Neumora Therapeutics, Inc. · NASDAQ:NMRA
Neumora Therapeutics — Investor Presentation (February 2026)
43 slides from Neumora Therapeutics's investor presentation, February 2026
Slide 1: Redefining Neuroscience Drug Development
Redefining Neuroscience Drug Development February 2026
Slide 2: Important Disclosures
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 brin
Slide 3: Our Mission
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 3
Slide 4: Led by experienced company builders and leading neuroscience drug developers
Led by experienced company builders and leading neuroscience drug developers Leadership Board of Directors Paul L. Berns Joshua Pinto, Ph.D. Bill Aurora, Pharm.D. Paul L. Berns Co-Founder, Chief Executive Officer & President Chief Operating & Development Officer Co-Founder, Chief Executive Officer,
Slide 5: Goal to address unmet needs across large markets
Goal to address unmet needs across large markets Biggest Health Disorders Facing U.S.1 Goal To Address Unmet Needs Patients Impacted (M) 0 20 40 60 80 100 120 140 Metabolic Disease Diabetes, Obesity & - Expanded oral treatment options Metabolic Disease - Improved tolerability profile - Novel MoAs wi
Slide 6: Advancing three franchises each anchored by a potential best-in-class program
Advancing three franchises each anchored by a potential best-in-class program PROGRAM INDICATION Preclinical Phase 1 Phase 2 Phase 3 Target/Mechanism U.S. Prevalence METABOLIC DISEASE NMRA-215 Obesity NLRP3 Inhibitor 103M Obesity Undisclosed 103M NEUROGENERATIVE DISEASE NMRA-511 Agitation in Alzheim
Slide 7: Multiple catalysts expected in 2026 across three core franchises
Multiple catalysts expected in 2026 across three core franchises ANTICIPATED KEY MILESTONES Metabolic Disease NMRA-215 biomarker data 3Q 2026 NMRA-215 human weight loss data Year end ‘26 Neurogenerative Disease NMRA-511 MAD extension data Year end ‘26 KOASTAL-2 and -3 topline data (joint readout) 2Q
Slide 8: NMRA-215: differentiated NLRP3 inhibitor for obesity and related metabolic diseases
NMRA-215: differentiated NLRP3 inhibitor for obesity and related metabolic diseases NMRA-215 Target Profile Multiple factors drive NLRP3-mediated inflammation resulting in disease Rationale/Pharmacology IP DRIVERS • Diet (e.g., lipids) • Genetics NLRP3-related inflammatory Composition of matter pate
Slide 9: Obesity represents one of the greatest public health challenges
Obesity represents one of the greatest public health challenges And yet, NLRP3 inhibition By 2030, Significant May address unmet opportunity remains needs 1.13 BILLION people worldwide will be living Approved incretin therapies offer weight NLRP3 inhibition may offer benefit across with obesity1 los
Slide 10: CNS penetrant NLRP3 inhibition provides broad benefit
CNS penetrant NLRP3 inhibition provides broad benefit System Drug Impact Outcome CNS Reduce Reduced appetite and neuroinflammation drive body weight loss in the brain Potential treatment benefits driven by both CNS and Protect organ Reduce the risk of Periphery comorbidities. peripheral and vascular
Slide 11: NMRA-215 has an optimized pharmacological profile including best-in-class CNS exposure
NMRA-215 has an optimized pharmacological profile including best-in-class CNS exposure NMRA-215 is highly potent with low NMRA-215 is NMRA-215 is extensively characterized nM potency across a range of assays highly selective for NLRP3 and optimized for brain exposure Rat Kpuu1-4 NMRA-215 Assay Forma
Slide 12: Doses selected for DIO studies to determine target coverage necessary for weight loss
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 Dose (BID) IC paradigms Target Dose 90 Mi
