Neumora Therapeutics, Inc. · NASDAQ:NMRA
Neumora Therapeutics — Investor Presentation (June 2026)
41 slides from Neumora Therapeutics's investor presentation, June 2026
Slide 1: Redefining Neuroscience Drug Development
Redefining Neuroscience Drug Development June 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 Neurodegenerative Disease - Novel mechanisms with favorable benefit/risk profiles Heart Disease & - Easy-to-maintain treatments that redu
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 NEURODEGENERATIVE DISEASE NMRA-511 Agitation in Alzheimer’s Disease V1aR Antagonist 7M NMRA-GCASE Parkinson’s Disease GCase Activator
Slide 7: Multiple catalysts expected in 2026 across three core franchises
Multiple catalysts expected in 2026 across three core franchises ANTICIPATED KEY MILESTONES NMRA-511 MAD data 4Q 2026 Neurodegenerative Disease Initiate NMRA-511 Phase 2 study End of 2026 Neuropsychiatric Disease NMRA-898 Phase 1 data 2H 2026 Metabolic Disease Initiate NMRA-215 clinical program End
Slide 8: 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 9: 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 Total population Elevated anxiety (NPI-AA ≥4) (RAID ≥12) • CMAI effect size similar to A
Slide 10: 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 11: 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
Slide 12: Data were consistent in the NPI-AA ≥4 population showing an unsurpassed clinical effect size
Data were consistent in the NPI-AA ≥4 population (matching other NPI-AA ≥ 4 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
Slide 13: With results in the NPI-AA ≥4 population supported by multiple endpoints
With results in the NPI-AA ≥4 population supported by NPI-AA ≥ 4 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
Slide 14: NMRA-511 demonstrated an unsurpassed clinical effect size in patients with elevated anxiety
NMRA-511 demonstrated an unsurpassed clinical effect size in RAID ≥ 12 patients with elevated anxiety CMAI Total Score Change from Baseline Mean Change in CMAI Factor Scores at Week 8 (pre-specified elevated anxiety sub-population) (pre-specified elevated anxiety sub-population) Physically non- Aggr
Slide 15: Unsurpassed clinical effect size in patients with elevated anxiety demonstrated across endpoints
Unsurpassed clinical effect size in patients with elevated anxiety RAID ≥ 12 demonstrated across endpoints CGI-S Agitation NPI Agitation/Aggression (NPI-AA) Change from Baseline Change from Baseline (pre-specified elevated anxiety sub-population) NMRA-511 Placebo (pre-specified elevated anxiety sub-
Slide 16: 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
Slide 17: 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 elevated anxiety 0.51 – 0.64 0.82 – 1.1 0.38
Slide 18: 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
Slide 19: 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 20: 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 21: 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
Slide 22: 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
Slide 23: 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
Slide 24: 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 25: 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 26: 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 27: 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 Kpuu1-4 NMRA-215 Assay Format IC50 • NMRA-
Slide 28: 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
Slide 29: 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 30: 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 31: 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 32: 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 33: 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
Slide 34: 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-
Slide 35: 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
Slide 36: Data supports utility of NMRA-215 across multiple treatment paradigms
Data supports utility of NMRA-215 across multiple treatment paradigms 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 like induction biomarkers NMRA-215 as add-on 2 to a GLP-1 Up t
Slide 37: Appendix
Appendix 37
Slide 38: 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 39: 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
Slide 40: 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 41: © Neumora
© Neumora
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