9:00 am Registration & Coffee

10:00 am Chair’s Opening Remarks

Targeting the PI3K Pathway: New Insights & Overcoming Key Challenges Associated with PI3K Inhibitors

10:05 am Co-Targeting PIM Kinase and PI3K/mTOR- A Promising Treatment Strategy by AUM302

Synopsis

• Delve into the main reasons for exploring combination therapies in targeting the PI3K Pathway i.e., reducing toxicity, overcoming resistance mechanisms, and improving potency of PI3K inhibitors
• Gain key insights into what combination therapies show promise
• Investigate the challenges and setbacks in developing successful combination therapies

10:35 am Gilead Case Study: Bringing the First PI3K-δ Inhibitor to the Market

Synopsis

• Gilead’s Idelalisib was the first PI3K delta inhibitor to gain approval from the FDA in selected hematological malignancies in 2014
• Revisit the key clinical trial data leading to approval, use in the clinic along with lessons learnt, how the safety profile can be potentially optimized and some possible future directions

11:05 am Morning Refreshments & Virtual Speed Networking

Targeting the PI3K Pathway- Preclinical, Translation & Clinical Advances

12:00 pm Selective Targeting of PI3Kδ for the Treatment of Solid Tumors: Immune Mediated & Direct Anti-Cancer Activity

Synopsis

• IOA-244 is a novel PI3Kδ inhibitor with a unique binding mode, conferring an excellent safety profile
• IOA-244 is in clinical development for the treatment of solid tumors burdened by an immune suppressive TME and characterised by high PI3Kδ expression
• The potential of IOA-244 is also being exploring as a safer PI3Kδ inhibitor for the treatment of hematological malignancies

12:30 pm TGB-β Mediated Epithelial to Mesenchymal Transformation (EMT) through PI3K

  • Andrew Brown Director Biomedical Research Strategy and Architecture, ZS Bio

Synopsis

• Computational and Experimental Approaches to Elucidate Biomarkers
in the Process of EMT and Metastasis
• Artificial Intelligence Based Therapeutic Design
• Machine Learning Models and Prognostic Indicators

1:00 pm PI3K Inhibitors for the Treatment of Venous and Lymphatic Malformations via Topical Formulations

Synopsis

• Many cutaneous VMs and LMs are driven by mutations in PI3K or its upstream driver, TIE2
• Venthera are currently developing a topical PI3K inhibitor in order to safely and effectively treat these lesions at their source

1:30 pm Targeted PI3K-hyperactivation in B-cell Malignancies

  • Markus Müschen, MD-PhD Arthur H. and Isabel Bunker Professor of Hematology
    Director, Center of Molecular and Cellular Oncology , Yale University

Synopsis

• 25% of all cancers are driven by PI3K-activating lesions, but B-cell malignancies are exempt
• The vast majority of newly formed B-cells express autoreactive antibodies and are removed through a mechanism termed “negative B-cell selection”, based on excessive activation of PI3K-signaling
• We propose to leverage “negative B-cell selection” by pharmacological PI3K-hyperactivation to overcome drug-resistance in refractory B-cell malignancies, including B-ALL, mantle cell lymphoma and CLL
• Discuss preliminary data supporting a rationale for PI3K-hyperactivating agents

2:00 pm Lunch & Networking

3:00 pm Panel Discussion: Making PI3K Inhibitors Work in the Clinic

  • Bart Vanhaesebroeck Professor of Cell Signaling, University College London 
  • Sathish Padi Assistant Professor (In Residence), Department of Molecular Biology and Biophysics, UConn Health
  • George Poulogiannis Team Leader, Signaling & Cancer Metabolism, The Institute of Cancer Research
  • Zoe Johnson Chief Scientific Officer, iOnctura

Synopsis

• Developing effective combination strategies
• Targeting beyond the PI3K pathway
• Disease specific resistance mechanisms
• Isoform specific vs Pan PI3K inhibitors in mitigating resistance

3:30 pm The Unexpected Function & Location of PIK3Cδ

Synopsis

• PIK3Cδ is mainly described to be expressed in myeloid/lymphoid cells
• We identified PIK3Cδ in fibroblasts derived from triple negative breast cancer patients
• Overexpression of PIK3Cδ drives fibroblast mediated cancer cell invasion
• In vivo, overall survival is markedly worse when levels of PIK3Cδ were high in cancer fibroblasts

4:00 pm Chair’s Closing Remarks

4:05 pm Scientific Poster Session

5:00 pm Close of Day 1