Bright Minds Biosciences Inc. · CSE:DRUG
Bright Minds Biosciences — Corporate Update (November 2025)
35 slides from Bright Minds Biosciences's corporate update, Nov 6, 2025
Slide 1: Announcement of Prader-Willi Syndrome Program
Announcement of Prader-Willi Syndrome Program November 6, 2025
Slide 2: Disclaimer and Cautionary Note regarding Forward Looking Statements
Disclaimer and Cautionary Note regarding Forward Looking Statements This corporate presentation (this “Presentation”) of Bright Minds Biosciences Inc. (the “Company”) is (viii) the ability to protect intellectual property rights throughout the world; (ix) market viability for current as of November
Slide 3: Event speakers
Event speakers Bright Minds Bio Participants Key Opinion Leaders Jennifer Miller, MD Dr. Miller is a Professor in the division of pediatric endocrinology at the University of Florida . She graduated with Ian McDonald her M.D. from the University of Florida in 1998, and her M.S. in Clinical Investiga
Slide 4: Topic, Themes, Speaker, Timing
Topic Themes Speaker Timing • Corporate update Introduction Ian McDonald 5 min • Announcement of new BMB-105 program Overview of • Clinical presentation (overview) Jennifer Miller 10 min Prader-Willi • Unmet need in PWS: not only hyperphagia, but also behavioral issues. Syndrome • Major neurobehavio
Slide 5: Prader-Willi Syndrome Targeting Serotonin
Prader-Willi Syndrome Targeting Serotonin Ian McDonald Chief Executive Officer Bright Minds Biosciences
Slide 6: Creating New Chemical Entities That Target Serotonin Signaling
Creating New Chemical Entities That Target Serotonin Signaling Key 5-HT2 Receptors Targets 5-HT2C 5-HT2A/2C 5-HT2A Agonists Agonists Agonists Epilepsy, Depression, Depression, PTSD Impulsivity control, Anxiety, Pain, Hyperphagia Migraine Serotonin (5-HT) is the most prominent neurotransmitter in the
Slide 7: Update on BREAKTHROUGH Ph.2a study
Update on BREAKTHROUGH Ph.2a study Absence Seizures and Developmental and Epileptic Encephalopathies BREAKTHROUGH study is ongoing in Absence Seizures and Developmental and Epileptic Encephalopathies. • To date, BMB-101 has been well tolerated, with no drug-related Serious Adverse Events nor any saf
Slide 8: Initiation of Prader-Willi Clinical Program
Initiation of Prader-Willi Clinical Program • Bright Minds has initiated clinical development of BMB-105, 5-HT2C agonist specifically for Prader-Willi patients • BMB will initiate Phase 2a – Proof-of-Pharmacology program in Prader Willi Syndrome with BMB-101 to pave the way forward for a pivotal stu
Slide 9: BMB-105 development plan in PWS
BMB-105 development plan in PWS BMB-101 Clinical Studies – Phase 2a – PoPh in PWS patients NOVA (Neuro-Obesity Validated Advancement) A Randomized, Double-Blind, Placebo-Controlled Phase 2 Study to Assess Efficacy, Safety and Tolerability of BMB-101 Oral Solution for the Treatment of Patients with P
Slide 10: PWS is a complex neurodevelopmental and neurobehavioral disorder with limited treatment options
PWS is a complex neurodevelopmental and neurobehavioral disorder with limited and insufficient treatment options Energy balance Neuropsychiatric symptoms Obesity Compulsion Cognitive impairment Glutides Hyperphagia Sleep Disturbances Self-injury Vykat Feeding problems Aggression Epilepsy Anxiety AED
Slide 11: Current treatments do not address the majority of PWS complex symptoms
Current treatments do not address the majority of PWS complex symptoms Need for a therapy which can address the entire complex Energy balance Neuropsychiatric symptoms Obesity Compulsion Cognitive impairment Glutides Sleep Disturbances Self-injury Feeding problems Aggression Epilepsy Anxiety SSRIs P
Slide 12: Prader-Willi Syndrome 5-HT2C mechanism of action
Prader-Willi Syndrome 5-HT2C mechanism of action Jan Torleif Pedersen, MSc PhD Chief Scientific Officer Bright Minds Biosciences
