Important Disclosures This presentation contains forward-looking statements about Neumora Therapeutics, Inc. (the "Company," "we," "us," or "our") within the meaning of the federal securities laws, including statements r

January 2026 Redefining Neuroscience

Drug Development Exhibit 99.1

Important Disclosures This

presentation contains forward-looking statements about Neumora Therapeutics, Inc. (the "Company," "we," "us," or "our") within the meaning of the federal securities laws, including statements related

to: Neumora's intention to redefine neuroscience drug development by bringing forward the next generation of novel therapies that offer improved treatment outcomes and quality of life for patients; the timing, progress and plans for its

therapeutic development programs, including the timing of clinical trial initiation and data readouts and upcoming milestones and catalysts; expectations and projections regarding future operating results and financial performance, including the

sufficiency of its cash resources, intellectual property protection, and expectation of the timing of its cash runway; and other statements identified by words such as "could," "expects," "intends,"

"may," "plans," "potential," "should," "will," "would," or similar expressions and the negatives of those terms. Other than statements of historical facts, all statements

contained in this presentation are forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995. These statements are subject to risks and uncertainties that could cause the

actual results to be materially different from the information expressed or implied by these forward-looking statements, including, among others: the risks related to the inherent uncertainty of clinical drug development and unpredictability and

lengthy process for obtaining regulatory approvals; risks related to the timely initiation and enrollment in our clinical trials; risks related to our reliance on third parties, including contract research organizations; risks related to serious or

undesirable side effects of our therapeutic candidates; risks related to our ability to utilize and protect our intellectual property rights; and other matters that could affect sufficiency of capital resources to fund operations. For a detailed

discussion of the risks and uncertainties that could cause actual results to differ from those expressed in these forward-looking statements, as well as risks relating to Neumora's business in general, please refer to the risk factors

identified in the Company's filings with the Securities and Exchange Commission (SEC), including but not limited to its Quarterly Report on Form 10-Q for the quarter ended September 30, 2025 which was filed with the SEC on November 6, 2025.

Forward-looking statements speak only as of the date hereof, and, except as required by law, Neumora undertakes no obligation to update or revise these forward-looking statements. Our results for the quarter ended September 30, 2025 are also not

necessarily indicative of our operating results for any future periods.

Our Mission We are focused on bringing

forward the next generation of novel therapies with brain-penetrant chemistry that offer improved treatment outcomes and quality of life for patients

Led by experienced company builders

and leading neuroscience drug developers Leadership Paul L. Berns Co-Founder, Chief Executive Officer & Chairman of Board of Directors Bill Aurora, Pharm.D. Chief Operating & Development Officer Joshua Pinto, Ph.D. President Board of

Directors Carol Suh Chief Strategy Officer & Co-Founder Nick Brandon, Ph.D. Chief Scientific Officer Jason Duncan Chief Legal & Administrative Officer Lori Houle Chief Technical Operations & Quality Officer Michael Milligan Chief

Financial Officer Amy Sullivan Chief Human Resources Officer Pablo Gersberg Chief Information Officer Paul L. Berns Co-Founder, Chief Executive Officer, Chairman Kristina Burow Managing Director, ARCH Venture Partners Matthew K. Fust Biotechnology

Advisor Alaa Halawa Executive Director, Mubadala Capital Maykin Ho, Ph.D. Retired Partner, Goldman Sachs David Piacquad Biotechnology Advisor

Goal to address unmet needs across

large markets 1Source: National Institutes of Health (NIH), "Our Biggest Health Challenges," last reviewed January 21, 2025; CDC/NCHS, NHANES 2021-2023; The Lancet Diabetes & Endocrinology Commission, 2025; NIMH, 2025.

*Includes: major depressive disorder, bipolar depression, schizophrenia, generalized anxiety disorder, post traumatic stress disorder, substance use disorder, Alzheimer's disease, Parkinson's disease, attention-deficit hyperactivity disorder Neumora

Focus Area Other Population Health Issue Biggest Health Disorders Facing U.S.1 Patients Impacted (M) Diabetes, Obesity & Metabolic Disease Neuropsychiatry & Neurodegenerative Disease* Infectious Disease Heart Disease & Stroke Traumatic

Brain Injury Cancer 0 20 40 60 80 100 120 140 Goal To Address Unmet Needs Metabolic Disease Expanded oral treatment options Improved tolerability profile Novel MoAs with potential for higher quality weight loss and maintenance Neurogenerative

Disease Improved tolerability and safety, particularly in elderly and high-risk populations Novel MoAs with greater brain penetration/efficacy Easy-to-maintain treatments that reduce caregiver burden Neuropsychiatric Disease Effective treatments

with favorable tolerability profiles Novel MOAs with the potential to treat multiple elements of disease (e.g., depressive symptoms, anhedonia)

