Conference Agenda

All Times Below - EST

08:30 am | Registration & Coffee

9:15 am Chair’s Opening Remarks

Keynote: Seizing the Histidine Phosphorylation Opportunity

9:30 am Will Histidine Phosphorylation Make a Good Drug Target?


  • Overcoming difficulties of studying labile phosphorylations to widen the therapeutic targeting of kinases and with non-canonical phosphorylations
  • Harnessing novel tools to study the functions behind histidine phosphorylation in normal and cancer cells, and the possibility for reversible post-translational modification for cell regulation
  • Discussing the prospects for targeting histidine phosphorylation therapeutically with small molecules

10:30 am | Structured Networking

Interrogating Cutting-Edge Technologies to Identify Novel Targets and Weaponize Against Existing Resistance

11:00 am An Approach for Identifying Protein Kinases That Phosphorylate All Identified Phosphorylation Sites


  • Describing an oriented peptide library approach for identifying amino acid preference at sites N-terminal and C-terminal of phosphorylated residues
  • Providing a software developed to utilize this information to predict kinases responsible for every identified phosphorylation site in a cell line or tissue
  • Applying this software to determine the selectivity of protein kinase inhibitors for their assumed target in cells or tissues

11:30 am Using Machine Learning-Based Approaches for the Discovery of Novel Kinase Inhibitors & Targeting Strategies


  • Explaining DeepCure’s AI approach to hit finding in drug discovery
  • Harnessing AI to discover novel kinase inhibitors and targeting strategies for maximal specificity
  • Evaluating the application of ML-based methods across the drug discovery pipeline to inform future drug development

12:00pm | Lunch & Networking

Advancing Development with the Next Generation of Selective Kinase Inhibitor Targets

1:00 pm Utilizing PROTACs to Degrade Kinases with Increased Selectivity, Improved Efficacy or PK/PD Disconnect Using Multiple Examples


  • Highlighting the advantages of using a degrader vs. catalytic site inhibitors and determining high specificity to minimize off-target effects
  • Optimizing the linkers and E3 ligand for maximal binding, optimize residency time and improving the durability of kinase inhibitor therapeutics
  • Discovering and characterizing a highly cooperative FAK-GSK215-VHL ternary complex

1:30 pm Characterizing the Structural & Functional Aspects of the Phosphatase Enzymes for Drug Development


  • Describing the disease relevance of members of the phosphatase family to inform indication-specific target selection
  • Providing a historical view to approaches towards targeted modulation of phosphatases to foster learnings going into future R&D
  • Grasping modern approaches towards phosphatase modulators using nonorthosteric mechanisms-of-action

2:00 pm Harnessing Multikinase Inhibitors to Weaponize the Next Generation Against Multiple Cancer Indications


  • Discussing the potential to treat multiple cancer indications by targeting multiple MOAs with multi-kinases
  • Introducing narazaciclib (ON123300) – discussing its unique MOA, targeting properties and safety profile through preclinical studies
  • Outlining phase 1 study results to date and the future clinical development pathway of narazacliclib

2:30 pm | Afternoon Refreshments

Leveraging Kinase Inhibitor Case Studies to Supercharge Further Target Selection to Supercharge Future R&D

3:00 pm Revealing IRAK1/4 as an Emerging Target to Override Adaptive Resistance Heme Malignancies


  • Reviewing IRAK1/4 signal transduction in cancer cells to inform future development
  • Clarifying the involvement of IRAK1/4 kinase signaling in the development of adaptive resistance
  • Identifying activated forms of IRAK4 in MDS/AML patients to inform effective drug selection

4:00 pm Enhancing Tyrosine Kinase Inhibitor Success in NSCLC Through Maximizing Potent Activity Against Exon20 Insertion (Ex20ins) Mutations with a Novel, Oral EGFR Inhibitor


  • Developing an EGFR inhibitor that targets Ex20ins mutations with high potency while sparing the WT EGFR activity
  • Overcoming toxicities related to inhibition of wild-type EGFR, including rash and diarrhea, which can compromise the use of EGFR Ins20 inhibitors
  • Presenting the latest clinical data from Cullinan’s phase 2a study with the selective candidate, CLN-081

4:30 pm Phenocopying IRAK1/4 Inhibition With R289 and Its Translation Into The Clinic Using a prodrug of R835 to inhibit IRAK1/4: R289

  • Vadim Markovtsov Executive Director, Translational Biology, Rigel Pharmaceuticals


  • Selectively inhibiting inflammatory innate immune signalling to tissue damage signals (PAMPs/DAMPs/IL-1 family of cytokines) in cells, animals and whole blood assays
  • Profoundly inhibiting inflammatory cytokine production induced by i.v. dosed LPS in healthy volunteers with R835
  • Phase 1 results position R289 attractively with respect to its translational PK/PD data

5:00 pm Chairman’s Closing Remarks & Close of Day 1