•‘Core Biologist’ for a small molecule tumor immune evasion target focused on selectivelyinducing tumor cell Type I IFN. Coordinated all in vitro and in vivo biology work for the project(MOA, potency, PK/PD/efficacy relationships, patient selection & biomarker/Project Optimusstrategies) from project conception to nominating a development candidate that was presented toand approved by the CSO and CMO• Project Lead for a second tumor immune evasion target focused on sensitizing tumor cells toextrinsic apoptosis ligands like TRAIL and TNFα. Responsible for overseeing work betweendepartments (~20 internal project team members) and at CROs. Team successfully identified apotential best-in-class strategy for this target focused on modulating compound stability• Management of 2 direct reports, with a focus on identifying and executing on novel tumorimmune evasion drug targets (such as inducing tumor cells to express Type I IFNs)• Conceived of and performed initial generation of CD8 T/NK cell : Tumor cell co-culture assays,which were utilized in the above two projects and modified by other project teams for theirprograms. Some of this co-culture work was published via a collaboration with the Dave Barbielab at DFCI on targeting TREX1• Member of the Tango Therapeutics collaboration team, helping to drive collaboration strategyaround identifying novel tumor cell immune evasion targets through Crispr screens• Assisted with diligence on two external assets, including presentations to the CSO and CMO

I lead the Translational Immunology and Immunopharmacology team for Adaptive Cellular Immunopharmacology. My team, consisting of 4 direct reports and myself, is focused on interrogating how Compass' drugs modulate in vitro T cell biology to help inform decisions on which molecules become drug candidates. We also perform IND enabling studies and write non clinical study reports for review by the FDA, such as for CTX-471. To do this work, we utilize industry standard T cell assays as well as custom-designed assays to look at T cell activation, signaling, tumor cell killing, proliferation, and release of Treg-mediated suppression.

In the immune education/cell therapy division I work on undisclosed immuno-oncology based cellular therapies (e.g., CAR-T / rTCR-T) against cancer. In my position, I routinely isolate primary human immune cells, expand them in vitro, manipulate them with lentivirus transduction or mRNA electroporation if needed, and then test their ability to be activated by and kill tumor cells. The majority of these assays utilize FACS/flow cytometry as the readout.Additionally, I was responsible for building the target cell lines and designing the assays used to measure the immune cell functions. These target cell lines and assays are now in use by multiple members of my and other teams at Agenus.

My Postdoctoral research fellowship is focused on studying an enigmatic subset of T cells called NKT cells. We identified microbe-derived lipids that activate NKT cells in vitro and are studying these cell populations in vivo (including human PBMCs and mouse organs). This work required us to develop methods of extracting lipids from microbes, purifying individual lipid species by HPLC and TLC, and then performing biological readout assays including isolation and ex vivo expansion of human and mouse T cells, intracellular flow cytometry, RT-PCR, qPCR, cell phenoytyping by FACS, ELISAs, flow-based killing assays, and ELISPOTs.

I have a joint appointment at Harvard Medical School as a research fellow. Both appointments are done in the lab of Michael Brenner, where I work on NKT cells.

My dissertation research was focused on MHC class I antigen presentation of proteins derived from Listeria monoctyogenes. Importantly, our work highlighted the fact that mammalian cells can tell when a protein comes from an exogenous source (such as from an intracellular pathogen) instead of host cell ribosomes. This work was published in two manuscripts (see below). For this project, I used PCR and cloning to designed recombinant Listeria that expressed and secreted chimeric proteins into the cytosol of infected host cells. Through western blotting and flow cytometry, we measured parameters such as the secretion/degradation rate of the chimeric proteins and the kinetics of surface peptide-MHC Class I production. Through careful measurement of those parameters, we calculated the economics of peptide-MHC Class I production from Listeria-derived proteins and found that peptide-MHC Class I complex formation was much more efficient than when the chimeric protein was expressed by host cell ribosomes. We also infected mice with recombinant Listeria and measured T cell responses to both the bacterium and the recombinant protein, including challenge studies with heterologous pathogens such as vaccinia virus and influenza virus.