Slide 13: Monotherapy: Up to 19% weight loss with NMRA-215 with incretin-like induction
Monotherapy: Up to 19% weight loss with NMRA-215 with incretin-like induction Induction Confirming STUDY 1 Pilot Study STUDY 2 Full DIO Study STUDY 3 Study* Body Weight Change (%) Body Weight Change (%) Body Weight Change (%) 5 10 5 5 0 0 -2% -2% 0 -5 -5 -4% -7% -5 -6% -7% -10% -7% -10 -10 -10 -15 -
Slide 14: Combination therapy: Up to 26% weight loss with NMRA-215 + semaglutide
Combination therapy: Up to 26% weight loss with NMRA-215 + semaglutide NMRA-215 + Combined with 3 nmol/kg semaglutide NMRA-215 + Combined with 1 nmol/kg semaglutide Body Weight Change (%) Body Weight Change (%) 10 10 5 5 0 0 - 4% -5 - 4% -5 -6% -10 -10 -15 -12% -17% -15 -20 -21% -18% -20 -25 -26% -3
Slide 15: Class-leading weight loss demonstrated with NMRA-215
Class-leading weight loss demonstrated with NMRA-215 NMRA-215 VTX3232 VENT-02 BGE-102 NT-0796 NMRA-215 monotherapy NLRP3i (end of study) 15%–19% 2% 11% 6% 17% demonstrates best-in-class weight loss semaglutide (end of 17%–19% 12% 21%^ 5% 21% study) NLRP3i (Day 7) 9% / 14% 3% 8% 6% 7% NMRA-215 monoth
Slide 16: NMRA-215 matches semaglutide weight loss with higher-quality outcomes
NMRA-215 matches semaglutide weight loss with higher-quality outcomes Reduced food intake Matches semaglutide weight loss, while preserving equivalent to semaglutide lean mass Cumulative food intake (g) 70 62.65 g 60 54.26 g Fat Mass (% to baseline) Lean Mass (% to baseline) 51.26 g 20 0 50 -1 15 -2
Slide 17: NMRA-215 drove positive results across key biomarkers
NMRA-215 drove positive results across key biomarkers Improved liver health Improved cardiovascular/lipid profile Improved insulin sensitivity similar to semaglutide relative to semaglutide Liver Weight HDL Insulin Tolerance Test 2500 5 1200 equiv. p<0.0001 2000 1000 4 AUC (0-150min) equiv. (mmol/L*
Slide 18: Data supports utility of NMRA-215 as monotherapy and combination therapy
Data supports utility of NMRA-215 as monotherapy and combination therapy Upcoming 12-week DIO data to evaluate maintenance paradigm NMRA-215 as weight loss 1 monotherapy Up to 19% body weight loss with semaglutide- Dose-dependent body weight loss confirmed Preserved lean mass and improved metabolic
Slide 19: Alzheimer's disease agitation represents large market opportunity with significant unmet need
Alzheimer’s disease agitation represents large market opportunity with significant unmet need Alzheimer’s disease agitation is a large and Anxiety is a key underlying driver of growing health burden aggression and irritability in dementia3 Millions currently living with AD; prevalence expected to in
Slide 20: NMRA-511 demonstrated unsurpassed efficacy in patients with AD agitation
NMRA-511 demonstrated unsurpassed efficacy in patients with AD agitation Simplified market segmentation and opportunities NMRA-511 Phase 1b key takeaways Safety • Well tolerated, with potential Mild for higher dosing side-effects Total population Elevated anxiety sub-population • CMAI effect size si
Slide 21: Study to evaluate the effects of NMRA-511 among healthy elderly and adults with agitation
Study to evaluate the effects of NMRA-511 among healthy elderly and adults with agitation associated with dementia due to Alzheimer's disease Part A: 2-Week Evaluation Period Enrolling Part B: 8-Week Evaluation Period Enrolling People Healthy Elderly Participants with Alzheimer’s Disease Agitation (
Slide 22: Demographics and baseline characteristics
Demographics and baseline characteristics Total Population Pre-specified elevated anxiety population NMRA-511 Placebo NMRA-511 Placebo n=40 n=40 n=16 n=21 Mean age 71.8 72.7 66.8 71.6 Sex, n (%) Male 18 (45.0%) 15 (37.5%) 7 (43.8%) 9 (42.9%) Female 22 (55.0%) 25 (62.5%) 9 (56.3%) 12 (57.1%) Race, n
