Neumora Therapeutics, Inc. · NASDAQ:NMRA

Neumora Therapeutics — Investor Presentation (August 2026)

37 slides from Neumora Therapeutics's investor presentation, August 2026

  1. Slide 1: Redefining Neuroscience Drug Development

    Redefining Neuroscience Drug Development August 2026

  2. 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

  3. 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

  4. 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, Ch

  5. 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 Cardiometabolic Disease Diabetes, Obesity & Metabolic Disease - Expanded oral treatment options - Improved tolerability profile Heart Dis

  6. 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 EXPECTED CATALYSTS Target/Mechanism U.S. Prevalence CARDIOMETABOLIC DISEASE Obesity / Cardiometabolic NMRA-215 Disease • Submit IND (4Q 2026) NLRP3 Inhibitor • Initia

  7. Slide 7: NMRA-215: differentiated NLRP3 inhibitor for obesity and cardiometabolic diseases

    NMRA-215: differentiated NLRP3 inhibitor for obesity and cardiometabolic 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 patent

  8. Slide 8: 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

  9. Slide 9: NMRA-215 has an optimized pharmacological profile including CNS exposure

    NMRA-215 has an optimized pharmacological profile including 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 Kpuu, brain1-4 NMRA-215 Assay Format IC50

  10. Slide 10: DIO data supports utility of NMRA-215 across multiple treatment paradigms

    DIO data supports utility of NMRA-215 across multiple treatment paradigms Combination Mechanism of Monotherapy Therapy Action Switch • Up to 19% weight loss with • Up to 26% weight loss when • Sustained weight loss following incretin-like induction combined with therapeutically active switch from se

  11. Slide 11: 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 class-leading weight loss semaglutide (end of 17%–19% 12% 21%^ 5% 21% study) NLRP3i (Day 7) 9% / 14% 3% 8% 6% 7% NMRA-215 monoth

  12. Slide 12: Totality of NMRA-215 non-clinical data support advancing to clinical studies

    Totality of NMRA-215 non-clinical data support advancing to clinical studies Study Study Outcome Study Supportive of Further Development GLP 28-Day Dog Toxicity Study ✓ ✓ DOGS GLP 3-Month Dog Toxicity Study ✓ ✓ GLP 28-Day Rat Toxicity Study ✓ ✓ RATS GLP 3-Month Unexpected adverse findings For-cause

  13. Slide 13: 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

  14. Slide 14: NMRA-511 has potential as a treatment for AD agitation

    NMRA-511 has potential as a treatment for AD agitation Simplified market segmentation and opportunities NMRA-511 Phase 1b key takeaways Safety • Well tolerated, with potential Mild for higher dosing side-effects NMRA-511 Ph. 1b data • CMAI effect size similar to Auvelity in total population Moderate

  15. Slide 15: 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 (

  16. Slide 16: Data consistent in the NPI-AA ≥4 population showing unsurpassed clinical effect size

    Data were consistent in the NPI-AA ≥4 population (matching other sponsors enrollment) showing an unsurpassed clinical effect size CMAI Total Score CMAI Factor Scores Change from Baseline Mean Change at Week 8 (modified analysis set, NPI-AA ≥4) (modified analysis set, NPI-AA ≥4) CMAI Total Score Chan

  17. Slide 17: Results in the NPI-AA ≥4 population supported by multiple endpoints

    With results in the NPI-AA ≥4 population supported by multiple endpoints CGI-S Agitation NPI Agitation/Aggression Domain Change from Baseline Change from Baseline (modified analysis set, NPI-AA ≥4) (modified analysis set, NPI-AA ≥4) * NMRA-511 Placebo NMRA-511 Placebo Week 6 Week 8 Week 4 Week 8 LSM

  18. Slide 18: Favorable tolerability and safety profile of NMRA-511

    Favorable tolerability and safety profile of NMRA-511 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 Naso

  19. Slide 19: NMRA-511 demonstrated consistent unsurpassed efficacy across measures and populations

    NMRA-511 demonstrated consistent unsurpassed efficacy across measures and populations 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 total population 0.32 – 0.34 0.50 – 0.51 0.46

  20. Slide 20: 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 designed for Epidemiology antipsychotic-like effic

  21. Slide 21: 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

  22. Slide 22: 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

  23. Slide 23: NMRA-898 has potential best-in-class potency and optimized brain penetration

    NMRA-898 has potential best-in-class potency and optimized brain penetration NMRA-8981 Emraclidine M4 EC50 13 nM 26 nM (human; cAMP)1 NMRA-898 is potentially more potent than emraclidine across multiple assays M4 EC50 8 nM 180 nM (human; Ca2+)1 NMRA–898 is selective for M4 over Selectivity at other

  24. Slide 24: Promising Phase 1 clinical results single ascending dose study

    Promising Phase 1 clinical results single ascending dose study Exposures support program On-target changes in heart rate advancement measures Phase 1 SAD PK Profile Phase 1 SAD Heart Rate Changes (healthy adults) (healthy adults) Exposures were dose proportional with low variability and Exposure-dep

  25. Slide 25: MAD study evaluating NMRA-898 in healthy adults and people with stable schizophrenia

    MAD study evaluating NMRA-898 in healthy adults and people with stable schizophrenia MAD – Part 2 CSP Study Objectives Dose Participants Randomization • Evaluate tolerable Cohort 1 Dose to be determined Healthy adults doses in people with stable schizophrenia Cohort 2 Dose to be determined Healthy a

  26. Slide 26: Appendix

    Appendix 26

  27. Slide 27: Doses selected for DIO mouse studies to determine target coverage necessary for weight loss

    Doses selected for DIO mouse 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

  28. Slide 28: 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 -

  29. Slide 29: 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

  30. Slide 30: 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

  31. Slide 31: 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*

  32. Slide 32: Sustained weight loss following switching from semaglutide to NMRA-215

    Sustained weight loss following switching from semaglutide to NMRA-215 12-Week DIO Data Full MoA Switch Key Takeaway % Change in Body Weight (Vehicle Adjusted) NMRA-215 demonstrated 4 sustained, semaglutide-like weight loss at 12 weeks following a 2 switch from semaglutide 0 -0% monotherapy to NMRA-

  33. Slide 33: NMRA-215 offers maintenance of weight loss

    NMRA-215 offers maintenance of weight loss 12-Week DIO Data Combination → NLRP3 maintenance Key Takeaway % Change in Body Weight (Vehicle Adjusted) Following switch from semaglutide 5 and NMRA-215 combination to NMRA-215 monotherapy at week 0 -0% 8, DIO mice maintained weight loss similar to mice wh

  34. Slide 34: 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

  35. Slide 35: 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 threat2 locomotor activity2 20 40 15 30 ** ** Postures (#) Jumps (#) 10 20 ** 5 10 0 0 V P1 0 0 0 0. 1. 1 1 1

  36. Slide 36: Demographics and baseline characteristics

    Demographics and baseline characteristics Total Population Pre-specified elevated anxiety population3 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

  37. Slide 37: © Neumora

    © Neumora

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