PROGRAM Target/Mechanism INDICATION

U.S. Prevalence Preclinical Phase 1 Phase 2 Phase 3 METABOLIC DISEASE NMRA-215 NLRP3 Inhibitor Obesity 103M Undisclosed Obesity 103M NEUROGENERATIVE DISEASE NMRA-511 V1aR Antagonist Agitation in Alzheimer's Disease 7M NMRA-GCASE GCase

Activator Parkinson's Disease 1M NMRA-CK1 CK1 Inhibitor ALS/Parkinson's Disease 25K/1M NEUROPSYCHIATRIC DISEASE Navacaprant KOR Antagonist Major Depressive Disorder 21M NMRA-898 M4 Modulator Schizophrenia 3M NMRA-861 M4

Modulator Schizophrenia 3M Advancing three franchises each anchored by a potential best-in-class program ALS = Amyotrophic lateral sclerosis; CK1 = Casein Kinase I Isoform delta; GCase = Glucocerebrosidase; IP = Intellectual Property; KOR =

kappa opioid receptor; M4 = Muscarinic Acetylcholine Receptor M4; NLRP3 = Nucleotide-binding Domain, Leucine-rich-containing Family, Pyrin Domain-containing-3; V1aR = Vasopressin 1a Receptor; DIO = diet induced obesity mouse model.

ANTICIPATED KEY MILESTONES Metabolic

Disease NMRA-215 biomarker data NMRA-215 human weight loss data Neurogenerative Disease NMRA-511 MAD extension data Neuropsychiatric Disease KOASTAL-2 and -3 topline data (joint readout) Provide M4 franchise update Multiple catalysts expected in

2026 across three core franchises Well capitalized with a cash runway to support operations into 3Q 2027 3Q 2026 Year end 26 Year end 26 2Q 2026 Mid-2026

NMRA-215: differentiated NLRP3

inhibitor for obesity and related metabolic diseases *Excluding any patent term adjustment or extension O'Brian et al. J Neuroinflammation. 2020;17(1):104. 2. Wani K et al. Int J Environ Res Public Health. 2021;18(2):511. 3. World Obesity

Federation. World Obesity Atlas 2024. London: World Obesity Federation, 2024. https://data.worldobesity.org/publications/?cat=22. AdipoGen Life Sciences. https://adipogen.com/inflammasomes/rce Rationale/Pharmacology NLRP3-related inflammatory

response via release of IL-1 , IL-18 and IL-6 cytokines is associated with obesity1,2 Indication Obesity, Parkinson's Disease Target Administration Oral, once-daily IP Composition of matter patent extending to 2043+* Epidemiology ~1.13

billion patients in the world with obesity by 20303 Expected Milestones Progress NMRA-215 into the clinic in 1H 2026 Report biomarker data (hsCRP, IC90) in 3Q 2026 Report human proof-of-concept data around end of 2026 NMRA-215 Target Profile

Multiple factors drive NLRP3-mediated inflammation resulting in disease DRIVERS Diet (e.g., lipids) Environment Genetics Aging NLRP3 Activation DISEASES Neurodegeneration (Parkinson's) Cardio-metabolic (obesity) Monogenic / autoimmune (CAPS)

ASC NLRP3 Caspase-1 NLRP3 inflammasome complex pro-caspase-1 pro-caspase-1 caspase-1 caspase-1 pro-IL-1 IL-1 IL-18 pro-IL-18

Obesity represents one of the greatest

public health challenges 1World Obesity Federation. World Obesity Atlas 2025. London: World Obesity Federation, 2025. https://data.worldobesity.org/publications/world-obesity-atlas-2025-v7.pdf 1.13 BILLION people worldwide will be living with

obesity1 By 2030, $130 - $170 BILLION estimated obesity market size in 2030 Driving a significant market for obesity treatments Significant opportunity remains And yet, NLRP3 inhibition NLRP3 inhibition may offer benefit across monotherapy,

combination therapy and maintenance paradigms: Incretin-like weight loss Increased response rates Better tolerability Convenience with no cold chain storage Lower COGS with oral small molecule Approved incretin therapies offer weight loss, but come

with challenges: Significant AEs, such as nausea, vomiting, constipation and diarrhea High discontinuation rates Weight regain following discontinuation Cold chain storage required Emerging oral treatments produce less weight loss and are burdened

by the same intolerable side effects May address unmet needs

CNS penetrant NLRP3 inhibition

provides broad benefit System Drug Impact Outcome Periphery Protect organ and vascular system from inflammation-related damage CNS Reduce neuroinflammation in the brain Reduced appetite and drive body weight loss Reduce the risk of comorbidities.

