CONFERENCE DAY TWO
FEBRUARY 19, 2025
7.30 am One-on-One PartneringTM portal meeting schedule starts, to sit down with key contacts up to 90 minutes before day two starts.
9:00 am Chair’s Opening Remarks
Section Two: How do we see Non-Hallucinogenic Psychedelics Impacting Disease Outcomes?
9:10 am Can You Separate the Hallucinogenic Effects from the Efficacy of Psychedelics
Synopsis
- Contextualizing the significant clinical interest generated in the last 50 years on the therapeutic benefit of psychedelics for psychiatric disorders
- Discussing major strides in the expansion of the clinical therapeutic findings with those molecules, as well as in the understanding of the biological effects responsible for their therapeutic benefit
- Reviewing the clinical and preclinical findings based on the mind-altering effects of psychedelics, their therapeutic benefits, and the relationship between those two
9:30 am Development of Non-Hallucinogenic Neuroplastogens Targeting 5-HT2A for the Treatment of Psychiatric Disorders
Synopsis
- Highlighting the profound therapeutic efficacy of psychedelics across numerous preclinical studies and clinical trials in psychiatry and neurology, and the commercialization involved in scaling access to psychedelic medicines.
- Describing the rational design and optimization of both hallucinogenic and nonhallucinogenic 5-HT2A agonists for clinical development.
- Discussing Psylo’s pipeline of novel neuroplastogens and the identification of development candidate PSYLO-1001
9:50 am Speed Networking:
Synopsis
This is a “speed dating” style networking, to maximize opportunity to meet everyone with time to still follow up. This session is not designed for long-form conversations, but to put faces to names with everyone before the conference ends. Ensure you’ve met with all your peers across biotech, pharma, and investors in a quick-fire format, 5 minutes per round!
10.45 am Morning Break & One-on-One Networking
11:40 am Medicine Just got a Digital Upgrade: Software-enhanced Drugs™
Synopsis
- Analyzing how prescription digital therapeutics can broaden access to neuropsychiatric care and improve clinical outcomes
- Highlighting the value of software-enhanced drug™treatments in bridging gaps in care and safely treating neuropsychiatric diseases
- Sharing how SE formulations of pharmaceuticals and biologics will impact the future standard of care
12:00 pm Effectively & Efficiently Structuring Deal Processes as Small Neuroscience Companies
Synopsis
- Discussing the panel’s experience executing and performing due diligence across neuroscience deals
- Sharing expectations for robust data packages and approaching partnerships
- Outlining opportunities for creative deal structures, and when and where they would be appropriate
12.30 pm Lunch Break & One-on-One Networking
Section Three: Patient Stratification & Mitigation of the Placebo Response to Support Clinical Outcomes
1:40 pm The Use of Biomarkers in Clinical Trials for Patient Stratification, & Supporting Key Efficacy & Safety Outcomes
Synopsis
- Sharing biomarker-driven enriched patient enrollment and/or clinical data
- Discussing biomarker-supported product differentiation of clinical efficacy and safety
- Reviewing pharmacoeconomics and biomarker-aided pricing and reimbursement strategies, specifically
Section Four: Neuroimmunology Target Biology Opportunities to Link Aggregation to Inflammation
2:00 pm IGFBPL1-Fusion Proteins: A Multi-targeted Approach for Retina that Promotes Neuroprotection & Mitigates Neuroinflammation
Synopsis
- Introducing IGFBPL1 and its interactions with two validated neuroscience targets: SORT1 and DCC/Netrin-1 receptor
- Discussing IGFBPL1-fusion proteins as first-in-class therapeutics being developed for glaucoma, Dry-AMD/GA, and other optic neuropathies, exhibiting both direct neuroprotective and anti-inflammatory pharmacologies
- Sharing IGFBPL1-based platform and its significant opportunity in neurodegenerative disorders of the brain
2:20 pm Impeding the Neurotoxic Cascade to Reduce Inflammation & Achieve Efficacy
Synopsis
- Inhibiting neurotoxic aggregating proteins overexpressed in chronic or acute neurodegeneration to reverse the toxic cascade that leads to inflammation, nerve cell death, and loss of function
- Discuss how removing several neurotoxic aggregating proteins that can induce the toxic cascade – Abeta, tau, alpha-synuclein, and TDP43 – has a larger effect size than only removing one.
- Discussing Annovis’ phase 2/3 AD study and phase 3 PD study that show by lowering the levels of neurotoxic aggregating proteins, cognitive function is improved in AD and motor function is improved in PD
2:40 pm Are we Seeing Inflammation because of Aggregation of Protein?
Synopsis
- Discussing targets considered efficacious in non-neuro settings and how they are translating into neuroscience
- The role of the immune system in the CNS specifically, and how this impacts future treatment landscapes and disease
- Within the components of neuroinflammation, where might future deals lie?