Slide 13: PWS is a complex neurodevelopmental and neurobehavioral disorder
PWS is a complex neurodevelopmental and neurobehavioral disorder Hyperphagia Serotonin pathway Obesity Feeding problems Executive functions: Compulsion cognitive and behavioural issues Sleep Disturbances Aggression Cognitive impairment Reward system: hyperphagia Self-injury Anxiety Epilepsy Satiety
Slide 14: Genetics of PWS is linked to 5-HT2C receptor
Genetics of PWS is linked to 5-HT2C receptor Genetic variants lead to heterozygous 5-HT2CR loss of function • About 50-74% of cases occur when part of the father's chromosome 15 is deleted. In 25-36% of cases, the affected person has two copies of the maternal chromosome 15 from the mother and lacks
Slide 15: 5-HT2C agonism directly targets underlying pathophysiology of PWS
5-HT2C agonism directly targets underlying pathophysiology of PWS • 5-HT2C receptors are Apex regulators of the neuroendocrine axis. • 5-HT2C+ neurons project to hypothalamic melanocortin neurons to suppress food intake and thereby directly regulating satiety and appetite. • 5-HT2C receptors are als
Slide 16: Loss of 5-HT2C receptor function leads to obesity and maladaptive behavior
Loss of 5-HT2C receptor function in humans leads to obesity and maladaptive behavior • Sporadic loss-of- function variants leads to obesity and maladaptive behaviour in humans • Sporadic loss-of- function variants lead to partial loss of 5-HT2C receptor tonus. • Phenotype is similar to that observed
Slide 17: 5-HT2C receptor is a key regulator of compulsive behavior and food intake
5-HT2C receptor is a key regulator of compulsive behavior and food intake Learnings from 5-HT2C KO mice • Increased locomotor behaviour • Over-eating • Pre-diabetic • Attenuated contextual fear phenotype response • Compulsive (OCD-like) behaviour Nebuka et al, Behav Brain Res. 2020 Feb 3:379:112394.
Slide 18: BMB 5-HT2C agonists dose-dependently reduce binge eating episodes in rats
BMB 5-HT2C agonists dose-dependently reduce binge eating episodes in rats Reduced binge eating episodes Reduced body weight in rat models in binge eating rat models V 3mg/kg V 10mg/kg V 30mg/kg V 3 10 30 NASDAQ: DRUG | BRIGHTMINDSBIO.COM 18
Slide 19: BMB 5-HT2C agonist reduces aggression in rat resident intruder model
BMB 5-HT2C agonist reduces aggression in rat resident intruder model Resident intruder attacks 90 80 % Reduction in attack duration 70 60 50 40 30 20 10 0 10 mg/kg 15 mg/kg 25 mg/kg NASDAQ: DRUG | BRIGHTMINDSBIO.COM 19
Slide 20: BMB 5-HT2C agonist improves spatial learning and memory in tau transgenic mice
BMB 5-HT2C agonist improves spatial learning and memory in tau transgenic mice (Radial arm water maze) 1 Training day Testing day 8 2 Errors 7 3 6 4 5 Start arm BMB-101 protects PS19 P301L tau mice mice from cognitive impairment in the radial arm water maze. Mice were tested in 5 blocks of three tri
Slide 21: BMB 5-HT2C agonist reverses compulsive behavior
BMB 5-HT2C agonist reverses compulsive behavior • BMB-101 dose-dependently suppressed fentanyl • SB242084 (5-HT2C antagonist) reversed the self infusions. suppression of intake induced by 20 mg/kg, • BMB-101 dose-dependently reduces the number • No full reversal when BMB-101 was administered of acti
Slide 22: BMB 5-HT2C agonists demonstrate preclinical efficacy across all key PWS symptom domains
BMB 5-HT2C agonists demonstrate preclinical efficacy across all key PWS symptom domains Hyperphagia Reduces binge eating and weight loss in rat model Reduces aggressive behaviors in resident intruder Aggression mice model Protects mice from cognitive impairment Cognitive improvements in the radial a
Slide 23: Clinical POC study in PWS: Efficacy with non-selective 5-HT2C agonist
Clinical POC study in PWS: Efficacy with non-selective 5-HT2C agonist Results with fenfluramine • Decreased weight • Decreased food related behaviour • Decreased aggressive behaviours • Parents and patients frequently reported Study design pronounced qualitative changes. Some parents reported that t