Reduces heart disease: improved CV outcomes Improves type II diabetes: reduced insulin resistance in mice Potential treatment benefits driven by both CNS and peripheral inhibition of NLRP3

MDCK permeability: Unknown 14.0

P-gp efflux ratio: Unknown 1.1 NMRA-215 has an optimized pharmacological profile including best-in-class CNS exposure *NT0796 = mouse Kpuu 1Neumora data on file. 2Thornton P, et al. JPET. 2024 Feb 15;388(3):813-826 . 3Ventus Data Presented at 5th

Annual Inflammasome Summit. November 28 - 30, 2023. Boston, MA. 4Ventyx R&D Day Presentation. Published Jan 2023. NMRA-215 is extensively characterized and optimized for brain exposure NMRA-215 is highly selective for NLRP3 NMRA-215 is

highly potent with low nM potency across a range of assays NMRA-215 is highly selective for NLRP3 versus other inflammasomes (NLRP1, NLRC4, AIM2) >250-fold selective for NLRP3 versus a broad panel of targets (Eurofins SafetyScreen87) Clean

profile in cardiac ion channel and kinase screening panels Higher Brain Exposure NMRA-215 Assay Format IC50 THP-1 (IL-1 ) 3 nM Target engagement (Nanobret) 5 nM iMicroglia (IL-1 ) 8 nM Human whole blood (IL-1 ) 16 nM

Doses selected for DIO studies to

determine target coverage necessary for weight loss NMRA-215 dose selection Semaglutide dose selection Goal: Sustained IC90 target coverage for 24 hours Goal: Select two doses that allow for evaluation of different treatment paradigms Dose (BID) IC

Target Dose 90 Mid-Dose 50 Low Dose 20 Ability to evaluate combination and dose sparing effects of NMRA-215 Therapeutic dose: 3 nmol/kg Sub-therapeutic dose (incretin-sparing): 1 nmol/kg Similar dosing paradigm used by other sponsors allows for

comparison across studies NMRA-215 Low Dose NMRA-215 Mid Dose NMRA-215 Target Dose free brain IC90 IC50 IC20 [Total Plasma] (log scale) Target dose drives IC90 in CNS and periphery over 24 hours based on human whole blood assay

Monotherapy: Up to 19% weight loss

with NMRA-215 with incretin-like induction NMRA-215 administered subcutaneously in Studies 1 and 3 and administered orally in Study 2. Semaglutide administered subcutaneously in all studies. In Study 2 beginning on Day 22, mice underwent daily

endpoint collections, including behavioral testing, MRI, and fasting on day 24 to support blood collection Days 25-27. *Study designed to run up to 28 days. Following achievement of study objective confirming incretin-like induction at Day 13, study

was stopped due to injection site irritation, which will not be present in the clinical setting, as NMRA-215 is being developed as an oral therapy. Day Body Weight Change (%) Pilot Study STUDY 1 -2% -10% -16% Day Body Weight Change (%) Induction

Confirming Study* STUDY 3 -18% -2% -7% Day Body Weight Change (%) Full DIO Study STUDY 2 -4% -6% -7% -7% -15% -17% Vehicle NMRA-215 Low Dose NMRA-215 Mid Dose NMRA-215 Target Dose semaglutide 1 nmol/kg semaglutide 3 nmol/kg -19%

Combination therapy: Up to 26%

weight loss with NMRA-215 + semaglutide Day Body Weight Change (%) Combined with 3 nmol/kg semaglutide NMRA-215 + Day Body Weight Change (%) Combined with 1 nmol/kg semaglutide NMRA-215 + -4% -17% -26% -21% -4% -6% -18% -12% Additive weight loss

with therapeutically active incretin dose Vehicle Combination with NMRA-215 Mid Dose semaglutide Combination with NMRA-215 Target Dose Potential for incretin-sparing combination with better tolerability

Combination demonstrates additive

effects of NMRA-215 Class-leading weight loss demonstrated with NMRA-215 NMRA-215 VTX3232 VENT-02 BGE-102 NT-0796 NLRP3i (end of study) 15%-19% 2% 11% 6% 17% semaglutide (end of study) 17%-19% 12% 21%^ 5% 21% NLRP3i (Day 7) 9% / 14%