Slide 23: NMRA-511 demonstrated unsurpassed clinical effect size on CMAI total score in patients with elevated anxiety
NMRA-511 demonstrated unsurpassed clinical effect size on CMAI total score in patients with elevated anxiety CMAI Total Score Change from Baseline Mean Change in CMAI Sub-Scores at Week 8 (pre-specified elevated anxiety sub-population) (pre-specified elevated anxiety sub-population) Physically non-
Slide 24: NMRA-511 drove unsurpassed reductions in CGI-S agitation scores
NMRA-511 drove unsurpassed reductions in CGI-S agitation scores in patients with elevated anxiety at baseline CGI-S Agitation Change from Baseline (pre-specified elevated anxiety sub-population) Week 6 Week 8 LSMD (SE) -0.5 (0.2) -0.3 (0.3) Effect size range (Cohen’s d) 0.78 0.38 * NMRA-511 Placebo
Slide 25: Strong clinical effect demonstrated on NPI agitation/aggression domain
Strong clinical effect demonstrated on NPI agitation/aggression domain in patients with elevated anxiety at baseline NPI Agitation/Aggression (NPI-AA) Change from Baseline (pre-specified elevated anxiety sub-population) Week 4 Week 8 LSMD (SE) -0.9 (0.8) -0.8 (0.6) Effect size range (Cohen’s d) 0.42
Slide 26: Favorable tolerability and safety profile demonstrated
Favorable tolerability and safety profile demonstrated NMRA-511 was safe and generally well tolerated • TEAEs were typically mild to moderate in severity TEAEs Incidence Placebo NMRA-511 (≥5% in either treatment group) n=40 n=40 • Low treatment Preferred Terms n (%) n (%) discontinuations due to Nas
Slide 27: NMRA-511 demonstrated consistent unsurpassed efficacy across measures
NMRA-511 demonstrated consistent unsurpassed efficacy across measures CMAI CMAI Total Aggressive CGI-S NMRA-511 in AD agitation NPI Score Behaviors Agitation Score • Well tolerated safety-profile, with potential for higher dosing NMRA-511 elevated anxiety 0.51 – 0.64 0.82 – 1.1 0.38 – 0.78 0.42 – 0.
Slide 28: Pre-clinical neurodegeneration programs each have a strong biological rationale
Pre-clinical neurodegeneration programs each have a strong biological rationale NMRA-CK1δ NMRA-GCASE Focused on inhibiting the protein casein kinase-1δ (CK1δ) to reduce levels Focused on elevating activity of the GCase enzyme, which is encoded by of the pathological form of TDP-43 and slow disease p
Slide 29: MDD represents a major population health challenge
MDD represents a major population health challenge MDD is the leading 280M 21M 30 years cause of disability since a novel mechanism of people worldwide adults in the U.S. have MDD2; the worldwide1 have MDD1 median onset is ~32.5 years of age action was approved for MDD Many people have Many people h
Slide 30: The role of kappa opioid receptor antagonism in MDD
The role of kappa opioid receptor antagonism in MDD navacaprant • The kappa opioid receptor (KOR) / dynorphin system is a well- characterized pathway, and results from preclinical studies support its potential to modulate depression, anhedonia, and anxiety • KOR system overactivation in response to
Slide 31: Near-term clinical development plan focused on MDD with opportunity for further expansion
Near-term clinical development plan focused on MDD with opportunity for further expansion PHASE 3 DEVELOPMENT PROGRAM IN MDD KOASTAL-1 KOASTAL-2 KOASTAL-3 Conducted in U.S. Conducted in U.S., Conducted in U.S. Topline data announced 01/25 Canada and Latin America and Europe Placebo-controlled, doubl
Slide 32: KOASTAL pivotal study design
KOASTAL pivotal study design KOASTAL Pivotal Efficacy Studies Navacaprant 80 mg QD Opportunity R to enroll in 1:1 Placebo QD KOASTAL-LT Randomized, double-blind treatment Baseline WK WK WK WK 1 2 4 6 Key Efficacy Assessments KOASTAL-1, KOASTAL-2, KOASTAL-3 Summary • Adults ages 18 – 65 diagnosed wit