Slide 24: Potential for best-in-class 5-HT2C agonist directly targeting pathophysiology in PWS
Potential for best-in-class 5-HT2C agonist directly targeting pathophysiology in PWS Clinical • Previously approved as weight loss drugs (lorcaserin and fenfluramine) 5-HT2C • Fenfluramine reduced hyperphagia and improved behaviors in a pilot clinical agonists trial in PWS Efficacy in multiple anima
Slide 25: BMB-101 NOVA Prader-Willi Syndrome
NOVA BMB-101 (Neuro-Obesity Validated Advancement) Novel 5-HT2C Selective Agonist Prader-Willi Syndrome Ph.2a clinical trial Stephen Collins, MD, PhD Chief Medical Officer Bright Minds Biosciences
Slide 26: BMB-101 – highly selective 5-HT2C agonist with excellent druggable qualities
BMB-101 – highly selective 5-HT2C agonist with excellent druggable qualities BMB-101 – selective 5-HT2C agonist, and Gq-protein biased to avoid desensitization and tolerance Well-tolerated in Phase 1 clinical trials, no SAEs, AEs were experienced at 2.5 or above predicted therapeutic dose, so enjoys
Slide 27: NOVA: BMB-101 Phase 2a for Prader-Willi Syndrome
NOVA: BMB-101 Phase 2a for Prader-Willi Syndrome Proof-of-Pharmacology study to demonstrate that 5-HT2C agonism will address symptom complex in PWS patients Eating behaviours PWS HQ-CT (Hyperphagia) As measured by instruments well accepted in the the PWS research Set of behavioural community and sym
Slide 28: NOVA: BMB-101 Phase 2a for Prader-Willi Syndrome
NOVA: BMB-101 Phase 2a for Prader-Willi Syndrome A Randomized, Double-Blind, Placebo-Controlled Phase 2 Study to Assess Efficacy, Safety and Tolerability of BMB-101 Oral Solution for the Treatment of Patients with Prader-Willi Syndrome Endpoints: • Hyperphagia scores (HQ-CT, CGI-S, CaGI-S) • Placebo
Slide 29: NOVA PWS study design
NOVA (Neuro-Obesity Validated Advancement) PWS study design Dose increase if drug Weight-based dosing is well tolerated Endpoints: • Hyperphagia scores (HQ-CT, CGI-S, CaGI-S) • Behaviors (PWS Profile) • Change in body weight • Safety endpoints Placebo-controlled 1:1 N=16 Multi-center study * Visit 1
Slide 30: BMB-105 Prader-Willi Syndrome Market Potential
BMB-105 Prader-Willi Syndrome Novel 5-HT2C Selective Agonist Market Potential Ian McDonald Chief Executive Officer, Director Bright Minds Biosciences
Slide 31: Novel mechanism for Prader Willi Syndrome
Novel mechanism for Prader Willi Syndrome Carbetocin ARD-101 BMB-10x Vykat (Soleno) (Acadia) (Aardvark) GLP-1 agonists Targeting hyperphagia ✓ ✓ ✓ ✓ ? Targeting behavioural ✓ x ✓ x x issues Targeting cognitive issues ✓ x x x x Twice daily-once Twice/once daily Intranasal Dosing (projected) Once dail
Slide 32: Attractive biologic rationale
Attractive biologic rationale Directly targeting PWS pathophysiology • Genetic link, preclinical and clinical evidence supports potential for tageting the PWS symptom complex with 5-HT2C agonism • Demonstrated tolerability and safety in Phase 1 clinical trial • Hyperpahgia and Behavioral endpoints s
Slide 33: With only two drugs approved there is significant market opportunity
With only two drugs approved there is significant market opportunity 1/15 000 births1 ~$4.6bn 10,000 – 20,000 U.S. market PWS patients in U.S.2 size ~400,000 Based on the annual price cases worldwide of approved therapy3 Additional research needed to assign a product-specific peak sales estimate Ref
Slide 34: Pipeline
Pipeline Rich and diverse portfolio in neurology and psychiatry with multiple programs Lead Indications Research Phase 1 Phase 2 5-HT2C agonists BMB-101 DEE Clinical Studies – Phase 2 Absence seizures BMB-101 Prader-Willi Syndrome Clinical Studies – Phase 2a - PoPh BMB-105 Prader-Willi Syndrome Clin
Slide 35: Q&A session
Announcement of Prader-Willi Syndrome Program Q&A session
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