8:55 am Chair’s Opening Remarks
Emerging Assays Which Will Streamline Epigenetic Drug Discovery & Development
9:00 am Evaluating Current Exploration into the Single Cell Space to Precisely Understand Epigenetic Behaviour
Synopsis
- Moving away from messy bulk, invasive analysis assays of millions of cells to better understand disease pathways
- Elevating understanding of epigenetic marks and gene expression by clustering single cell studies into sub-populations
- Increasing pathway specificity with single cell clustering to ensure patient safety
9:30 am Opportunities for non-invasive cancer detection and classification through epigenetic analysis of cell-free DNA
Synopsis
- Exploring novel methods for epigenetic analysis of cell-free DNA
- Utilizing cell-free DNA methylation analysis for non-invasive cancer detection and identifying clinically actionable resistance phenotypes
- Examining the role of epigenetic liquid biopsies in precision oncology in the future
Unveiling Novel Approaches to Epigenetic Therapy
10:00 am Targeting Transcription Factor-BAF Interactions in Cancer
Synopsis
- Understanding how transcription factors make for compelling drug targets, but have been historically hard-to-drug
- Spotlighting transcription factors involvement with the BAF chromatin remodeling complex to open chromatin
- Developing a drug discovery platform to inhibit TF-BAF interactions; the Foghorn approach
10:30 am
Morning Break & Structured Networking
11:00 am Regulating Gene Expression by Targeting Regulatory RNAs: A Novel Therapeutic Approach
Synopsis
- Highlighting regRNAs, non-coding transcripts derived from gene regulatory elements, as key regulators of transcription
- Targeting regRNAs with antisense oligonucleotides (ASO) leads to specific modulation of gene expression
- Unveiling the potential of ASOs targeting regRNAs have to be a novel class of programmable therapeutics for a range of diseases
11:30 am CFT8634, a Potent & Selective Degrader of BRD9 for the Treatment of SMARCB1-perturbed Cancers
Synopsis
- CFT8634 is an orally bioavailable heterobifunctional degrader that induces ubiquitination and degradation of BRD9 by the proteasome.
- CFT8634 promotes potent and selective BRD9 degradation and dosedependent tumor growth inhibition in cell- and patient-derived preclinical SMARCB1-perturbed xenograft models.
- Degradation of BRD9 by CFT8634 offers a promising and novel approach to address this class of difficult-to-treat diseases.
12:00 pm Considering Combinatorial Approaches: Using an Antiviral Prodrug to Target EBV+ Malignancies
Synopsis
- Inducing expression of certain viral kinase genes within the EBV genome using nanatinostat
- Disrupting the DNA replication cycle leading to chain termination and apoptosis
12:30 pm
Lunch & Structured Networking
Spearheading Conversation Around Drug Resistance Across Epigenetic Drug Development
1:30 pm Studying Neuroendocrine Transdifferentiation as a Mechanism of Drug Resistance
Synopsis
- How do mutiple tumors acquire resistance to targeted therapeutics by transdifferentiation?
- Understanding if there is a common epigenetic state in the resulting neuroendocrine tumor type
- Exploring how intratumoral heterogeneity is detected in these tumors
2:00 pm PANEL DISCUSSION: Let’s Talk About Epigenetic Drug Resistance
Synopsis
- Exploring the ways in which drug resistance develops in relation to epigenetics
- Considering epigenetic mechanisms implicit in drug resistance
- Combating drug resistance with epigenetic drugs in combinational therapies
Revising How We Approach Translational Medicine to Enhance Epigenetic Research & Development
2:45 pm Translating Established Targets: Potent anti-Tumor Activity of a KAT6A/KAT6B Inhibitor PF-9363/CTx-648 in KAT6A dysregulated ER+ Breast Cancer
Synopsis
- Understanding molecular dysregulation of KAT6A has been observed in several cancers, including amplifications in breast, lung, ovarian cancer along with oncogenic fusions in AML
- Examining CTx-648 (PF-9363), a first-in-class potent KAT6A/KAT6B inhibitor that possess high selectivity versus other MYST family members (KAT7, KAT5, KAT8)
- Learn how CTx-648 (PF-9363) inhibits expression of ESR1 expression leading to potent antitumor activity in ER+ breast cancer models