Slide 33: Optimizing KOASTAL-2 and -3 Phase 3 trials
Optimizing KOASTAL-2 and -3 Phase 3 trials Joint topline data readout expected in the second quarter of 2026 Site Selection Medical Monitoring Screening Tools Target Enrollment Adjusted clinical sites Using clinician-rated Verified Clinical Trial Option included in included in studies, with Massachu
Slide 34: M4 PAM franchise: differentiated M4R PAMs for schizophrenia
M4 PAM franchise: differentiated M4R PAMs for schizophrenia M4 Franchise Target Profile Pharmacology IP Neumora has multiple series Composition of matter patent of chemically distinct, highly extending to 2044+* selective M4 muscarinic receptor PAMs, including Epidemiology NMRA-861 and NMRA-898, Est
Slide 35: An optimized muscarinic drug profile would include selectivity and potency in the CNS
An optimized muscarinic drug profile would include selectivity and potency in the CNS Preclinical data and clinical Non-selective muscarinic PAMs offer the benefits of data in acute schizophrenia agents are associated with a greater selectivity supports M4 as a driver of range of peripheral AEs anti
Slide 36: Emraclidine receptor occupancy disconnected from plasma exposures
Emraclidine receptor occupancy disconnected from plasma exposures Receptor Occupancy for Emraclidine in Humans Suggests the Compound has Limited Brain Exposure • In a human PET study, peripheral concentration of emraclidine shows dose linear response • However, CNS receptor occupancy unchanged when
Slide 37: NMRA-861 & NMRA-898 have potential best-in-class potency and optimized brain penetration
NMRA-861 & NMRA-898 have potential best-in-class potency and optimized brain penetration NMRA-8611 NMRA-8981 Emraclidine M4 EC50 6 nM 13 nM 26 nM (human; cAMP)1 NMRA-861 and –898 potentially more potent than emraclidine across multiple assays M4 EC50 2 nM 8 nM 180 nM (human; Ca2+)1 NMRA-861 and –898
Slide 38: SAD/MAD studies evaluating NMRA-861 and NMRA-898 in healthy adults and people with stable schizophrenia
SAD/MAD studies evaluating NMRA-861 and NMRA-898 in healthy adults and people with stable schizophrenia SAD – Part 1 CSP Study Objectives Dose Cohorts Participants Randomization Dose 1, Dose 2, Part 1A Healthy adults 6:2 active:placebo Dose 3, etc. • Confirm once-daily dosing – based on PK profile i
Slide 39: Appendix
Appendix 39
Slide 40: Vasopressin/V1a receptor (V1aR) mediates anxiety-related behaviors
Vasopressin/V1a receptor (V1aR) mediates anxiety-related behaviors Robust preclinical data supports V1aR inhibition V1a antagonists and vasopressin modulate for treating anxiety in rodents anxiety and stress related behaviors in humans • V1a knock-out1 or reduction by siRNA2 drives reduced anxiety b
Slide 41: NMRA-511 reduced anxiety-related behaviors in a preclinical human threat test
NMRA-511 reduced anxiety-related behaviors in a preclinical human threat test Human threat test induces anxiety NMRA-511 reduces behavioral NMRA-511 does not reduce in marmosets1 response to threat locomotor activity 20 40 15 30 ** ** Postures (#) Jumps (#) 10 20 ** 5 10 0 0 V P1 0 0 0 0. 1. 1 1 1 3
Slide 42: NMRA-511 demonstrated clinically meaningful reduction in CMAI total score and CMAI aggression sub-score
NMRA-511 demonstrated clinically meaningful reduction in CMAI total score and CMAI aggression sub-score NMRA-511 demonstrated a 15.7-point reduction in CMAI CMAI aggression sub-score results suggest improvement total score at Week 8 on clinically relevant symptoms of AD agitation CMAI Total Score Ch
Slide 43: © Neumora
© Neumora
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