-511 Initiate study in agitation in Alzheimer's disease (1H24) Innovative Approach Maximizing the value of our programs to potentially increase the odds of clinical success and expand indications 2025 Navacaprant Data readout from KOASTAL-2 and KOASTAL-3 studies (1H25) ● NDA submission in MDD monotherapy (2025) Confidential 28#29Neumora Appendix Confidential 29#30Differentiated IP Position Includes Composition of Matter Protection with Favorable Expiration Dates Across Programs and Process Protection for Precision Platform Target Neurodegen Neuropsychiatry erative Navacaprant (NMRA-140)(1) KOR Antagonist NMRA-511 V1aR Antagonist NMRA-266(1) M4R PAM NMRA-NMDA NMDA PAM NMRA-CK18 Ck16 Inhibitor NMRA-NLRP3 NLRP3 NMRA-GCASE GCase *All dates are approximate / estimates / projections only PTE = US patent term extension +Estimates do not include PTE Portfolio of Drugs All new chemical entities Composition of matter patents for each program Favorable expiration dates Composition of Matter Patent Status US + Foreign Patents Issued US Patent Issued Foreign Patent Applications Pending US and Foreign Patents Pending Patent Pending Patent Pending Multiple Patents Pending In process Precision Platform AI/ML approach to find higher responding patients High-level, AI/ML process patent protection for Data Processing, Patient Stratification and Target / Drug Discovery + Translation Trade secret protection of underlying details Base Patent Expiration / Patent Expiration with PTE* 2038 / 2041 2038 / 2043 2041 / 2042 Pending (2044+) Pending (2043+) Pending (2043+) Pending (2044+) Biomarkers Approximate higher responding clusters Method of treatment patent protection Cover selecting patients with biomarker and treating with drug/class#31Navacaprant Phase 2 Efficacy Population: Patient Demographics and Baseline Characteristics Similar Across Treatment Groups Demographics Age Sex - n (%) Male Female Ethnicity - n (%) Mean (SD), years Race Hispanic or Latino Not Hispanic or Latino - n (%) White Black/African American Asian American Indian or Alaskan Native Not collected Select Baseline Disease Characteristics BMI - mean (SD), kg/m² HAMD-17 total score - mean (SD) Placebo QD n = 83 Min, max n (%) ≥ 22 > SHAPS total score - mean (SD) Min, max 42.7 (13.4) 25 (30.1) 58 (69.9) 14 (16.9) 69 (83.1) 54 (65.1) 22 (26.5) 6 (7.2) 0 1 (1.2) Navacaprant 80 mg QD n = 88 42.2 (13.3) 26 (29.5) 62 (70.5) 10 (11.4) 78 (88.6) 28.4 (4.7) 22.3 (3.4) 16, 30 47 (56.6) 38.0 (5.7) 27, 56 27.5 (4.8) 21.8 (3.5) 14, 30 53 (60.2) 37.5 (5.8) 28, 55 The Efficacy population includes all randomized subjects who received at least 1 dose of study drug, have a baseline HAMD-17 assessment total score, and have at least 1 valid post-baseline HAMD-17 assessment total score. 54 (61.4) 30 (34.1) 4 (4.5) 0 0 || Confidential 31#32Navacaprant Demonstrated Statistically Significant and Clinically Meaningful Improvements in Depression and Anhedonia Despite Inclusion of Mild Patients Change form baseline HAMD-17, LS Mean (SE) 0 -2 co -10 -12 Week 0 HAMD-17 Primary endpoint Week 4 -5.1 -7.9 ALSM = -2.7 P = 0.003 Week 8 -7.4 -9.0 ALSM = -1.7 P = 0.121 Improvement - Placebo Change form baseline SHAPS, LS Mean (SE) -Navacaprant 0 -2 + 6 CO -10 -12 Week 0 SHAPS Anhedonia scale Week 4 -3.7 -6.5 ALSM = -2.8 P = 0.004 Week 8 -4.4 -7.8 ALSM = -3.4 P = 0.002 Improvement Confidential 32