(Study 2) (Study 3) 3% 8% 6% 7% semaglutide (Day 7) 9% / 14% (Study 2) (Study 3) 9% 15%^ 11% 11% NLRP3i + semaglutide (Day 28) 26% 19% 29%^ 21% 24%# NMRA-215 monotherapy demonstrates best-in-class weight loss NMRA-215 monotherapy matches semaglutide

induction Studies in humanized transgenic obese mice are not directly comparable to other DIO studies ^Ventus semaglutide dose = 10 nmol/kg. #Nodthera combination study semaglutide dose = 5 g/kg. Other market participant data obtained through

company, scientific and Wall Street research publications

NMRA-215 matches semaglutide weight

loss with higher-quality outcomes Neumora data on file. *Unpaired t-test, semaglutide 3 nmol/kg compared with NMRA-215 Target Dose Day Cumulative food intake (g) Reduced food intake equivalent to semaglutide Fat Mass (% to baseline) Vehicle NMRA-215

Target Dose semaglutide 3 nmol/kg Matches semaglutide weight loss, while preserving lean mass Lean Mass (% to baseline) 62.65 g 54.26 g 51.26 g * p<0.05

NMRA-215 drove positive results

across key biomarkers Equiv. = equivalent. Neumora Data on File. Improved liver health similar to semaglutide Improved cardiovascular/lipid profile relative to semaglutide Vehicle NMRA-215 Target Dose semaglutide 3 nmol/kg Cytokine data from 28-day

study available in early 2026 Additional Data Improved insulin sensitivity LDL TC Liver Weight HDL Insulin Tolerance Test equiv. p<0.0001 equiv. equiv. equiv. equiv. p<0.0001

Data supports utility of NMRA-215

as monotherapy and combination therapy Upcoming 12-week DIO data to evaluate maintenance paradigm 1 2 3 NMRA-215 as weight loss monotherapy NMRA-215 as add-on to a GLP-1 NMRA-215 as weight maintenance treatment Up to 19% body weight loss with

semaglutide-like induction Dose-dependent body weight loss confirmed Preserved lean mass and improved metabolic biomarkers Up to 26% body weight loss; additive to semaglutide alone Potential for incretin-sparing combination with better tolerability

Report 12-week DIO mouse data in 1Q26 Initiate clinical program with NMRA-215 in monotherapy and combination settings in 1H 2026 and deliver proof of concept weight loss data around the end of 2026 Next Step

Alzheimer's disease agitation

represents large market opportunity with significant unmet need 1Alzheimer's Association. 2025 Alzheimer's Disease Facts and Figures. Alzheimer's Dementia 2025;21(5). 2Van der Mussele S, et al. Aging Ment Health 2015;19(3):247-257. 3Image from

Alzheimer's Society Alzheimer's disease agitation is a large and growing health burden Millions currently living with AD; prevalence expected to increase as the population ages1 ~7M 13M U.S. Adults with Alzheimer's Disease (M)1

>70% of people with AD experience agitation at some point in their disease2 Anxiety is a key underlying driver of aggression and irritability in dementia3

Significant opportunity for a

product with a differentiated benefit/risk profile For illustrative purposes only. NMRA-511 has not been studied in head-to-head trials against Auvelity or Rexulti, and there are differences in compounds, trial designs and other factors which must

be considered. 1Calculated from data: Addressing Dementia Via Agitation-Centered Evaluation (ADVANCE). https://clinicaltrials.gov/study/NCT03226522?intr=AXS-05&page=1&rank=9&tab=results. 2Lee D, Slomkowski M, Hefting N, et al.

Brexpiprazole for the Treatment of Agitation in Alzheimer Dementia: A Randomized Clinical Trial. JAMA Neurol. 2023;80(12):1307-1316. doi:10.1001/jamaneurol.2023.3810 0.25 Safety Effect size (Cohen's d)1,2,3 Boxed Warning Moderate

side-effects Mild side-effects Simplified market segmentation and opportunities Increased morbidity and mortality Earlier placement in long-term care facilities Reduced quality of life for patients and caregivers Inability to maintain independence

There is an unmet medical need for therapies that reduce agitation with improved tolerability and safety profiles3,4 AD agitation associated with: Standard-of-care treatment options are insufficient: The only currently approved therapy carries a

boxed warning for mortality in elderly people with dementia-related psychosis. 0.35 0.45 Efficacy Unmet need for new treatments

NMRA-511 demonstrates positive

signal in Phase 1b; potential to treat unmet need NMRA-511 Phase 1b key takeaways Well tolerated, with potential for higher dosing CMAI effect size similar to Auvelity in total population Unsurpassed CMAI effect size in patients with elevated

anxiety For illustrative purposes only. NMRA-511 has not been studied in head-to-head trials against Auvelity or Rexulti, and there are differences in compounds, trial designs and other factors which must be considered. 1Calculated from data: